Search

Sulfur mustard (SM) is a chemical warfare agent that increases oxidative stress in veterans. The literature assessing oxidant/antioxidant parameters in SM-exposed veterans contains conflicting results. A total of 11 relevant studies were identified and screened. Data were extracted, and effect size and heterogeneity were assessed. The analysis revealed significant elevations in levels of malondialdehyde (MDA, an indicator of lipid peroxidation), catalase (CAT), and a reduction in glutathione (GSH) following SM exposure while superoxide dismutase (SOD) and total antioxidant levels did not change. The meta-analysis revealed that the MDA and CAT levels significantly increased in the two post-exposure sampling times (15-20 and 21-33 years) except for theGSH level, which decreased only in the post-exposure sampling time of 21-33 years. The subgroup meta-analysis of the type of analyzed samples indicated that SOD and CAT levels were only increased in the serum/plasma samples, while GSH was decreased. BALF/sputum and erythrocyte samples also revealed significant increases in MDA and SOD levels while GSH level was significantly decreased. This meta-analysis concluded that SM exposure affects the balance between oxidants and antioxidants, promoting oxidative stress that may persist long after exposure. This condition highlights the need for strategies to enhance antioxidant defenses in SM-exposed veterans., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025 Elsevier B.V. All rights reserved.)

BACKGROUND The aim of this study was to identify the changes in the levels of total oxidant status (TOS) and total antioxidant status (TAS) in gingival crevicular fluid (GCF) samples of patients treated with conventional brackets (CBs) and clear aligners (CAs) over a 30-day period. MATERIAL AND METHODS Thirty-four patients who received non-extraction treatment with either CBs or CAs were included in the study. GCF samples were obtained at baseline (T0) and on days 7 (T1) and 30 (T2) following initial phase of treatment. Clinical periodontal parameters were used to determine periodontal conditions of patients. ELISA method was used to determine TAS and TOS levels in GCF samples. RESULTS In the group treated with CAs, TOS levels in GCF were significantly high at T1 but approached T0 after the first month (T2) of treatment. In contrast, the group treated with CBs showed significantly high TOS levels in GCF at both T1 and T2 compared with T0. No significant changes were observed in GCF TAS data at T1 and T2 in either group (CA and CB), compared with T0. When comparing TOS data between the groups at T1 and T2, the CA group had lower TOS levels than the CB group (Mann-Whitney U with Bonferroni correction). Additionally, the CA group had lower periodontal clinical indexes than did the CB group. CONCLUSIONS Oxidative tissue damage during orthodontic teeth movements may be lower with CA treatment. In cases in which higher oxidative stress is anticipated, CA treatment may be preferred over CB treatment.

Background: Thiol/disulphide homeostasis (TDH) has a critical role in many cellular activities such as antioxidant protection. Alterations of oxidative stress in the transition period play an important role in development of some diseases and disorders in dairy cows., Objectives: The purpose of this study is to assess the total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), total thiol, native thiol, disulphide and lipid profile in Simmental and Montofon dairy cows (aged 2-3) before and after calving., Methods: Blood samples were collected 233-280 days of pregnancy and the 30 days of post-partum. Serum total thiol, native thiol and disulphide levels were determined as well as TAS, TOS and paraoxonase-1 (PON-1) levels were measured using colorimetric assays. Triglycerides (TG), total cholesterol, HDL cholesterol and LDL cholesterol levels were measured with an automatic analyser., Results: Total thiol (p = 0.038) and disulphide (p = 0.015) levels were higher after calving compare to pregnancy in Montofon. TAS was found lower (p < 0.001), and OSI was higher in both breeds (Montofon p = 0.012, Simmental p = 0.028) after calving than in pregnancy. When compared between pregnancy and after calving levels in the same breed, HDL was found to be higher after calving (p < 0.001) and TG was lower after calving (p = 0.020) in Montofon. PON (p = 0.090), HDL (p < 0.001) and cholesterol levels were found higher (p < 0.001) and TG level was lower (p < 0.001) after calving in Simmental., Conclusions: According to our results, we observed different responses between two breeds before and after calving. There are few studies about TDH in animal research, and this is the first study in the literature that evaluates the TDH along with oxidative stress and lipid profiles in dairy cows in the periparturient and post-partum period., (© 2024 The Author(s). Veterinary Medicine and Science published by John Wiley & Sons Ltd.)

Fuchs endothelial corneal dystrophy (FECD) stands as the most prevalent primary corneal endothelial dystrophy worldwide, posing a significant risk to corneal homeostasis and clarity. Corneal endothelial cells exhibit susceptibility to oxidative stress, suggesting a nuanced relationship between oxidant-antioxidant imbalance and FECD pathogenesis, irrespective of FECD genotype. Given the constrained availability of corneal transplants, exploration into non-surgical interventions becomes crucial. This encompasses traditional antioxidants, small molecule compounds, biologics, and diverse non-drug therapies, such as gene-related therapy, hydrogen therapy and near infrared light therapy. This review concentrates on elucidating the mechanisms behind oxidant-antioxidant imbalance and the evolution of strategies to restore oxidant-antioxidant balance in FECD. It provides a comprehensive overview of both conventional and emerging therapeutic approaches, offering valuable insights for the advancement of non-surgical treatment modalities. The findings herein might establish a robust foundation for future research and the therapeutic strategy of FECD., Competing Interests: Declaration of competing interest The authors have no financial/non-financial competing interest., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

An actin binding protein, gelsolin (GSN) has two isoforms, plasma (pGSN) and cytosolic (cGSN). Changes in pGSN and/or cGSN levels have been shown to be associated with the pathogenesis of several diseases. The aim of this study was to evaluate changes in intracellular and extracellular GSNlevels with HIF-1 in animals exposed to chronic sustained hypoxia (CSH), in addition to apoptosis and the cellular redox status. The rats in the Sham group were exposed to 21% O 2 , and the rats in the hypoxia groups were exposed to 13 and 10% O 2 , respectively. Plasma pGSN, HIF-1α, Total Antioxidant Status (TAS) and Total Oxidant Status (TOS), and lung tissue pGSN, HIF-1α, TAS, TOS, GSN levels, and apoptotic cell numbers were measured. HIF-1α levels were found to increase significantly in the tissue, especially in the group with severe hypoxia, both in biochemical and histological examinations. pGSN levels were also significantly decreased in both plasma and tissue. Significant increases in tissue were observed in cGSN. It was observed that while the antioxidant activity was dominant in the tissue, the oxidant activity was dominant in the plasma. In particular, the response to hypoxia regulated by HIF-1 is very important for cellular survival. The results of this study showed that the increase in cGSN and TAS levels in the lung tissue together with HIF-1α can be considered as the activation of mechanisms for cellular protection., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Several recent studies have attempted to understand how fasting has benefits for body health, especially the nervous system. To evaluate the impact of intermittent fasting on body weight, brain neurotransmitters, brain oxidative stress, and brain-derived neurotrophic factor (BDNF) in several areas of the brain, this study was conducted in rats. Thirty male Wistar rats were randomly divided into two groups. Group 1 (15 rats) served as the control and group 2 (15 rats) underwent intermittent fasting (IF; 24 h) for 1, 7, or 15 days. The findings demonstrated that intermittent fasting significantly reduced body weight. In this sense, brain monoamines and amino acids, namely dopamine, glutamate, aspartate, and oxidative stress markers (malondialdehyde and nitric oxide), decreased significantly after 1 day of IF. However, norepinephrine, serotonin, gamma-amino butyric acid, and glycine increased significantly. Additionally, glutathione levels were markedly elevated in IF. Surprisingly, the neuromodulatory effect of intermittent fasting fluctuates depending on the IF period. To support this fluctuation, BDNF levels increased after 1 day in the hippocampus and decreased after 15 days of intermittent fasting in all areas of the brain tested. In conclusion, our results show that intermittent fasting has beneficial influences on the brain; however, prolonged intermittent fasting can also induce some unfavorable physiological outcomes that prevent optimal neurological function., (© 2024. The Author(s).)

Background and Objective: Damage to the hippocampus leads to increased anxiety, memory problems, and learning disabilities. Melatonin (MLT), a hormone secreted by the pineal gland, serves as an antioxidant and provides defense against nerve damage. Omega-3 (ω3) is known for improving brain function. This study aims to examine the impact of melatonin and omega-3, both individually and in combination, on cognitive function, histological changes, and the balance between oxidants and antioxidants in male rats with injuries to the dorsal CA1 hippocampus., Material and Methods: Five rat groups (n = 8) were examined. The sham group was given normal saline via intraperitoneal (ip) and gavage routes. After a local lesion in the hippocampus, the lesion group underwent the same treatment. The MLT group was given melatonin (10 mg/kg, ip), the ω3 group was provided with omega-3 (0.8 g/kg, gavage), and the MLT + ω3 group received both treatments. Injections were administered every other day for 10 days. On the 11th day, behavioral assessments were conducted, and then pyramidal cells were quantified using image analysis software. Serum samples were assessed for levels of oxidants and antioxidants., Results: The results from the open field test indicated a significant increase in distance moved in the Lesion + MLT + ω3 group compared to the lesion group (P < 0.05). Performance in the novel object recognition test showed improvement in the ω3 and MLT + ω3 treated groups compared to the lesion group (P < 0.05). Additionally, social interaction duration notably increased in the ω3, MLT, and MLT + ω3 treated groups compared to the lesion group. The number of degenerated cells in the CA1, CA2, and CA3 areas of the lesion group significantly increased compared to the sham group, but melatonin and omega-3 notably reduced this number (P < 0.05). The serum levels of the antioxidant enzymes,include superoxide dismutase, glutathione peroxidase, and catalase in the lesion group notably changed compared to the sham group, but omega-3 effectively restored them to control levels., Conclusion: According to increase in distance moved, memory function, learning and social interactions of the animal in the behavioral results and the reduction of degenerate cells in the histological results, it can be said that these effects may be part of the neuroprotective effects of melatonin and omega-3. The increase in levels of antioxidant enzymes, particularly omega-3, indicates their promise as therapeutic agents for reducing oxidative stress-induced damage in neurological disorders., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Epilepsy is a disorder characterized by a predisposition to generate seizures. Levetiracetam (LEV) is an antiseizure drug that has demonstrated oxidant-antioxidant effects during the early stages of epilepsy in several animal models. However, the effect of LEV on oxidant-antioxidant activity during long-term epilepsy has not been studied. Therefore, the objective of the present study was to determine the effects of LEV on the concentrations of five antioxidant enzymes and on the levels of four oxidant stress markers in the hippocampus of rats with temporal lobe epilepsy at 5.7 months after status epilepticus (SE). The results revealed that superoxide dismutase (SOD) activity was significantly greater in the epileptic group (EPI) than in the control (CTRL), CTRL + LEV and EPI + LEV groups. No significant differences were found among the groups' oxidant markers. However, the ratios of SOD/hydrogen peroxide (H 2 O 2 ), SOD/glutathione peroxidase (GPx) and SOD/GPx + catalase (CAT) were greater in the EPI group than in the CTRL and EPI + LEV groups. Additionally, there was a positive correlation between SOD activity and GPx activity in the EPI + LEV group. LEV-mediated modulation of the antioxidant system appears to be time dependent; at 5.7 months after SE, the role of LEV may be as a stabilizer of the redox state.

Cyclophosphamide (CTX) is the most commonly used effective alkylating drug in cancer treatment, but its use is restricted because its toxic side effect causes testicular toxicity. CTX disrupts the tissue redox and antioxidant balance and the resulting tissue damage causes oxidative stress. In our study based on this problem, kefir against CTX-induced oxidative stress and testicular toxicity were investigated. Rats were divided into 6 groups: control, 150 mg/kg CTX, 5 and 10 mg/kg kefir, 5 and 10 mg/kg kefir + 150 CTX. While the fermented kefirs were mixed and given to the rats for 12 days, CTX was given as a single dose on the 12th day of the experiment. Testis was scored according to spermatid density, giant cell formation, cells shed into tubules, maturation disorder, and atrophy. According to our biochemical findings, the high levels of total oxidant status (TOS), and the low levels of total antioxidant status (TAS) in the CTX group, which are oxidative stress markers, indicate the toxic effect of CTX, while the decrease in TOS levels and the increase in TAS levels in the kefir groups indicate the protective effect of kefir. In the CTX-administered group, tubules with impaired maturation and no spermatids were observed in the transverse section of the testicle, while in the kefir groups, the presence of near-normal tubule structures and tubule lumens despite CTX showed the protective effect of kefir. In our study, it was observed that kefir had a protective and curative effect on CTX-induced toxicity and oxidative stress and could be a strong protector., (© 2024. The Author(s).)

Oxidative stress has been known about in biological sciences for several decades; however, the understanding of this concept has evolved greatly since its foundation. Over the past years, reactive oxygen species, once viewed as solely deleterious, have become recognized as intrinsic components of life. In contrast, antioxidants, initially believed to be cure-all remedies, have failed to prove their efficacy in clinical trials. Fortunately, research on the health-promoting properties of antioxidants has been ongoing. Subsequent years showed that the former assumption that all antioxidants acted similarly was greatly oversimplified. Redox-active compounds differ in their chemical structures, electrochemical properties, mechanisms of action, and bioavailability; therefore, their efficacy in protecting against oxidative stress also varies. In this review, we discuss the changing perception of oxidative stress and its sources, emphasizing everyday-life exposures, particularly those of dietary origin. Finally, we posit that a better understanding of the physicochemical properties and biological outcomes of antioxidants is crucial to fully utilize their beneficial impact on health.

Background: Periodontal diseases are the most frequently diagnosed problem in cats. It has been well-established that periodontal diseases could not only cause various oral health issues but could also contribute to systemic diseases. Oxidative stress is a possible link between systemic diseases and periodontitis. Our study aimed to illustrate the influence of periodontitis on oxidative stress development in cats. Furthermore, the changes in the bacterial flora of the gums were investigated., Methods: Based on the clinical and laboratory examinations, fifty cats were divided into two groups normal (n = 25) and moderate to advanced periodontitis (n = 25). Serum total antioxidant capacity (TAC), total oxidant status (TOS), reduced (GSH) and oxidized glutathione (GSSG) were measured. In addition, samples were taken from the subgingival plaques of all cats for bacterial culture., Results: Serum TOS, GSSG, GSSG to GSH ratio, and oxidative stress index (OSI), calculated as the ratio of TOS to TAC in cats with periodontal disease were significantly higher, and TAC was significantly lower (p < 0.05) compared with controls. The results of bacterial culture indicated that the number of isolated bacterial colonies is higher in patients than in the control group. Additionally, the analysis of these data showed a positive association between periodontal index and oxidative stress., Conclusions: Our results revealed that periodontitis in cats is related to a main oxidative stress. Furthermore, oxidant factors such as TOS and OSI, compared to antioxidant factors, may better indicate the presence of oxidative stress conditions in patients with periodontitis., (© 2024. The Author(s).)

Dramatic metabolic changes during pregnancy and post-partum period resulted in alteration of the biochemical parameters in dromedary she-camels. The current study focused on assessment of stress indicators in post-partum dromedary she-camels on days 14, 28 and 42 post-calving through monitoring the clinical findings, serum steroid hormones, serum or milk oxidant/antioxidant indicators, and milk somatic cell count (SCC) status with reference to serum lipid profile changes. The study also stated several correlations between reproductive cyclicity parameters, stress biomarkers and serum-milk oxidant/antioxidant indicators. The study was conducted on clinically healthy recently calved she-camels (n = 25). They were subjected to clinical and laboratory assays including lipid profiles, serum steroid hormones [Progesterone (P4) and estradiol (E2)], serum or milk oxidant/antioxidant biomarkers [Malondialdehyde (MDA), reduced glutathione (GSH) and cortisol], and milk SCC on days 14, 21 and 28 post-calving. The study concluded the influence of stress as a result of lactation in post-partum period in recently calved she-camels and its relationship with reproductive cyclicity as well as changes in serum steroids, lipid profiles, serum-milk oxidant/antioxidants parameters, and milk SCC that was reflected through significant elevations in serum levels of P4, E2, cortisol, MDA and glucose, and milk values of MDA, cortisol and SCC as well as significant drop in serum levels of GSH, TPs, albumins and globulins on day 14 post-calving comparing with their values particularly on day 42. The study stated variable correlation relationships between reproductive cyclicity parameters, lipid profiles, serum-milk oxidant/antioxidants parameters and milk SCC., (© 2024. The Author(s).)

Background: Unexplained infertility is defined as the absence of any pathology in the basic evaluation performed in couples who cannot achieve pregnancy after 1 year of unprotected sexual intercourse. The results of tests examining the causes of infertility show no identifiable cause in almost 15% of couples., Aim: The aim of this study was to investigate the effects of reactive oxygen species (ROS) on pregnancy and embryos., Methods: This study included 200 patients, aged between 20-44 years, with unexplained infertility, who had recurrent intrauterine inseminations failures and hence started in vitro fertilization (IVF)/intracytoplasmic sperm injection treatment. Some amounts of waste follicular fluid samples were collected by embryologists from the oocytes of these patients during the ovum pick-up procedure. Next, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) values were calculated in the biochemistry laboratory., Results: In terms of pregnancy status, both follicular TOS and OSI values were not significantly different in patients with biochemical and clinical pregnancy, whereas TAS values were significantly higher in patients with pregnancy (P < 0.05). In terms of embryo quality, no significant difference was observed in TAS, TOS, and OSI values between grade 1 and 2 embryos, whereas pregnancy rates were significantly higher in patients who received grade 1 embryo transfer (P < 0.05). However, the follicular fluid TAS levels were significantly lower in smoking patients than in those who did not smoke; TOS and OSI levels were significantly higher., Conclusion: This study showed that exposure to oxidative stress might be a causative factor for infertility. In addition, ROS decreased the level of TAS by increasing OSI in the follicular fluid; thus, antioxidant supplementation might be a necessity., (Copyright © 2024 Copyright: © 2024 Nigerian Journal of Clinical Practice.)

Parabens are being used as preservatives due to their antifungal and antimicrobial effects. They are emerging as aquatic pollutants due to their excessive use in many products. The purpose of this study was to determine the toxic effect of ethyl paraben (C9H10O3) on the hematobiochemical, histological, oxidative, and anti-oxidant enzymatic and non-enzymatic activity; the study also evaluates the potential of ethyl paraben to cause genotoxicity in Rohu Labeo rohita. A number of 15 fish with an average weight of 35.45±1.34g were placed in each group and exposed to ethyl paraben for 21 days. Three different concentrations of ethyl paraben, i.e., T1 (2000μg/L), T2 (4000 μg/L), andT3 (6000 μg/L) on which fish were exposed as compared to the control T0 (0.00 μg/L). Blood was used for hematobiochemical and comet assay. Gills, kidneys, and liver were removed for histological alterations. The results showed a significant rise in all hemato-biochemical parameters such as RBCs, WBCs, PLT count, blood sugar, albumin, globulin, and cholesterol. An increase in aspartate aminotransferase (AST) and alanine transaminase (ALT) levels directed the hepatocytic damage. Histological alterations in the liver, gills and kidneys of fish were found. Ethylparaben induces oxidative stress by suppressing antioxidant enzyme activity such as SOD, GSH, CAT and POD. Based on the comet assay, DNA damage was also observed in blood cells, resulting in genotoxicity. Findings from the present study indicate that ethyl paraben induces hemato-biochemical alterations, tissue damage, oxidative stress, and genotoxicity., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Akmal et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Background: Although oxidative stress is involved in the pathophysiological process of chronic rhinosinusitis with nasal polyps (CRSwNP), the specific underlying mechanism is still unclear. Whether antioxidant therapy can treat CRSwNP needs further investigation., Methods: Immunohistochemistry, immunofluorescence, western blotting and quantitative polymerase chain reaction (qPCR) analyses were performed to detect the distribution and expression of oxidants and antioxidants in nasal polyp tissues. qPCR revealed correlations between oxidase, antioxidant enzymes and inflammatory cytokine levels in CRSwNP patients. Human nasal epithelial cells (HNEpCs) and primary macrophages were cultured to track the cellular origin of oxidative stress in nasal polyps(NPs) and to determine whether crocin can reduce cellular inflammation by increasing the cellular antioxidant capacity., Results: The expression of NOS2, NOX1, HO-1 and SOD2 was increased in nasal epithelial cells and macrophages derived from nasal polyp tissue. Oxidase levels were positively correlated with those of inflammatory cytokines (IL-5 and IL-6). Conversely, the levels of antioxidant enzymes were negatively correlated with those of IL-13 and IFN-γ. Crocin inhibited M1 and M2 macrophage polarization as well as the expression of NOS2 and NOX1 and improved the antioxidant capacity of M2 macrophages. Moreover, crocin enhanced the ability of antioxidants to reduce inflammation via the KEAP1/NRF2/HO-1 pathway in HNEpCs treated with SEB or LPS. Additionally, we observed the antioxidant and anti-inflammatory effects of crocin in nasal explants., Conclusion: Oxidative stress plays an important role in the development of CRSwNP by promoting various types of inflammation. The oxidative stress of nasal polyps comes from epithelial cells and macrophages. Antioxidant therapy may be a promising strategy for treating CRSwNP., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhou, Zhou, Liu, Liu, Meng, Wen, Luo, Liu, Li, Ba and Du.)

Objectives: To examine the influence of hirudotherapy on parameters of oxidative stress., Methods: The cross-sectional study was conducted from March 29 to September 29, 2021, at the Alanya Research and Training Hospital's Traditional and Complementary Medicine Application Centre, Turkey, and comprised adult volunteers of either gender. The participants were subjected to two sessions of hirudotherapy 4 weeks apart. Total antioxidant status, total oxidant status, oxidative stress index values, ischaemia-modified albumin level, paraoxonase 1, disulfide, native thiol, total thiol, and arylesterase levels were assessed at baseline and after the second hirudotherapy session. Data was analysed using SPSS 15., Results: Of the 50 subjects, 30(60%) were females and 20(40%) were males. The overall mean age was 47.10±15.16 years. Oxidative stress, ischaemia-modified albumin and disulfide levels decreased, but not significantly (p>0.05). The reduction in disulfide levels was significant (p=0.021)., Conclusions: Hirudotherapy, within its limitations, could reduce oxidative stress.

High sodium intake is decisive in the incidence increase and prevalence of hypertension, which has an impact on skeletal muscle functionality. Diazoxide is an antihypertensive agent that inhibits insulin secretion and is an opener of K ATP channels (adosine triphosphate sensitive potasium channels). For this reason, it is hypothesized that moderate-intensity exercise and diazoxide improve skeletal muscle function by reducing the oxidants in hypertensive rats. Male Wistar rats were assigned into eight groups: control (CTRL), diazoxide (DZX), exercise (EX), exercise + diazoxide (EX + DZX), hypertension (HTN), hypertension + diazoxide (HTN + DZX), hypertension + exercise (HTN + EX), and hypertension + exercise + diazoxide (HTN + EX + DZX). To induce hypertension, the rats received 8% NaCl dissolved in water orally for 30 days; in the following 8 weeks, 4% NaCl was supplied to maintain the pathology. The treatment with physical exercise of moderate intensity lasted 8 weeks. The administration dose of diazoxide was 35 mg/kg intraperitoneally for 14 days. Tension recording was performed on the extensor digitorum longus and the soleus muscle. Muscle homogenates were used to measure oxidants using fluorescent probe and the activity of antioxidant systems. Diazoxide and moderate-intensity exercise reduced oxidants and increased antioxidant defenses., (© 2024 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

First in the literature this study aimed to investigate the effects of Tartrazine, a common industrial food dye, on kidney and whether Thymoquinone has a protective effect in tartrazine-induced nephrotoxicity. The study conducted on the rats bred at İnönü University Experimental Animals Production and Research Center. Wistar albino rats were randomly divided into 4 groups, where each group included 8 rats: control, Tartrazine, Thymoquinone, and Tartrazine + Thymoquinone groups. The experiments continued for 3 weeks and then, kidney tissues and blood samples were collected from the rats under anesthesia. Malondialdehyde (MDA), super oxidized dismutase (SOD), total oxidant status (TOS), increase in Oxidative stress index (OSI), glutathione (GSH), Glutathione peroxidase (GSH-Px), catalase (CAT), Total antioxidant status (TAS) levels decreased in the kidney tissues collected from the tartrazine group. Serum Bun and Creatinine levels increased in the tartrazine group. Tartrazine administration damaged and degenerated the glomeruli and cortical distal tubes in the histopathology of kidney tissues, also different degrees of inflammatory cell infiltration were observed in the renal cortex and medulla. Thymoquinone and tartrazine administration improved both biochemical and histopathological parameters. Tartrazine administration induced nephrotoxicity. This could be observed with the increase in oxidant capacity and the deterioration of kidney functions. Thymoquinone was observed to demonstrate strong antioxidant properties. Thymoquinone could be used primarily as a protective agent against Tartrazine-induced toxicity., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Objective: Acrylamide (AA) is toxic and forms in food that undergoes high-temperature processing. This study aimed to investigate the effects of AA-induced toxicity on renal tissue in pinealectomized rats and the possible protective effect of exogenous Melatonin (ML) administration., Materials and Methods: Sixty rats were randomized into 6 groups (n = 10): Sham, Sham+AA, Sham+AA+ML, PX, PX+AA, and PX+AA+ML. Sham and pinealectomized rats received AA (25 mg/kg/day orally) and ML (0.5 ml volume at 10 mg/kg/day, intraperitoneal) for 21 days., Results: The results showed that malondialdehyde (MDA), total oxidant status (TOS), oxidative stress index (OSI), tumor necrosis factor-α (TNF-α), and interleukin 1β (IL-1β) levels of the kidney and urea and creatinine levels of serum in the PX (pinealectomy)+AA group were more increased than in the Sham+AA group. In addition, glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and total antioxidant status (TAS) levels decreased more in the PX+AA group than in the Sham+AA group. Also, we observed more histopathologic damage in the PX+AA group. On the other hand, up-regulation of kidney tissue antioxidants, down-regulation of tissue oxidants, and improvement in kidney function were achieved with ML treatment. Also, histopathological findings such as inflammatory cell infiltration, shrinkage of glomeruli, and dilatation of tubules caused by AA toxicity improved with ML treatment., Conclusion: ML supplementation exhibited adequate nephroprotective effects against the nephrotoxicity of AA on pinealectomized rat kidney tissue function by balancing the oxidant/antioxidant status and suppressing the release of proinflammatory cytokines., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflict of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Acrylamide (ACR) is a toxic chemical frequently encountered in daily life, posing health risks. This study aimed to elucidate the molecular-level mechanism of ACR's toxic effects on testicles and investigate whether Vitamin E can mitigate these effects. A total of 40 adult pregnant rats were utilized, divided into four groups: Control, ACR, Vitamin E, and ACR + Vitamin E. ACR and Vitamin E were administered to the mother rats during pregnancy and lactation, and to the male offspring until the 8th week post-birth. Serum hormone levels, oxidant-antioxidant parameters, histopathological examination of testicular tissue, and mRNA and protein levels of the testicular and liver aromatase gene were analyzed. Spermiogram analysis was conducted on the collected sperm samples from the male offspring. The results revealed that ACR exposure adversely affected hormone levels, oxidant-antioxidant parameters, histological findings, as well as aromatase gene and protein expressions. However, Vitamin E administration effectively prevented the toxic effects of ACR. These findings demonstrate that ACR application significantly impairs the reproductive performance of male offspring rats by increasing liver aromatase activity., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Introduction: The flavonoid-rich fraction of Rosa damascena (FRFRD) contains antioxidant and active compounds. Therefore, this study aimed to investigate the role of FRFRD, rich in quercetin and kaempferol, in liver fibrosis induced by CCl4., Materials and Methods: The FRFRD fraction was separated and standardized by High-Performance Liquid Chromatography (HPLC) based on the levels of quercetin and kaempferol. Liver fibrosis was induced over CCl4 over 12 weeks in 30 male Wistar rats, and three concentrations of FRFRD were administered to them during the last four weeks. Subsequently, after evaluation of liver serum markers and fibrotic parameters, the relative expression of transforming growth factor-beta-1 (TGF-β 1 ), platelet-derived growth factor (PDGF), and lysyl oxidase homolog 2 (Loxl2) genes were assessed, along with the measurement of lysyl oxidase activity and oxidative markers., Results: Fibrotic markers demonstrated progressive recovery of liver damage in the treated group compared to the non-treatment group (p < 0.01). These results were accompanied by a significant decrease in the expression of TGF-β 1 , PDGF, and Loxl2 genes, as well as, a reduction in lysyl oxidase activity (p < 0.001). The antioxidant effects of the treatment were observed through a significant decrease in malondialdehyde (MDA) levels and an increase in catalase enzyme (CAT) and glutathione peroxidase (GPx) activity in the treatment group compared to the fibrotic group (p < 0.01)., Conclusion: The flavonoid-rich fraction of Rosa damascena ameliorates liver damage by affecting collagen cross-linking and lowering oxidative and inflammatory levels., Competing Interests: Declaration of competing interest The authors declare that there are no conflicts of interest, (Copyright © 2023. Published by Elsevier Inc.)

Toxic doses of formaldehyde (FA) can cause oxidative damage and impair energy metabolism. Asprosin (ASP) and subfatin (SUB) are adipokines produced by adipose tissue that help regulate energy metabolism. We investigated the effects of carvacrol (CAR), an antioxidant with hepatoprotective properties, on ASP and SUB in rats exposed to FA using immunohistochemistry and biochemistry. We used 42 male Wistar albino rats divided into six groups of seven: group 1, untreated control; group 2, FA (10 ppm FA by inhalation 8 h/day, 5 days/week); group 3, CAR-20 (20 mg/kg); group 4, CAR-40; group 5, FA (10 ppm FA by inhalation 8 h/day, 5 days/week) + CAR-20 (20 mg/kg); group 6, FA (10 ppm FA by inhalation 8 h/day, 5 days/week) + CAR-40 (40 mg/kg). Levels of ASP and SUB, and total oxidant status (TOS) and total antioxidant status (TAS) in blood and liver tissue were measured using ELISA. ASP and SUB immunoreactivity was assessed using immunohistochemistry. The number of apoptotic cells was determined using the TUNEL method. The number of apoptotic cells in group 2 was increased compared to group 1. TOS in group 2 was increased compared to group 1. The numbers of apoptotic cells and TOS in group 3 were decreased compared to group 1. TOS was decreased in group 6 compared to group 2, but TOS was increased compared to group 1. We found ASP and SUB immunoreactivity in the liver. All alterations were reversed by addition of CAR. It appears that FA disrupts energy metabolism and CAR ameliorates the destructive effects of FA when used at appropriate doses, although CAR might be harmful at high doses.

Levetiracetam (LEV) is an anticonvulsant for epilepsy. The toxic effects of this medication in tissues have been associated with redox state imbalance, which can lead to salivary gland dysfunction. Therefore, the current work investigated the effects of LEV on the biochemical, functional, and redox parameters of the parotid and submandibular glands in rats. For this, male Wistar rats (Rattus norvegicus albinus) were randomly divided into 3 groups (n = 10/group): Control (0.9% saline solution), LEV100 (100 mg/kg), and LEV300 (300 mg/kg). After 21 consecutive days of intragastric gavage treatments, pilocarpine stimulated saliva secretion was collected for salivary biochemical analysis. The extracted salivary glands were utilized for histomorphometry and redox state analyses. Our results showed that LEV300 increased plasma hepatotoxicity markers and reduced salivary amylase activity and the acinar surface area of the parotid gland. Total oxidant capacity and oxidative damage to lipids and proteins were higher in the parotid gland, while total antioxidant capacity and uric acid levels were reduced in the submandibular gland of the LEV100 group compared to Control. On the other hand, total oxidant capacity, oxidative damage to lipids and proteins, total antioxidant capacity, and uric acid levels were lower in both salivary glands of the LEV300 group compared to Control. Superoxide dismutase and glutathione peroxidase activities were lower in the salivary glands of treated animals compared to Control. In conclusion our data suggest that treatment with LEV represents a potentially toxic agent, that contributes to drug-induced salivary gland dysfunction., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Industrial products containing PdCu@GO can gain access to the aquaculture environment, causing dangerous effects on living biota. In this study, the developmental toxicity of zebrafish treated with different concentrations (50, 100, 250, 500 and 1000 μg/L) of PdCu@GO was investigated. The findings showed that PdCu@GO administration decreased the hatchability and survival rate, caused dose-dependent cardiac malformation. Reactive oxygen species (ROS) and apoptosis were also inhibited in a dose-dependent manner, with acetylcholinesterase (AChE) activity affected by nano-Pd exposure. As evidence for oxidative stress, malondialdehyde (MDA) level increased and superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) activities and glutathione (GSH) level decreased due to the increase in PdCu@GO concentration. Our research, it was determined that the oxidative stress stimulated by the increase in the concentration of PdCu@GO in zebrafish caused apoptosis (Caspase-3) and DNA damage (8-OHdG). Stimulation of ROS, inflammatory cytokines, tumor Necrosis Factor Alfa (TNF-α) and interleukin - 6 (IL-6), which act as signaling molecules to trigger proinflammatory cytokine production, induced zebrafish immunotoxicity. However, it was determined that the increase of ROS induced teratogenicity through the induction of nuclear factor erythroid 2 level (Nrf-2), NF-κB and apoptotic signaling pathways triggered by oxidative stress. Taken together with the research findings, the study contributed to a comprehensive assessment of the toxicological profile of PdCu@GO by investigating the effects on zebrafish embryonic development and potential molecular mechanisms., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Previous studies have shown that Allium cepa ( A. cepa ) has relaxant and anti-inflammatory effects. In this research, A. cepa extract was examined for its prophylactic effect on lung inflammation and oxidative stress in sensitized rats., Methods: Total and differential white blood cell (WBC) count in the blood, serum levels of oxidant and antioxidant biomarkers, total protein (TP) in bronchoalveolar lavage fluid (BALF), and lung pathology were investigated in control group (C), sensitized group (S), and sensitized groups treated with A. cepa and dexamethasone., Results: Total and most differential WBC count, TP, NO 2 , NO 3 , MDA (malondialdehyde), and lung pathological scores were increased while lymphocytes, superoxide dismutase (SOD), catalase (CAT), and thiol were decreased in sensitized animals compared to controls (p < 0.01 to p < 0.001). Treatment with all concentrations of extract significantly improved total WBC, TP, NO 2 , NO 3 , interstitial fibrosis, and emphysema compared to the S group (p < 0.05 to p < 0.001). Two higher concentrations of the extract significantly decreased neutrophil and monocyte count, malondialdehyde, bleeding and epithelial damage but increased lymphocyte, CAT, and thiol compared to the S group (p < 0.05 to p < 0.001). Dexamethasone treatment also substantially improved most measured parameters (p < 0.05 to p < 0.001), but it did not change eosinophil percentage. It was proposed that A. cepa extract could affect lung inflammation and oxidative stress in sensitized rats., Competing Interests: No conflict of interest.

Aims: The imbalance between reactive oxygen species (ROS) and the antioxidant response has been linked to various airway diseases, including asthma. However, knowledge on cell-specific responses of the airway resident and inflammatory cells against increased oxidant stress is very limited. We aim to better understand the cell-specific antioxidant response that contributes to the pathophysiology of lung disease in response to oxidative stress., Materials and Methods: The human cell lines of epithelial, fibroblast, endothelial, monocyte, eosinophil and neutrophil were incubated with tert-butyl hydroperoxide (tBHP) or cigarette smoke condensate (CSC). Following stimulation, cell viability, total oxidant and antioxidant activity were assessed in both residential and inflammatory cells. Human Oxidative Stress Plus RT 2 Profiler PCR array was used to determine 84 gene expression differences in oxidant and antioxidant pathways following oxidant stimulus in all cells., Key Findings: We showed that various cell types respond differently to oxidative stress inducers, with distinct gene expression and oxidant-antioxidant generation. Most importantly, eosinophils increased the activity of all main antioxidant enzymes in response to both oxidants. Monocytes, on the other hand, showed no change in response to each stimulation, whereas neutrophils only increased their CAT activity in response to both stimuli. The increase in NRF2-regulated genes HSPA1A, HMOX1 and DUSP1 after both tBHP and CSC in epithelial cells and fibroblasts indicates Nfr2 pathway activation., Significance: This study advances our knowledge of the molecular and cellular mechanisms of cell-specific antioxidant response upon exposure to oxidative stress. Additionally, our observations imply that the eosinophils' distinct biological response may be utilized for endotype-based cell-targeted antioxidant therapy., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

1. Ammonia is one of major air pollutants in intensive poultry houses, where it causes immunosuppression in broilers. Although previous studies have focused on a particular organ, data on multiple organs have not been reported.2. In the following work, broilers were exposed to environmental ammonia (0, 10, 20, and 40 mg/m 3 from 1-21 d old; and 0, 15, 30, and 60 mg/m 3 from 22-42 d old).3. Ammonia exposure reduced bird spleen index at 42 d and thymus index at 14, 28, 35 and 42 d, meaning that ammonia caused immunosuppression in birds. Moreover, high ammonia exposure down-regulated the expression of toll-like receptor 4 (TLR4) in lung tissue at 21 d, as well as TLR4 in lung and tracheal mucosa at 42 d when analysed using qRT-PCR. It increased SIgA in saliva at 42 d when analysed by ELISA. Ammonia increased interleukin-6 (IL-6), IL-1β, interferon-α (IFN-α), and IFN-γ in serum at 28 d from the ELISA assay, which indicated that all of these factors took part in ammonia-immunosuppression in birds.4. Three antioxidants (CAT, SOD, T-AOC) decreased, and one oxidant MDA increased after ammonia exposure in the liver and blood, which indicated that ammonia caused oxidative stress via the imbalance of antioxidants/oxidants in birds.5. Correlation analysis showed that TLR4 and TLR15 in the tracheal mucosa were significantly positively related to IFN-γ and negatively related to IL-6. TLR2 in the lung was significantly positively related to IL-1β, and TLR2 in bird tracheal mucosa was negatively related to IL-6 in serum.6. The results suggested that oxidative stress mediated immunosuppression caused by ammonia gas via antioxidant/oxidant imbalance in broilers.

The objective of this study was to examine the effects of early-life host specific probiotic and lactoferrin (LF) supplementations on diarrhoea incidence, iron (Fe)-zinc (Zn) balance and antioxidant capabilities in serum of neonatal piglets. A total of eight sow litters obtained from parity matched sows were randomly divided into four groups and assigned to one of the four interventions: control (2.0 ml normal saline), bovine lactoferrin (bLF) (100 mg bLF in normal saline), probiotic (Pb) (1×109 cfu of swine origin Pediococcus acidilactici FT28 strain) and bLF+Pb (both 100 mg bLF and 1×109 cfu of P. acidilactici FT28). All the piglets received supplementations once daily orally for first 7 days of life. The incidence of diarrhoea markedly decreased in bLF group compared to control group. Notably, no incidences of diarrhoea were recorded in Pb and bLF+Pb groups. The Zn and Fe concentrations were significantly increased from day 7 to 21 in bLF and on day 21 in bLF+Pb group. No such changes were noted in Pb group. Total antioxidant capacity (TAC) in serum was significantly increased on days 7 and 15 in bLF group and on days 7 and 21 in bLF+Pb group. Malonaldehyde concentration was markedly reduced from day 7 to 21 in bLF and bLF+Pb groups. The concentrations of nitrate on days 15 and 21 and malonaldehyde on day 7 were significantly higher in Pb group, but mean TAC was unaltered from day 0 to 21. Although no correlation between the incidence of diarrhoea and Zn/Fe and oxidant/antioxidant homeostasis was noted in the Pb group, the supplementation of P. acidilactici FT28 alone was sufficient to prevent the incidence of diarrhoea in neonatal piglets. Taken together, it is concluded that strategic supplementation of P. acidilactici FT28 in early life could help in preventing diarrhoea until weaning of piglets.

Avian musculoaponeurotic fibrosarcoma (Maf) proteins play an important role in Nrf2/Keap1 signaling pathway, which mainly resist the oxidant stress. The members of sMaf have a high homology basic leucine zipper (bZIP) and lack trans activation domain, and could interact with other transcriptional regulatory factors as a molecular chaperone. In this study, a full-length MafG-like gene was cloned from Procambarus Clarkii, designated as PcMafG-like, which consisted of an ORF length of 246 bp encoding 82 amino acids, a 5' untranslated region (UTR) of 483 bp, and a 3' UTR of 111 bp. The domain of PcMafG-like had a bZIP-Maf domain that binds to DNA. The cDNA sequence of PcMafG-like was 99 % similar to that of Penaeus vannamei. The mRNA of PcMafG-like was expressed in all tested tissues, and the highest expression was in muscle tissue. Under stimulation of Cu 2+ and Cd 2+ , PcMafG-like was significantly up-regulated in hepatopancreas and gill, and the same result was testified by situ hybridization. The representative antioxidant genes, CAT, GPx and CZ-SOD, were significantly induced by Cu 2+ ; CAT and GPx was induced by Cd 2+ . PcMafG-dsRNA significantly inhibited the expression of these up-regulated genes, but also inhibited the expression of other detected genes CZ-SOD, GST-θ and GST-1like. The antioxidant effect of PcMafG-like was further verified by oxidative stress markers (T-SOD, CuZnSOD, GPx, CAT, GSH and MDA) kits. Cu 2+ and Cd 2+ could induce the contents of these oxidative stress markers (MDA, GSH, CZ-SOD, CAT in Cu 2+ /Cd 2+ treated group, and GSH-Px in Cd 2+ group), while interference of PcMafG-like significantly inhibited the up-regulation. Furthermore, hematoxylin-eosin staining experiments showed that the degree of pathological damage was dose-dependent and time-dependent, and the pathological damage was more serious after dsRNA interfered with PcMafG-like. In addition, subcellular localization showed that PcMafG-like gene existed in nucleus. The recombinant protein PcMafG-like was expressed and purified in prokaryotic expression. The affinity analysis of promoter by agarose gel electrophoresis suggested that PcMafG-like could bind with CAT promoter in vitro. This indicated that PcMafG-like could activate antioxidant genes., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022. Published by Elsevier B.V.)

The aim of this study was to investigate the impact of heat stress on production performance and oxidative stress in different plumage colors of Japanese quail. For this purpose, a total of 100 birds were used in this study. The 25 birds belonged to Wild-type (n=25, grey), Tuxedo (n=25, black), Golden (n=25, yellow) and Recessive white (n=25). The birds were reared for 42 days in an environmentally controlled room at 39°C and relative humidity of 60-65%. The body weight, body weight gain (g/bird/day), and feed conversion ratio were not different between the groups (p>0.05). However, the feed intake (g/bird/day) of the Wild-type had a higher value than the Tuxedo (black) group counterparts between 15 and 21 days different (p⟨0.05). There was no significant effect of heat stress on the carcass traits (p>0.05). Spleen weights were different between the groups (p⟨0.05). The yellow group had the highest spleen weight. The highest MDA level was found in the Recessive White variety, followed by Wild-type (grey), Golden (yellow) and Tuxedo (black), respectively. However, there were no statistical differences amongst the groups (p>0.05). There was also no statistical significance in glutathione (GSH) and superoxide dismutase (SOD) levels (p>0.05). The heat shock protein 70 kDa (HSP70) level was significantly different between the groups (p⟨0.001). The highest percentage was observed in the Golden (5.06%) and the lowest in the White (1.43%) variety. There was no superior color variety of Japanese quail regarding fattening performance and carcass traits. It is conceivable that when considering the stress response of the different colors, the Golden group is more sensitive to stress due to the hepatic and cellular level of HSP70., (Copyright© by the Polish Academy of Sciences.)

Abamectin, an avermectin member, can induce significant neurodegeneration symptoms in non-target organisms. However, its neurodevelopmental influences in mammals are unclear. Here, we focus on the antiapoptotic action of alpha-mangostin against the developmental neurotoxicity of abamectin with the possible involvement of reelin and nestin mRNA gene expression. Thirty-two pregnant rats were allocated to four groups (8 rats/group); control, alpha-mangostin (20 mg/kg/d), abamectin (0.5 mg/kg), and co-treated group (alpha-mangostin + abamectin). The animals have gavaged their doses during the gestation period. The fetotoxicity and many signs of growth retardation were observed in the abamectin-intoxicated rats. In comparison with the control group, abamectin prompted a significant elevation ( p  < 0.05) in the levels of malondialdehyde and nitric oxide, along with many symptoms of histopathological changes in the fetal cerebral cortex. However, the glutathione, dopamine, and serotonin concentrations together with the activities of glutathione-S-transferase, catalase, and superoxide dismutase were markedly decreased ( p  < 0.05) in the abamectin group. Moreover, abamectin remarkably upregulated ( p  < 0.05) the brain mRNA gene expression of reelin, nestin, and caspase-9 as well as the immunoreactivity of Bax and caspase-3 proteins in the cerebral cortex. It should be noted that alpha-mangostin mitigated the developmental neurotoxicity of abamectin to the normal range by recovering the levels of oxidant/antioxidant biomarkers, catecholamines; and apoptosis-related proteins with the involvement of reelin and nestin genes regulation. Those records revealed that the transcription regulation of reelin and nestin could be involved in the neuroprotective efficacy of alpha-mangostin, especially avermectin's developmental neurotoxicity.

Iron [Fe(II)] and copper [Cu(II)] overloads in rat brain are associated with oxidative stress and damage. The purpose of this research is to study whether brain antioxidant enzymes are involved in the control of intracellular redox homeostasis in the brain of rats male Sprague-Dawley rats (80-90 g) that received drinking water supplemented with either 1.0 g/L of ferrous chloride (n = 24) or 0.5 g/L cupric sulfate (n = 24) for 42 days. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione transferase (GT) activities in brain were determined by spectrophotometric methods and NO production by the content of nitrite concentration in the organ. Chronic treatment with Fe(II) and Cu(II) led to a significant decrease of nitrite content and SOD activity in brain. Activity of NADPH oxidase increased with Cu(II) treatment. Concerning Fe(II), catalase and GT activities increased in brain after 28 and 4 days of treatment, respectively. In the case of Cu(II), catalase activity decreased whereas GT activity increased after 2 and 14 days, respectively. The regulation of redox homeostasis in brain involves changes of the activity of these enzymes to control the steady state of oxidant species related to redox signaling pathways upon Cu and Fe overload. NO may serve to detoxify cells from superoxide anion and hydrogen peroxide with the concomitant formation of peroxynitrite. However, the latest is a powerful oxidant which leads to oxidative modifications of biomolecules. These results suggest a common pathway to oxidative stress and damage in brain for Cu(II) and Fe(II)., (© 2022. The Author(s), under exclusive licence to Society for Biological Inorganic Chemistry (SBIC).)

This study investigated the effect of potato peel extract (PPE), orally administrated to rabbits, on serum blood metabolites and ameliorating oxidative stress induced by cold stress under Egyptian winter conditions. Twenty-four bucks grouped into three treatments (8 animals per group) were used for the experiment. The animals received 1.5 ml of water orally, containing 0 (PPE0), 25 (PPE25) or 50 (PPE50) mg PPE/kg live weight. Bucks were randomly assigned into three homogenous equal groups according to the level of PPE. Treatments were applied to each animal every two days over a period of three months including one month as an adaptation period. At the 8th week of the experiment, blood samples were collected from each buck and at the end of the experiment, bucks were slaughtered, and some organs were collected and weighed. The PPE improved ( p  < 0.05) blood total protein, albumin, globulin and glucose. The blood concentration of total lipid, cholesterol, triglyceride, low density lipoprotein and very low-density lipoprotein (were increased ( p  < 0.02) in PPE rabbits. Furthermore, PPE extract doses decreased ( p  < 0.001) oxidant thiobarbituric reactive substance (TBARS) in both blood and liver. Other liver and blood antioxidant system enzymes such as catalase, glutathione peroxidase, and superoxide dismutase were improved ( p  < 0.005) by PPE supplementation. Overall, oral administration of PPE up to 50 mg/kg live weight can have positive effects on rabbit health under cold stress.

This study aims to investigate the effect of Premna odorata (P. odorata) (Lamiaceae) on the hepatic and nephrotoxicity induced by aluminum chloride (AlCl 3 ) in rat. Wistar male rats were equally classified into four groups: control, P. odorata extract (500 mg/kg B.W.), AlCl 3 (70 mg/kg B.W.), and P. odorata extract plus AlCl 3 groups. All treatments were given orally for 4 weeks. Serum transaminases and some biochemical parameters, hepatic and renal antioxidant/oxidant biomarker; tumor necrosis factor-α (TNF-α); matrix metalloproteinase (MMP9) and transforming growth factor-β (TGF-β) mRNA expression; histopathological examination of the liver, and kidneys were investigated. The obtained results revealed that AlCl 3 significantly increased the activities of serum aspartate transaminase, alanine transaminase, and alkaline phosphatase as well as produced a significant increase in total cholesterol, triglyceride, urea, and creatinine concentrations, while there were no changes observed in the total protein, albumin, and globulin concentrations. Also, aluminum administration significantly decreased the reduced glutathione content and increased the catalase activity, malondialdehyde, and TNF-α concentrations in the liver and kidney tissue. Moreover, AlCl 3 results in congestion, degeneration, and inflammation of the liver and kidney tissue. Co-treatment of P. odorata extract with AlCl 3 alleviated its harmful effects on the previous parameters and reduced the histopathological alterations induced by AlCl 3 . Therefore, Premna odorata may have a potent protective effect against oxidative stress induced by Al toxicity through downregulation of MMP9 and TGF-β gene expression., (© 2022. The Author(s).)

Background: The present study aimed to evaluate the effect of nanocurcumin and curcumin on liver transaminases, lipid profile, oxidant and antioxidant system, and pathophysiological changes in aluminium phosphide (ALP) induced hepatoxicity. Material and Methods . In this experimental study, thirty-six male Wistar rats were randomly divided into six groups curcumin (Cur), nanocurcumin (Nanocur), ALP, ALP+Cur, and ALP+Nanocur. All treatments were performed by oral gavage for seven days. After treatment, animals were sacrificed, and liver and blood samples were taken. Serum levels of aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (AP), total bilirubin, cholesterol, triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL) were measured by photometric methods. Total antioxidant capacity (TAC) and malondialdehyde (MDA) as parameters of oxidative stress and mRNA expression of the nonenzyme protein including Sirtuin 1 (STR1), Forkhead box protein O1 (FOXO1) and protein O3 (FOXO3), catalase (CAT), and glutathione peroxidase (GPX) as the enzyme protein in homogenized tissues have been investigated. A histologist analyzed liver tissue sections after staining with hematoxylin-eosin., Results: In the aluminium phosphide group, there was a significant increase in MDA, ALT, AST, and AP and total bilirubin, cholesterol, triglyceride, LDL, and VLDL; AST, ALT, total bilirubin, LDL, VLDL, cholesterol, and MDA were significantly decreased; and HDL and TAC were significantly increased compared to ALP ( P < 0.05). In the ALP+Nanocur group, ALT, AST, ALP, total bilirubin, cholesterol, LDL, VLDL, triglyceride, and MDA were significantly decreased and HDL and TAC were increased significantly ( P < 0.05). The effect of nanocurcumin on controlling serum levels of LDL, VLDL, triglyceride, and MDA in ALP-poisoned rats was significantly more than curcumin ( P < 0.05). The ALP group had significant changes in genes SIRT1 , FOXO1a , FOXO3a , CAT , and GPX compared to healthy controls ( P < 0.05). Nanocurcumin mice expressed more SIRT1 , FOXO1a , CAT , and GPX genes than controls, and curcumin-treated mice expressed more SIRT1 and FOXO1a genes ( P < 0.05). Histopathological findings also indicated a more significant protective effect of nanocurcumin relative to curcumin against ALP-induced hepatotoxicity., Conclusion: Nanocurcumin significantly protects the liver against aluminum phosphide toxicity. It is suggested that nanocurcumin-based drugs be developed to reduce the toxic effects of ALP in poisoned patients., Competing Interests: The authors declare that they have no conflict of interest., (Copyright © 2022 Ali Salimi et al.)

Previous studies reported that, with aging, Leydig cell intracellular antioxidants are reduced in concentration and intracellular ROS levels increase, suggesting that oxidant/antioxidant imbalance may contribute to the reduced testosterone production that characterizes the aging cells. As yet, little is known about how the Leydig cell oxidant/antioxidant environment is regulated. Sirt1, an enzyme that deacetylates transcription factors, and the transcription factor Nrf2, have been shown to be associated with cellular response to oxidative stress. We hypothesized that Sirt1 and/or Nrf2 might be involved in regulating the oxidant/antioxidant environment of Leydig cells, and therefore, the testosterone production. We found that Sirt1 and Nrf2 are present in the Leydig cells of Brown Norway rats, though reduced in aged cells. In MA-10 cells in which Sirt1 or Nrf2 were suppressed by nicotinamide (NAM) or ML385, respectively, or in which siRNAs were used for knockdown of Sirt1 or Nrf2, increased ROS levels and decreased progesterone production occurred. In rat Leydig cells, inhibition of Sirt1 by culturing the cells with NAM resulted in increased ROS and reduced testosterone production, and subsequent removal of NAM from the culture medium resulted in increased testosterone production. Activation of rat Leydig cells Sirt1 with honokiol or of Nrf2 with sulforaphane resulted in the maintenance of testosterone production despite the exposure of the cells to oxidizing agent. These results, taken together, suggest that Sirt1 and Nrf2 are involved in maintaining the Leydig cell oxidant/antioxidant environment, and thus in maintaining steroid production., (© The Author(s) 2021. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Early detection of oxidant-antioxidant levels and special care in severe patients are important in combating the COVID-19 epidemic. However, this process is costly and time consuming. Therefore, there is a need for faster, reliable and economical methods., Methods: In this study, antioxidant/oxidant levels of patients were estimated by Expert-models using biomarkers, which are effective in the diagnosis/prognosis of COVID-19 disease. For this purpose, Expert-models were trained and created between the white-blood-cell-count (WBC), lymphocyte-count (LYM), C-reactive-protein (CRP), D-dimer, ferritin values of 35 patients with COVID-19 and antioxidant/oxidant parameter values of the same patients. Error criteria and R 2 ratio were taken into account for the performance of the models. The validity of the all models was checked by the Box-Jenkis-method., Results: Antioxidant/Oxidant levels were estimated with 95% confidence-coefficient using the values of WBC, LYM, CRP, D-dimer, ferritin of different 500 patients diagnosed with COVID-19 with the trained models. The error rate of all models was low and the coefficients of determination were sufficient. In the first data set, there was no significant difference between measured antioxidant/oxidant levels and predicted antioxidant/oxidant levels. This result showed that the models are accurate and reliable. In determining antioxidant/oxidant levels, LYM and ferritin biomarkers had the most effect on models, while WBC and CRP biomarkers had the least effect. The antioxidant/oxidant parameter estimated with the highest accuracy was Native-Thiol divided by Total-Thiol., Conclusions: The results showed that the antioxidant/oxidant levels of infected patients can be estimated accurately and reliably with LYM, ferritin, D-dimer, WBC, CRP biomarkers in the COVID-19 outbreak., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background: Oxidative stress and inflammation play a critical role in the etiopathogenesis of bronchopulmonary dysplasia (BPD). The aim of this study was to evaluate the preventive effect of Chrysin (CH), an antioxidant, antiinflammatory, antiapoptotic and antifibrotic drug, on hyperoxia-induced lung injury in a neonatal rat model., Methods: Forty infant rats were divided into four groups labeled the Control, CH, BPD, and BPD + CH. The control and CH groups were kept in a normal room environment, while the BPD and BPD + CH groups were kept in a hyperoxic (90-95%) environment. At the end of the study, lung tissue was evaluated with respect to apoptosis, histopathological damage and alveolar macrophage score as well as oxidant capacity, antioxidant capacity, and inflammation., Results: Compared to the BPD + CH and control groups, the lung tissues of the BPD group displayed substantially higher levels of MDA, TOS, TNF-α, and IL-1β (p < 0.05). While the BPD + CH group showed similar levels of TNF-α and IL-1β as the control group, MDA and TOS levels were higher than the control group, and significantly lower than the BPD group (p < 0.05). The BPD group exhibited considerably lower levels of TAS, SOD, GSH, and GSH-Px in comparison to the control group (p < 0.05). The BPD and BPD + CH groups exhibited higher mean scores of histopathological damage and alveolar macrophage when compared to the control and CH groups (p ≤ 0.0001). Both scores were found to be lower in the BPD + CH group in comparison to the BPD group (p ≤ 0.0001). The BPD + CH group demonstrated a significantly lower average of TUNEL and caspase-3 positive cells than the BPD group., Conclusion: We found that prophylaxis with CH results in lower histopathological damage score and reduces apoptotic cell count, inflammation and oxidative stress while increasing anti-oxidant capacity., (Copyright © 2021. Published by Elsevier B.V.)

Introduction: The prevalence of metabolic syndrome among the elderly population is growing. The elements of metabolic syndrome in an aging society are currently being researched. Atherosclerosis is a slow process in which the first symptoms may be observed after many years. The mechanisms underlying the progression of atherosclerosis are oxidative stress and inflammation. Inflammation and oxidative stress are associated with the increased incidence of metabolic syndrome. Taking the above into consideration, metabolic syndrome is thought to be a clinical equivalent of atherosclerosis., Aim: The aim of this paper is to review the impact of the interplay of oxidant-antioxidant and inflammation markers in metabolic syndrome in general as well as its components in the pathophysiology which underlies development of atherosclerosis in elderly individuals., Methods: A systematic scan of online resources designed for elderly (≥65 years) published from 2005 to the end of 2020 were reviewed. This was supplemented with grey literature and then all resources were narratively analyzed. The analysis included the following terms: "atherosclerosis or metabolic syndrome" and "oxidative stress or inflammation" and "elderly" to find reports of atherosclerotic disease from asymptomatic to life-threatening among the elderly population with metabolic syndrome ., Results: The work summarizes articles that were applicable to this study, including systematic reviews, qualitative studies and opinion pieces. Current knowledge focuses on monitoring the inflammation and oxidant-antioxidant imbalance in disentangling atherosclerosis in patients diagnosed with metabolic syndrome. The population-based studies described inflammation, increased oxidative stress and weak antioxidant defense systems as the mechanisms underlying atherosclerosis development. Moreover, there are discussions that these targets could potentially be a point of intervention to reduce the development of atherosclerosis in the elderly, especially those with altered glucose and lipid metabolism. Specific markers may be used as an approach for the prevention and lifestyle modification of atherosclerotic disease in such population., Conclusion: Metabolic syndrome and its components are important contributors in the progression of atherosclerotic disease in the elderly population but constant efforts should be made to broaden our knowledge of elderly groups who are the most susceptible for the development of atherosclerosis complications., Competing Interests: The author declares no conflict of interest., (© 2021 Dziegielewska-Gesiak.)

Toxoplasma gondii is an apicomplexan parasite causing toxoplasmosis, a common disease, which is most typically asymptomatic. However, toxoplasmosis can be severe and even fatal in immunocompromised patients and fetuses. Available treatment options are limited, so there is a strong impetus to develop novel therapeutics. This review focuses on the role of oxidative stress in the pathophysiology and treatment of T. gondii infection. Chemical compounds that modify redox status can reduce the parasite viability and thus be potential anti- Toxoplasma drugs. On the other hand, oxidative stress caused by the activation of the inflammatory response may have some deleterious consequences in host cells. In this respect, the potential use of natural antioxidants is worth considering, including melatonin and some vitamins, as possible novel anti- Toxoplasma therapeutics. Results of in vitro and animal studies are promising. However, supplementation with some antioxidants was found to promote the increase in parasitemia, and the disease was then characterized by a milder course. Undoubtedly, research in this area may have a significant impact on the future prospects of toxoplasmosis therapy.

We suppose that apigenin may inhibit the cellular process of sepsis-induced lung injury, which is considered to be a major cause of morbidity and mortality, and may improve inflammation and oxidative stress. The aim of this study was to investigate the potential protective effect of apigenin in a rat model of polymicrobial sepsis. Eight groups consisting of a total of 64 female Wistar albino rats were used for this study. Pro-inflammatory (TNF-α, IL-1-β, IL-6) and anti-inflammatory (TGF-β, IL-10) cytokine levels were measured with the enzyme-linked immunosorbent assay technique, oxidant/antioxidants parameters were measured using the spectrophotometric method and Bax and Caspase-3 immunohistochemical methods. TNF-α, TGF-β, IL-1β, and IL-6 levels significantly increased in the sepsis-induced group than in the control groups, while IL-10 levels decreased. Lipid peroxidase (LPO), an oxidative stress marker, increased, while the antioxidant defense parameters of superoxide dismutase (SOD), catalase (CAT) activities, glutathione (GSH) levels decreased. Although Bax and Caspase-3 immunoreactivity and H score levels significantly increased in the sepsis group, significant decreases were found in the groups treated with apigenin. In conclusion, we are of the opinion that apigenin treatment improves lung injury by inhibiting oxidative stress and inflammatory cell damage., (© 2021 Wiley Periodicals LLC.)

Objective: Multiple sclerosis (MS) is a demyelinating chronic inflammatory disease of the central nervous system (CNS). Recent studies have shown that oxidative stress plays an important role in MS pathogenesis. This study aimed to investigate the relationship between total oxidative stress (TOS) and total antioxidant capacity (TAC), which were reported to be effective in the pathogenesis of MS, and therapeutic efficacy of fingolimod used in the treatment of MS., Materials and Methods: Serum TOS and total TAC levels of 25 patients with relapsing-remitting MS (RRMS) were measured before fingolimod treatment was initiated and in the third month of treatment and compared with those of 40 healthy individuals. Measurement of TOS activity was performed with TOS Assay Kit (Rel Assay Diagnostics, Turkey). Measurement of TAC activity was also performed with TAC Assay Kit (Rel Assay Diagnostics, Turkey)., Results: A statistically significant increase was observed in the TOS levels measured before fingolimod treatment in the patient group compared to the control group. The TOS levels measured in the third month of the treatment were found to decrease significantly compared to the pre-treatment TOS levels. An increase was observed in TAC levels after the treatment; however, no significant difference was found between the groups in terms of TAC levels. There was a positive correlation between the pre- and post-treatment Expanded Disability Status Scale (EDSS) scores and TOS values whereas no significant correlation was observed between the pre- and post-treatment EDSS scores and TAC values., Conclusion: The present study has revealed that fingolimod reduced oxidative stress. There was a positive correlation between the pre- and post-treatment EDSS and TOS values, which confirmed that there was a close correlation between the MS and oxidative stress. There are some limitations in this study. The small number of patients and the short follow-up times can be listed among these limitations. Our study does not contain a definitive answer to what is the mechanism of increased TOS in MS patients and how fingolimod reduces TOS levels. More detailed studies are needed on this subject., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Physiological balance between pro- and antioxidative processes is crucial for placentation and further development of fetus and placenta. Parameters of pro- and antioxidative profile may serve as markers of proper course of pregnancy. The aim of study was to assess whether the balance between pro- and antioxidative parameters during placentation phase in bovine placenta is maintained. Placental and blood samples were collected from healthy, HF, pregnant (2nd-3rd month) cows (n = 8) in slaughterhouse and in farm, respectively. Formylokinurenine and bityrosine content were measured spectrofluorimetrically in blood plasma and tissue homogenates while metabolites of lipid peroxidation, total antioxidant capacity, SH groups and activity of antioxidative enzymes (glutathione peroxidase and superoxide dismutase) were determined in examined tissues by spectrophotometry. Western blotting was used to confirm the presence of enzymatic proteins in placenta. Results: Local profile in tissues was more pronounced than general profile in blood plasma. Activities of antioxidative enzymes were significantly (p < 0.05) higher in 2nd compared to 3rd month of pregnancy in maternal part of placenta while prooxidant parameters showed opposite relationship. Obtained results showed significant differences when compared to data from non-pregnant animals or time of parturition. Further studies are necessary for elucidation of placentation phase in cows.

The aim of the current study is to investigate the effect of daily long-term radio-frequency electromagnetic field (RF-EMFs) exposure on thiol/disulphide homeostasis and oxidant-antioxidant status in the serum of rats. Fourteen male Sprague Dawley rats were divided into two equal groups (n = 7). They were grouped as group 1 (sham-control) and group 2 (2100 MHz exposed). Group 2 rats were exposed to GSM-like signals for 5 h/day, 7 days per week for 14 days. In serum of blood samples, the native, total and native/total thiol levels and antioxidant-oxidant parameters were analyzed. The study revealed that the mean serum total thiol levels of GSM exposure group was rather higher than sham-control group ( p = 0,219); the mean serum native thiol levels of GSM exposure group was rather higher than sham-control group ( p = 0,416), and the mean serum disulphide levels of GSM exposure group was rather higher than sham-control group ( p = 0,566). On the other hand, the mean serum total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) of GSM exposure group were higher than sham-control group. There are no data in the literature, that examine the effects of RF-EMFs on thiol/disulphide homeostasis. The results of this study, indicate that RF-EMFs did not cause oxidative stress and statistically changes in thiol/disulphide homeostasis. More sample sizes and longer-term exposures are needed to confirm the results of this study.

Aim and Objective: Cells and tissues of the body are prone to oxidative damage as a result of an increased level of reactive oxygen species and nitrogen radical beyond the detoxifying ability of the endogenous antioxidant system. This study aimed to evaluate the ameliorative effect of methanolic extracts of Nigella sativa (MENS) against cadmium-induced blood oxidative stress and testicular toxicity in albino rats., Materials and Methods: Twenty-five (25) male albino rats, weighing (200 ± 20g), were randomly grouped into five groups (A-E). Group B (Negative Control) received intraperitoneal administration of cadmium chloride (CdCl 2 , 5 mg/kg) only, group C received CdCl 2 and low dose MENS (300 mg/kg, oral), group D received CdCl 2 and high dose MENS (600 mg/kg, oral), group E (Positive control) received CdCl 2 and Vitamin C (200 mg/kg, oral), for 14 days. No treatment was administered to group A (Normal control). The oxidative state of the blood was assessed by measuring the blood levels or activities of MDA, CAT, GSH and SOD; while testicular injury was assessed by measuring serum testosterone level using ELISA. The testes were harvested for histopathological examination., Results: The results showed that cadmium induced a marked elevation in the level of MDA, and a decrease in SOD, CAT and GSH levels or activities (p<0.05 or p<0.01); but no significant alteration in the serum testosterone level was found (p>0.05); Histopathological studies on the testes showed that cadmium significantly induced testicular injury, which was however ameliorated by the seed extract of N. sativa., Conclusion: We conclude that N. sativa seed extract is potentially testiculoprotective and attenuates oxidative stress against harmful chemical toxins such as cadmium., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objective: To evaluate the effect of pasteurization on antioxidant and oxidant properties of human milk., Methods: 42 samples of milk before and after pasteurisation were used to evaluate the antioxidant activity by the ferric reducing capacity and by scavenging the 2,2'-azino-bis 3-ethylbenzthiazoline-6-sulfonic acid radical. Lipid peroxidation was estimated by the concentration of malondialdehyde product using the thiobarbituric acid reactive substances assay and by the evaluation of advanced oxidation protein products., Results: No significant difference was observed in fresh human milk and after pasteurization in relation to antioxidant properties determined by the ferric reducing capacity (50.0±3.4% and 48.8±3.0%, respectively) and by scavenging the 2,2'-azino-bis 3-ethylbenzthiazoline-6-sulfonic acid radical (28.9±1.5% and 31.2±1.3%, respectively). The results of malondialdehyde (62.6±4.1 and 64.3±3.6 µM/mg) and protein oxidation products (59.4±3.4 and 54.2±3.8 µM/L) of fresh and pasteurized milk, respectively, did not exhibited any significant difference., Conclusions: This data showed that human milk has an important antioxidant activity and that the pasteurizing process does not influence the antioxidant capacity, avoiding the peroxidation of breast milk lipids and the formation of advanced protein oxidation products.

The purpose of this study was to evaluate the prophylactic effects of quercetin (QUE) against oxidative damages and histological changes induced by 1, 2, 3, 4-tetrachlorodibenzo-p-dioxin (TCDD) in rat heart. For this purpose, 20 adult male Wistar rats were divided into four groups as fellow control group, TCDD group (10µg/kg BW/day by gavage daily for 60 consecutive days), QUE group (30 mg/kg BW/day) and TCDD + QUEgroup. The oxidative biomarkers of heart tissue and the levels of cTnI and lipid profile in serum were measured. Our results showed that the cTnI serum level and the heart lipid peroxidation significantly increased and the heart level of antioxidant profile significantly decreased in the TCDD group compared to control and QUEgroups. While pretreatment with QUEcould significantly improved these factors in serum and heart tissue in animals that consumed TCDD. It can be concluded that QUEat doses of 30 mg/kg/day could alleviate heart oxidative damage and histological changes induced by TCDD.

Amazon fish are vulnerable to climate change. Current temperature increases in Amazonian rivers are likely to continue in the coming years. Elevated temperatures impair homeostasis and subject fish to oxidative stress; nevertheless, the effects of elevated temperature on plasma and muscle oxidative stress as well as fillet fatty acid composition in matrinxã (Brycon amazonicus) remain unknown. Therefore, the aims of the present study were to determine whether antioxidant system is able to withstand acute thermal stress to avoid plasma and muscle oxidative damage and to determine the manner in which matrinxã adjust their muscle fatty acid metabolism in a response to acute heat stress. We exposed juvenile matrinxã to four temperatures (28 °C as control and 30, 32, and 34 °C) for 72 h and observed the effects on plasma and muscle oxidant/antioxidant status and on fatty acid composition. Plasma reactive oxygen species (ROS) and lipid peroxidation (LPO) levels were significantly higher in matrinxã exposed to 34 °C compared with the control group, while they were significantly higher in the muscle of matrinxã exposed to 32 °C and 34 °C compared with the control group. Superoxide dismutase (SOD) activity and total antioxidant capacity (TAC) levels were significantly lower in the plasma and muscle of matrinxã exposed to 34 °C compared with the control group. Plasma glutathione peroxidase (GPx) activity was significantly lower in matrinxã exposed to 32 and 34 °C compared with the control group, while it was significantly lower in the muscle of matrinxã exposed to 34 °C. The total content of saturated fatty acid (SFA) was significantly higher in the fillet of matrinxã exposed to 34 °C compared with the control group, while the total content of polyunsaturated fatty acid (PUFA) was significantly lower. Based on this evidence, we conclude that acute heat stress at 32 °C and 34 °C causes plasma and muscular oxidative stress, and the enzymatic and non-enzymatic antioxidant system is unable to prevent oxidative damage. Moreover, increased levels of total SFA and decreased levels of PUFA occur in an attempt to withstand heat stress and maintain membrane fluidity; nevertheless, these responses can represent negative impacts for consumers.