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Silver nanoparticles (AgNPs) are prominent nanomaterials that are efficiently used in different industries including medical products, water treatment, and cosmetics. However, AgNPs are known to cause adverse effects on the ecosystem and human health. In this study, aqueous extract of Rumex patientia (RP) was used as a reducing and stabilizing agent in AgNP biosynthesis. The obtained activated carbon (AC) from Chenopodium album (CA) plant was combined with RP-AgNPs to synthesize RP-Ag/AC NPs. Next, the effects of these green synthesis RP-Ag/AC NPs on zebrafish (Danio rerio) embryos and larvae were investigated. First, we characterized the RP-Ag/AC NPs by using X-ray diffraction (XRD) and transmission electron microscopy (TEM) and determined LC50 value as 217.23 mg/L at 96 h. Next, the alterations in survival rate, hatching rate, and morphology of the larvae at 96 h were monitored. The survival rates decreased in a dose-dependent manner. Morphological defects such as yolk sac edema, pericardial edema, spinal curvature, and tail malformation in the NP-treated larvae were observed. RP-Ag/AC NPs stimulated the production of neuronal NOS (nNOS) and 8-OHdG in zebrafish brain tissues in a dose-dependent manner and enhanced neutrophil degeneration and necrosis at concentrations of 50 and 100 mg/L. Thus, the obtained data suggest that the green synthesis process is not sufficient to reduce the effect of oxidative stress caused by AgNPs on oxidative signaling.

This study was conducted to assess the impacts of prolonged fasting (70 and 120days) on the morphological, biochemical, oxidative stress responses, immune-related gene expression, histopathology, and DNA damage in rainbow trout. Final weight (FW), hepatosomatic index (HSI), and condition factor (CF) significantly decreased in both 70 and 120days of fasting compared to the pre-fasting group (p p p

In the scope of the study, the protective effect of hesperidin (HES), a flavanone glycoside, was investigated against sodium arsenite (NaAsO2, SA) induced heart and brain toxicity. For this purpose, 35 Sprague-Dawley male rats were divided into 5 different groups, 7 in each group. Physiological saline was given to the first group. Dose of 200 mg/kg of HES to the second group, 10 mg/kg dose of SA to the 3rd group, 100 mg/kg HES and 10 mg/kg SA to the 4th group, 200 mg/kg HES, and 10 mg/kg SA to the 5th group were given orally for 15 days. At the end of the study, biochemical, histopathological, and immunohistochemical examinations were performed on the heart and brain tissues of the rats. According to the results, SA increased malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels and decreased glutathione (reduced, GSH) level and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in both tissues. Also, it increased cardiac lactate dehydrogenase (LDH) and creatine kinase isoenzyme-MB (CK-MB) activities and cardiac troponin-I level (cTn-I), cerebral acetylcholine esterase activity, nuclear factor kappa-B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-one beta (IL-1β), and cysteine aspartate-specific protease-3 (caspase-3) levels. In addition, as a result of histopathological examination, it was determined that SA damaged tissue architecture, and as a result of immunohistochemical examination, it increased cardiac Bcl-2-associated X protein (Bax) and cerebral glial fibrillary acidic protein (GFAP) expression. The results have also shown that HES co-treatment has an antioxidant, anti-inflammatory, antiapoptotic effect on SA-induced toxicity and aids to protect tissue architecture by showing a regulatory effect on all values. Consequently, it was determined that HES co-treatment had a protective effect on SA-induced heart and brain toxicity in rats.

Diabetes mellitus (DM) may cause specially health problem which can effect most of tissue such as liver, kidney and brain. Thus, this research aimed to examining the effects ofLupinus albusL. seed ethanol extract (LA) on the liver and renal tissues malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione (GSH) level of diabetic rats. Sprague–Dawley, adult a total of 28 male rats were used in the study that were randomly divided into four groups with 7 animals in each group: Control, STZ-DM, LA and STZ-DM+LA group. Diabetes was induced in rats by a single dose of 60 mg/kg/i.p. Streptozotocin (STZ) injection (STZ-DM and STZ-DM+LA groups).Lupinus albusL. ethanol extract was given at a dose of 10 mg/kg/p.o. via intragastric tube for 20 days (LA and STZ-DM+LA groups). At the end of the study, biochemical and histopathological examination in kidney and liver tissues were examined. STZ application significantly increased the oxidative stress and lipid peroxidation. When the dose of 10 mg/kg of LA significantly decreased the level of plasma glucose and liver and renal MDA. Meanwhile, the levels of liver and renal CAT, SOD, GPx and GSH were significantly increased in diabetic rats treated withLupinus albusL. seed ethanol extract. These results indicate the role ofLupinus albusL. seed extract might as antidiabetic, antioxidant and reducing of the oxidative stress and lipid peroxidation. Extracted afterLupinus albusseed’ roasting is a pioneer in literature and the use of LA in ethnomedicine for diabetes.&nbsp

Living organisms have an innate ability to regulate the synthesis of inorganic materials, such as bones and teeth in humans. Cadmium sulfide (CdS) can be utilized as a quantum dot that functions as a unique light-emitting semiconductor nanocrystal. The increased use in CdS has led to an increased inhalation and ingestion rate of CdS by humans which requires a broader appreciation for the acute and chronic toxicity of CdS. We investigated the toxic effects of CdS on cerebellar cell cultures and rat brain. We employed a ‘green synthesis’ biosynthesis process to obtain biocompatible material that can be used in living organisms, such as Viridibacillus arenosi K64. Nanocrystal formation was initiated by adding CdCl2 (1 mM) to the cell cultures. Our in vitro results established that increased concentrations of CdS (0.1 μg/mL) lead to decreased cell viability as assessed using 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT), total antioxidant capacity (TAC), and total oxidant status (TOS). The in vivo studies showed that exposure to CdS (1 mg/kg) glial fibrillary acidic protein (GFAP) and 8-hydroxy-2' -deoxyguanosine (8-OHdG) were increased. Collectively, we describe a model system that addresses the process from the synthesis to the neurotoxicity assessment for CdS both in vitro and in vivo. These data will be beneficial in establishing a more comprehensive pathway for the understanding of quantum dot-induced neurotoxicity.

Objective Mercury is a global environmental pollutant and is responsible for several organ pathophysiology including oxidative stress-induced liver disorders. Therefore, the present study was conducted to evaluate the potential ameliorative effects of rutin on mercury chloride (HgCl2)-induced hepatotoxicity in adult male rats. Methods HgCl2 was intraperitoneally injected at a dose of 1.23 mg/kg body weight for 7 days alone or in combination with the orally rutin (50 and 100 mg/kg body weight). Results Rutin treatment significantly improved liver function tests [alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT)], and increased activities of antioxidant defense system [catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)] and glutathione (GSH) content. The histological alterations and epidermal growth factor receptor (EGFR) expression in the HgCl2-induced liver tissues were decreased by administration of rutin. Furthermore, rutin reversed the changes in levels of apoptosis and inflammation related proteins involving p53, Bcl-2 associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), cytochrome c, nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), B-cell lymphoma-3(Bcl-3) and interleukin-1β (IL-1β), and inhibited p38α mitogen-activated protein kinase (MAPK) and cysteine aspartate specific protease-3 (caspase-3) activations. Conclusion The data of the present study suggest that rutin effectively suppress HgCl2‐induced hepatotoxicity by ameliorating oxidative stress, inflammation and apoptosis.

Probiotics have been shown to have positive effects when it comes to combating various health issues when consumed, preventing even the absorption of environmental toxins. One of the main environmental toxins encountered today is pesticide residues. Neonicotinoids, widely applied today in countries that have approved of them, are a known class of insecticides with an excellent and effective potency. Neonicotinoids have been shown to cause various toxic effects, either acutely or chronically, on human health and on beneficial insects when exposed. To clarify the assumption that probiotics could counteract these toxic effects, especially on vital organs, the probiotic yeast “Saccharomyces boulardii” (S. boulardii) was tested against the neonicotinoids, acetamiprid (ACE) and imidacloprid (IMI), as it has outstanding physiological and metabolic properties. The results obtained from the studies indicated that although ACE and IMI induced liver, kidney, brain and bowel damage, there was a considerable level of protection by the dietary supplementation of S. boulardii, as it reduced the absorption of these insecticides.

Cyclophosphamide (CYP) is a chemotherapeutic agent used in the treatment of autoimmune disorders and malignant diseases. However, its usage is restricted due to its severe side effects, especially hepatotoxicity and nephrotoxicity. This study aimed to investigate the protective role of chrysin (CH) against CYP-induced hepatotoxicity and nephrotoxicity in rats. In the present study, 35 male Wistar rats were randomly divided into 5 groups with each group consisting of 7 rats. The rats were pretreated with CH orally in doses of 25- and 50-mg/kg body weight for 7 consecutive days, and CYP (200-mg/kg body weight, i.p.) was administrated on the 7th day 1 h after the last dose of CH. It was found that CH could ameliorate CYP-induced elevations of ALT, ALP, AST, urea, creatinine, MDA, and hepatorenal deterioration, and enhance antioxidant enzymes' activities such as SOD, CAT, and GPx, and GSH's level. Furthermore, CH reversed the changes in levels of inflammatory, apoptotic, and autophagic parameters such as NF-κB, TNF-α, IL-1β, IL-6, iNOS, COX-2, Bax, Bcl-2, and LC3B in liver and kidney tissues. To conclude, the findings of this study demonstrated that CH has a protective effect against CYP-induced hepatorenal toxicity.

Although Doxorubicin (DOX) is a widespread drug used in the treatment of cancer, its clinical use is restricted due to its common side effects. In addition, administrating DOX with an antioxidant has recently become a new strategy in preventing the side effects of DOX. The protective effects of morin, a natural flavonoid, against DOX-induced liver and kidney damage in rats were investigated biochemically, immunohistochemically and histopathologically in this study. The experimental procedure was planned as 10 days, and 5 groups consisting of seven rats were formed. Morin was given orally to rats at a dose of 50 and 100 mg/kg for 10 days and DOX was given a single dose of 40 mg/kg intraperitoneally on day 8. In order to determine the protective effect of morin against oxidative stress caused by DOX, reduced glutathione (GSH) and malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) enzyme activities were measured in liver and kidney tissues. Liver and kidney tissue damage were determined both histopathologically and by serum alanine transaminase (ALT), aspartate transaminase (AST), urea and creatinine analysis. In order to determine the effect of DOX-induced inflammation and against the effect of morin, tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and nuclear factor kappa B (NF-kappa B) levels were determined in both tissues. Liver and kidney B-cell lymphoma-2 (Bcl-2) levels were determined biochemically. In addition, Bax expression in liver tissue and aquaporin-2 (AQP-2) and nephrin expression in renal tissue were determined immunohistochemically. It was determined that oxidative damage caused by DOX decreased and improvement of liver and kidney function markers were observed in the groups that were treated with morin. In addition, pre-treatment of morin showed a regulatory effect on TNF-alpha, IL-1 beta and NF-kappa B levels. It prevented the increase in DOX-induced Bax expression and decrease in Bcl-2 level, AQP-2 and nephrin expression. Histopathological examination revealed that it prevented tissue damage in liver and kidney tissues., Unit of Scientific Research Projects of University of Agri Ibrahim Cecen [ECZF.17.001], This research was supported by the Unit of Scientific Research Projects of University of Agri Ibrahim Cecen [Grant number ECZF.17.001].

Objectives Cisplatin is employed for chemotherapeutic purposes in several types of adult and pediatric cancer. However, side-effects including nephrotoxicity, ototoxicity, gastrointestinal effects and neuropathy restrict the use of the drug due to their adverse impacts on quality of life. This study aimed to determine whether levosimendan exhibits a protective effect against cisplatin-related ototoxicity in a rat model by means of functional, biochemical and histochemical analysis. Methods The study was employed with 24 female Sprague Dawley rats. After distortion product otoacoustic emissions (DPOAE) tests applied to all rats, rats were randomly assigned into four groups of six animals each. A single intraperitoneal 15 mg/kg dose of cisplatin was administered to Cisplatin group. Levosimendan group received intraperitoneal levosimendan at a dose of 100 mg/kg for five consecutive days. Cisplatin + Levosimendan group received intraperitoneal levosimendan at a dose of 100 mg/kg for five consecutive days and a single intraperitoneal dose of 15 mg/kg cisplatin at 3rd day of the study. Control group received 8 mL/kg/day intraperitoneal saline solution for five consecutive days. The DPOAE test was repeated on the 6th day of the study. All rats were then sacrificed, the cochleas were removed and set aside for biochemical and histopathological analyses. Results A significant increase in levels of Malondialdehyde (MDA) and significantly lower activities of superoxide dismutase (SOD) and Glutathione peroxidase (GPx) were observed at rats of cisplatin group. Administration of levosimendan showed significantly lower cochlear MDA levels, while SOD and GPx activities both increased significantly. The DPOAE test performed at 6th day of the study showed a significant impairment in the signal-noise ratio (SNR) levels of rats in Cisplatin group. The SNR levels of rats treated with levosimendan were significantly higher than those of cisplatin group and were similar to those of the control group. Cisplatin impaired the cochlear structure and a severe Caspase 3 and 8-hydroxy-2' -deoxyguanosine (8-OHdG) immunopositivity was observed at cochlea of the rats of cisplatin group. Administration of levosimendan protected the structure of cochlea and there was a mild Caspase 3 and 8OHdG immunopositivity. Conclusion Our data demonstrate that levosimendan protects hearing against cisplatin-induced ototoxicity and obviates cellular degeneration. It also significantly reduces oxidative stress and apoptosis, probable mechanisms involved in ototoxicity.

Introduction: Cisplatin is an antineoplastic agent widely used in the treatment of a variety of cancers. Ototoxicity is one of the main side-effects restricting the use of cisplatin. Objective: The purpose of this study was to investigate the protective efficacy of gallic acid, in biochemical, functional and histopathological terms, against ototoxicity induced by cisplatin. Methods: Twenty-eight female Sprague Dawley rats were included. Rats were randomly assigned into four groups of seven animals each. Cisplatin group received a single intraperitoneal dose of 15 mg/kg cisplatin. Gallic acid group received intraperitoneal gallic acid at 100 mg/kg for five consecutive days. Cisplatin + gallic acid group received intraperitoneal gallic acid at 100 mg/kg for five consecutive days and a single intraperitoneal dose of 15 mg/kg cisplatin at 3rd day. A control group received 1 mL intraperitoneal saline solution for five consecutive days. Prior to drug administration, all rats were exposed to the distortion product otoacoustic emissions test. The test was repeated on the 6th day of the study. All rats were then sacrificed; the cochleas were removed and set aside for biochemical and histopathological analyses. Results: In cisplatin group, Day 6 signal noise ratio values were significantly lower than those of the other groups. Also, malondialdehyde levels in cochlear tissues were significantly higher, superoxide dismutase and glutathione peroxidase activities were significantly lower compared to the control group. Histopathologic evaluation revealed erosion in the stria vascularis, degeneration and edema in the connective tissue layer in endothelial cells, impairment of outer hair cells and a decrease in the number of these calls. In the cisplatin + gallic acid group, this biochemical, histopathological and functional changes were reversed. Conclusion: In the light of our findings, we think that gallic acid may have played a protective role against cisplatin-induced ototoxicity in rats, as indicated by the distortion product otoacoustic emissions test results, biochemical findings and immunohistochemical analyses. Resumo: Introdução: A cisplatina é um agente antineoplásico amplamente usado no tratamento de vários tipos de câncer. A ototoxicidade é um dos principais efeitos colaterais que restringem o uso da cisplatina. Objetivo: O objetivo deste estudo foi investigar a eficácia protetora do ácido gálico, em termos bioquímicos, funcionais e histopatológicos, contra a ototoxicidade induzida por cisplatina. Método: Vinte e oito ratas Sprague-Dawley foram incluídas. As ratas foram distribuídas aleatoriamente em quatro grupos de sete animais cada. O grupo cisplatina recebeu uma única dose intraperitoneal de 15 mg/kg de cisplatina. O grupo ácido gálico recebeu ácido gálico via intraperitoneal a uma dose de 100 mg/kg durante cinco dias consecutivos. O grupo cisplatina + ácido gálico recebeu ácido gálico via intraperitoneal a uma dose de 100 mg/kg durante cinco dias consecutivos e uma única dose intraperitoneal de 15 mg/kg de cisplatina no terceiro dia. O grupo controle recebeu 1 mL de solução salina via intraperitoneal por cinco dias consecutivos. Antes da administração do fármaco, todos os ratos foram expostos ao teste de emissões otoacústicas - produto de distorção. O teste foi repetido no sexto dia do estudo. Todos os ratos foram então sacrificados; as cócleas foram removidas e reservadas para análises bioquímicas e histopatológicas. Resultados: No grupo cisplatina, os valores da relação sinal-ruído do dia 6 foram significativamente mais baixos aos dos outros grupos. Além disso, os níveis de malondialdeído nos tecidos cocleares foram significativamente mais altos, e as atividades de superóxido dismutase e glutatione peroxidase foram significativamente mais baixas em comparação com o grupo controle. A avaliação histopatológica revelou erosão na estria vascular, degeneração e edema na camada de tecido conjuntivo em células endoteliais, comprometimento das células ciliadas externas e diminuição do número dessas células. No grupo cisplatina + ácido gálico, estas alterações bioquímicas, histopatológicas e funcionais foram revertidas. Conclusão: Tendo em vista os nossos achados, consideramos que o ácido gálico pode ter desempenhado um papel protetor contra a ototoxicidade induzida por cisplatina em ratas, conforme indicado pelos resultados do teste emissões otoacústicas - produto de distorção, achados bioquímicos e análises imuno-histoquímicas. Keywords: Cisplatin-induced ototoxicity, Gallic acid, Oxidative stress, DPOAE, Palavras-chave: Ototoxicidade induzida por cisplatina, Ácido gálico, Estresse oxidativo, EOAPD

Bu calismada, ratlarda Cyclophosphamide (CP) ile induklenen hemorajik sistitte izole mesane duz kas kontraksiyonlari ve mesane histopatolojisi uzerine Rutin’in etkileri arastirildi. Calismada 24 adet eriskin disi Sprague Dawley rat kullanildi ve ratlarin agirliklari ortalama 200-250 gramdi. Dort deney grubu olusturuldu ve her bir grupta 6 rat vardi. Kontrol ve CP grubuna 7 gun intraperitoneal (ip) serum fizyolojik uygulandi. Ayrica, CP grubuna serum fizyolojik uygulamasinin 5. gunu tek doz CP (150 mg/kg, ip) enjekte edildi. Rutin uygulanan gruplara serum fizyolojikte cozdurulmus Rutin (50 mg/kg, ip) 7 gun enjekte edildi. Rutin+CP grubuna, Rutin uygulamasinin 5. gunu tek doz CP uygulandi. Deneysel uygulamanin 8. gunu ratlar anestezi esliginde dekapite edilerek mesaneleri izole edildi. Izole mesane duz kas seritlerinde Asetilkolin (Ach) (10-4 M) ve Potasyum Klorur (KCI) (60 mM) ile induklenen kontraksiyon degerleri elde edildi. Ayrica mesaneler hematoksilen eozin ile boyanarak histopatolojik degerlendirme yapildi. CP grubundaki ratlarda ACh ve KCl ile induklenen in vitro kontraksiyonlarin arttigi fakat istatistiksel onem arz etmedigi (P>0.05) ve Rutin uygulamasinin artan kontraksiyon cevaplarini azalttigi belirlendi. Histopatolojik incelemede mesane lumeninde epitel dokuntu, mukoza epitelinde deskuamasyon, koagulasyon nekrozu ve siddetli duzeyde eritrosit gorulurken, Rutin’in bu degisiklikleri azalttigi goruldu. Sonuc olarak; CP ile induklenen hemorajik sistitte mesane kontraktilitesi ve histopatolojisi uzerine Rutin uygulamasinin protektif etkili oldugu belirlendi.

This study was aimed to detect the effect of butylated hydroxytoluene (BHT) on the liver glutathione level and glutathione-dependent enzyme activities in female Wistar albino rats. BHT was adminis-tered by oral gavage at a dose of 250 mg/kg (Group I) and 500 mg/kg (Group II) for 28 days, 1000 mg/kg (Group III) and 1500 mg/kg (Group IV) for 4 days. The serum ALT, AST and LDH activities were measured on an autoanalyzer, and liver gluthathione (GSH), gluthathione peroxidase (GPx), gluthathione S-transferase (GST), and gluthathione reductase (GR) activities were analysed with commercial ELISA kits. The ALT activity was significantly higher in Groups III and IV (P

Ethyl carbamate (EC, urethane), which is used as an anesthetic especially by veterinarians due to its very long duration of action, is also a naturally occurring compound in all fermented foods and beverages. Although the health problem of EC is related to its carcinogenic potential, the scarcity of current studies that can be used in the evaluation of usage limits encouraged us to do this study. In this context, zebrafish embryos were exposed to serial doses of EC. According to the results, it was observed that EC exposure caused a significant decrease in survival and hatching rates as well as significant body malformations. Whole-mount staining results showed that EC caused dose-dependent increased apoptosis. Oxidative stress caused by EC exposure was demonstrated by whole-mount staining, transcriptional and immunohistochemically. Furthermore, it has been shown histochemically that EC exposure causes necrosis and degeneration in the brain. In behavioral tests, it was observed that EC caused hyperactivity associated with these neuronal degenerations. In addition, a dramatic decrease in blood flow was detected in association with pericardial edema. In the light of the current results, it should be carefully considered that EC can be found naturally in many human diets, especially fermented foods.

Nephrotoxicity is a very important complication of 5-fluorouracil (5-FU)-treated cancer patients. Increased oxidative stress, kidney damage, and apoptosis play an important role in the pathogenesis of nephrotoxicity caused by 5-FU. In this study, protective effects of two natural compounds, hesperidin and curcumin, on experimentally induced kidney damage in mice with 5-FU were determined. Application of 5-FU resulted in severe histopathological changes and severe renal failure with increased serum urea and creatinine levels. Also, 5-FU-induced kidney damage, increased levels of malondialdehyde (MDA), decreased superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) activity, and glutathione (GSH) level have been demonstrated. Also, where 5-FU is in the concentration of caspase-3 and 8-OHdG immune-positive cells and therefore causes apoptosis and DNA damage in kidney tissue cells. However, especially high doses of hesperidin and curcumin treatment significantly improved 5-FU-induced oxidative stress/lipid peroxidation, apoptosis/DNA damage, and renal dysfunction. Based on these data, our results suggest that hesperidin and curcumin may be used as new and promising agents against 5-FU-induced nephrotoxicity.

Phosphodiesterase-5 inhibitors (PDE-5Is) exert positive effects on bone healing and mineralization by activation the nitric oxide/cyclic guanosine monophosphate/protein kinase-G (NO/cGMP/PKG) signaling pathway. In this study, the effects of zaprinast and avanafil, two PDE-5Is, on the NO signaling pathway, estrogen levels, selected bone formation and destruction marker levels, whole-body bone mineral density (WB-BMD), right femur trabecular bone thickness (RF-TBT) and epiphyseal bone width, angiogenesis in the bone-marrow, and selected oxidative stress parameter levels were investigated in rats with ovariectomy-induced osteoporosis. Twenty four adult rats (8 months old) were equally divided into four groups. The first group was the sham operated group. Groups 2, 3 and 4 included ovariectomized rats. At six months after ovariectomy, the 3rd and 4th groups were administered 10 mg/kg zaprinast and avanafil daily as a single dose for 60 days, respectively. Increases in the activity of the NO/cGMP/PKG signalling-pathway, C-terminal collagen peptide levels, angiogenesis in the bone marrow, RF-TBT, epiphy seal bone width and WB-BMD were observed compared to the ovariectomized positive control group (OVX), while the pyridinoline and deoxypyridinoline levels were decreased in the OVX+zaprinast and OVX+avanafil groups (p

Alzheimer’s disease (AD) is associated with metabolic abnormalities linked to critical elements of neurodegeneration. Here, we analysed the brain transcriptomics data of more than 600 AD patients using genome-scale metabolic models and provided supporting evidence of mitochondrial dysfunction related to the pathophysiologic mechanisms of AD progression. Subsequently, we investigated, in a rat model of AD, the oral administration of Combined Metabolic Activators (CMA), consisting of NAD+ and glutathione precursors, to explore the effect for improvement of biological functions in AD. CMA includes L-serine, nicotinamide riboside, N-acetyl-L-cysteine, and L-carnitine tartrate, salt form of L-carnitine. The study revealed that supplementation of the CMA improved the AD-associated histological parameters in the animals. Finally, we designed a randomized, double-blinded, placebo-controlled human phase 2 clinical trial and showed that the administration of CMA improves cognitive functions in AD patients. As decreased AD Assessment Scale-cognitive subscale (ADAS-Cog) score is the indicator of the improved cognitive function in AD patients, we observed a significant decrease of ADAS-Cog scores on Day 84 vs Day 0 (Log2FC= -0.37, (29% improvement), p-value=0.00001) in the CMA group. We also observed a significant decrease in the placebo group on Day 84 vs Day 0 (Log2FC= -0.19, (14% improvement), p-value=0.001) possibly due to the recommendations of exercise and Mediterranean diet to all AD patients and/or a placebo effect apparent in the early stages of AD clinical trials. A comprehensive analysis of the human plasma metabolome and proteome revealed that plasma levels of proteins and metabolites associated with redox metabolism are significantly improved after treatment. In conclusion, our results show that treating AD patients with CMA leads to enhanced cognitive functions, suggesting a role for such a therapeutic regime in treating AD and other neurodegenerative diseases. Funding: This work was financially supported by ScandiBio Therapeutics and Knut and Alice Wallenberg Foundation. The authors would like to thank the Metabolon Inc. (Durham, USA) for generation of metabolomics data, and ChromaDex Inc. (Irvine, CA, USA) for providing NR. AM and HY acknowledge support from the PoLiMeR Innovative Training Network (Marie Sklodowska-Curie Grant Agreement No. 812616) which has received funding from the European Union’s Horizon 2020 research and innovation programme. Declaration of Interest: AM, JB and MU are the founder and shareholders of ScandiBio Therapeutics. The other authors declare no competing interests. Ethical Approval: All experiments for the treatment of the animals were approved by the Ethics Committee of Ataturk University, and were conducted following the National Institutes of Health Guide for Care and Use of Laboratory Animals.

In the present study, the protective effects of chrysin (CHR) against testicular damage caused by lead acetate (PbAc) were examined. In this way, 30 min after rats were given 25 and 50 mg/kg/b.w CHR orally for seven consecutive days, 30 mg/kg/b.w PbAc was administered orally. In biochemical analysis of testicular tissue, it was found that PbAc-reduced antioxidant parameters [glutathione peroxidase (GPx), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)], while it increased lipid peroxidation, inflammatory markers [nuclear factor kappa-B (NF-κB), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE-2), and inducible nitric oxide synthase (iNOS)], and 8-hydroxy-2'-deoxyguanosine (8-OHdG). In the immunohistochemical examination, it was determined that PbAc increased the expression of tumor necrosis factor-α (TNF-α) and caspase-3. Accordingly, PbAc was found to cause a decrease in sperm motility and an increase in the percentage of dead sperm. However, it has been observed that CHR relieves oxidative stress due to its antioxidant properties, thus protecting against inflammation and apoptosis. It also allowed the CHR sperm parameters to return to control group levels. The results revealed that CHR could be a natural substance to be used in Pb-induced testicular toxicity. PRACTICAL APPLICATIONS: Lead (Pb) is an important environmental contaminant heavy metal. Pb is believed to reduce fertility in men. Oxidative stress plays a significant role in the damage caused by Pb to testicular tissue. CHR is an antioxidant substance that occurs naturally in various plants and has various pharmacological properties. In the present study, it was investigated whether CHR has a protective effect against testicular toxicity induced by PbAc. The results revealed that in rats, CHR protects the testicular tissue from PbAc toxicity by showing antioxidant, anti-inflammatory and anti-apoptotic effects, thus bringing sperm parameters closer to normal.

Bu çalışmada zeytin ağacı (Olea europeae) ağacının yaprağından saflaştırılan oleanolik asidin (OEA) ratlarda çekal ligasyon ve punksiyonla (CLP) indüklenen sepisisin oluşturduğu kalp hasarı üzerine etkileri incelendi. Her gruba eşit olacak şekilde 30 adet Wistar erkek rat sham, sepsis, OEA-150, OEA-300 ve CEFT olarak 5 gruba ayrıldı. Kromatografik metotlarla zeytin yaprağından saflaştırılan oleanolik asit OEA gruplarına 150 ve 300 mg/kg dozlarda oral yolla uygulandı. CEFT grubuna seftriakson 150 mg/kg dozda intraperitoneal yolla uygulandı. Uygulamadan 24 saat sonra ratlardan kan serumu ve kalp dokuları, histopatolojik, immünohistokimyasal ve biyokimyasal analizler için alındı. Yapılan histopatolojik ve immünohistokimyasal incelemede, sepsis grubunun doku tümör nekrozis faktör (TNF)- ve interlökin (IL)-1β ekspresyonlarında artış, myokartta kas liflerinde şiddetli düzeyde hyalin dejenerasyon, Zenker nekrozu ve damarlarda şiddetli düzeyde hiperemi gözlendi. OEA ve seftriakson (CEFT) sitokin ekspresyonlarında ve histopatolojik bulgularda azalma sağladı. Sepsis, doku superoksit dismutaz aktivitesini (SOD) azalttı. Ayrıca lipid peroksidasyonu (LPO) ve glutatyon (GSH) seviyeleri ile doku katalaz (KAT), serum kreatin kinaz (CK-MB) ve serum laktat dehidrojenaz (LDH) aktivitelerini önemli şekilde arttırdı. OEA ve CEFT, SOD aktivitesini önemli derecede arttırırken diğer parametrelerde belirgin düşüşe neden oldu. Bu çalışmadan elde edilen bulgular ışığında oleanolik asidin sepsis sırasında oluşan kalp dokusu hasarının azaltılmasında faydalı olabileceği düşünülmektedir., In the present, the effects of oleanolic acid (OEA) purified from leaf of the olive tree (Olea europeae) on heart damage caused by cecal ligation and puncture (CLP) induced sepsis model in rats were examined. Thirty Wistar rats equally were divided into six groups as sham, sepsis, OEA-150, OEA-300 and CEFT. Oleanolic acid purified from olive leaf by chromatographic methods was orally administered at doses of 150 and 300 mg/kg to OEA groups. Ceftriaxone was intraperitoneally administered at a dose of 150 mg/kg to the CEFT group. Twenty-four hours after the application, blood serum and heart tissues were taken from rats for histopathological, immunohistochemical and biochemical analysis. In histopathological and immunohistochemical examination, an increase in tissue tumor necrosis factor (TNF)- and interleukin (IL)-1β expressions of the sepsis group, severe hyaline degeneration in muscle fibers in the myocardium, Zenker necrosis and severe hyperemia in the vessels were observed. OEA and ceftriaxone (CEFT) provided a decrease in cytokine expressions and histopathological findings. Sepsis reduced tissue superoxide dismutase activity (SOD). It also significantly increased lipid peroxidation (LPO), glutathione (GSH) levels, catalase (CAT), serum creatine kinase (CK-MB) and serum lactate dehydrogenase (LDH) activities. OEA and CEFT significantly increased SOD activity while causing a significant decrease in other parameters. In the light of the findings from this study, it is thought that oleanolic acid may be beneficial in reducing heart tissue damage during sepsis.

Butylated hydroxyanisole (BHA) has been widely used in the cosmetics, pharmaceutical, and food industries due to its antioxidant activity. Despite the antioxidant effects, reported adverse effects of BHA at the cellular level have made its use controversial. In this regard, this study was performed to elucidate the potential toxicity mechanism caused by BHA at the molecular level in zebrafish embryos. For this purpose, zebrafish embryos were exposed to BHA at levels of 0.5, 1, 5, 7.5 and 10 ppm and monitored at 24, 48, 72 and 96 hours. Survival rate, hatching rate and malformations were evaluated. We examined the potential for reactive oxygen species (ROS) production and apoptosis signalling accumulation in the whole body. Moreover, we evaluated histopathological and immunohistochemical (8-OHDG) characterization of the brain in zebrafish embryos at the 96th hour. We also examined apoptosis, histopathological and immunohistochemical (8-OHDG) characteristics in 96 hpf zebrafish larvae exposed to tertiary butylhydroquinone (TBHQ), one of the major metabolites of BHA, at doses of 0.5, 2.5, 3.75 and 5 ppm. Consequently, it has been considered that increased embryonic and larval malformations in this study may have been caused by ROS-induced apoptosis. After 96 h of exposure, positive 8-OHdG immunofluorescence, degenerative changes, and necrosis were observed in the brain of BHA and TBHQ-treated zebrafish larvae in a dose-dependent manner. BHA and TBHQ exposure could lead to an increase in 8-OHdG activities by resulting oxidative DNA damage. In particular, the obtained data indicate that the induction of ROS formation, occurring during exposure to BHA and/or multiple hydroxyl groups, could be responsible for apoptosis.

This study was performed to evaluate the effect of chrysin on testicular torsion and detorsion damage in rats in terms of biochemistry, histopathology and immunohistochemistry. The study was performed on Wistar albino rats between 250 g and 300 g. A total of 40 rats were used. Five groups were created with eight rats in each group. Group 1 was the control group, and no torsion procedure was performed. In Group 2, 2 hr of torsion and 2 hr of detorsion were applied. In Group 3, 2 hr of torsion and 24 hr of detorsion were applied. In Group 4, 2 hr of torsion, 2 hr of detorsion and 50 mg/kg intraperitoneal chrysin were applied. In Group 5, 2 hr of torsion, 24 hr of detorsion and 50 mg/kg of chrysin were applied. In the torsion/detorsion groups, the study determined decreases in glutathione and testosterone levels, increases in tumour necrosis factor-alpha, interleukin-4, interleukin-6 and interleukin-10 levels, and increases in expression levels of caspase-3 and caspase-8. Chrysin application reduced malondialdehyde, tumour necrosis factor-alpha, caspase-3 and caspase-8 expression levels. We can say that chrysin can be used to reduce damage in cases of testicular ischaemia/reperfusion. For more reliable results, further clinical trials are recommended.

Allergic rhinitis (AR) is a ubiquitous chronic disease with a growing incidence. We aimed to investigate the protective effect of naringenin against AR induced in rats. Thirty-two Sprague Dawley rats were divided into four groups of eight animals each. Group 1 represented the control group. The other 24 rats were sensitized with intraperitoneal 0.3 mg ovalbumin (OVA) and 30 mg aluminum hydroxide every other day for 14 days to induce AR. Ten microliters OVA was administered to both nostrils by inhalation for the following seven days to provoke AR. Group 2 represented the AR group and received no treatment. Group 3 was treated as the reference group and received 5 mg/kg desloratadine every day between days 15 and 21. Group 4 received 100 mg/kg naringenin orally between days 15 and 21. All animal’s sneezing and nasal itching scores were recorded on day 22. The rats were then sacrificed. Serum total IgE, IL4 and IL5 values were studied, and nasal structures were extracted ‘en bloc’ for histopathological examination. Significant clinical recovery was achieved in the group treated with naringenin. Serum total IgE, IL4 and IL5 values in the naringenin group were significantly lower than in the AR group, and significant histopathological improvement was observed compared to the AR group. Naringenin produced significant clinical, biochemical and histopathological benefits in rats with induced AR. These effects suggest that naringenin is a promising agent for the treatment of AR.

We aimed to study the effect of coenzyme Q10 on pro-inflammatory cytokine, matrix metalloproteinase, oxidative DNA damage, caspase 3 and caspase 8 in ischaemia/reperfusion injury led to by testicular torsion/detorsion. Our research is a controlled experimental animal research using rats. This study was conducted with fifty-six adult male Albino Wistar rats. Interleucine-1 beta, 2, 6, 10, tumour necrosis factor-alpha, matrix metalloproteinase-2, 3, 9, 13, tissue inhibitor matrix metalloproteinase-1, 2, malondialdehyde and leucocyte 8-hydroxy-2-deoxy guanosine/10(6) deoxyguanosine was detected in serum and tissue samples. In addition, immunohistochemical analysis of caspase 2 and caspase 8 was performed. In testicular I/R injury, especially 24 hr after detorsion, oxidative damage pro-inflammatory cytokines and matrix metalloproteinases were increased. At the coenzyme Q10 group, a meaningful decrease was observed in these parameters. In addition, a decrease in the expression of caspase3 and caspase 8 was viewed in coenzyme Q10-treated groups. The coenzyme Q10 has beneficial effects on oxidative damage, pro-inflammatory cytokine levels, remodelling of extracellular matrix and apoptosis in testicular I/R injury.

Ferulic acid is a kind of phenolic compound that can be found in various fruits and vegetables. This study aims to investigate the effect of ferulic acid on nephrotoxicity induced by gentamicin (GM). In this study, rats were separated into 4 groups such that each containing 8 randomly selected rats: Control group, Ferulic Acid (FA) group, Gentamicin (GM) group and Gentamicin + Ferulic acid (GM + FA) group. Blood samples were collected after 24 hours following the 8-day trial period, and kidneys were taken out for histopathological evaluation. Serum urea, creatinine, uric acid and LDH analyses were performed in autoanalyzer while Malondialdehyde (MDA), Advanced Oxidized Protein Products (AOPP), Glutathione (GSH), Superoxide dismutase (SOD), Catalase (CAT), Interleukin 6 (IL-6), Tumor Necrosis Factor-alpha (TNF-alpha) analyses were performed in ELISA, and kidney tissues were also examined histopathologically. Urea (p < .001), creatinine (p < .001), MDA (p < .01), AOPP (p < .001), IL-6 (p < .01) and TNF-alpha (p < .001) levels were found to be statistically and significantly lowered in GM + FA group when compared to GM group. As a result, ferulic acid has reduced the inflammation in nephrotoxicity induced by GM, causing decreased oxidative stress. In this study, anti-inflammatory features of ferulic acid have come to the forefront rather than the antioxidant features. It can be said that ferulic acid reduces nephrotoxic damage and has protective properties for kidneys.

Aim Vancomycin (VCM) is a glycopeptide antibiotic widely used to treat serious infections caused by methicillin-resistant Staphylococcus aureus and has been associated with some severe side effects such as hepatotoxicity and nephrotoxicity. However, the underlying mechanism of VCM-induced hepatotoxicity is not yet fully understood. Therefore, the current study was designed to evaluate the protective effects of zingerone (Zin) against VCM-induced hepatotoxicity in rats. Materials and methods VCM was intraperitoneally administered at a dose of 200 mg/kg body weight (b.w.) for 7 days alone and in combination with the orally administered Zin (25 and 50 mg/kg b.w). Key findings Zin treatment significantly improved VCM-induced hepatic lipid peroxidation, glutathione depletion, reduced antioxidant enzyme (superoxide dismutase, catalase and glutathione peroxidase) activities and liver function markers (aspartate aminotransferase, alkaline phosphatase and alanine aminotransferase). Histopathological integrity and immunohistochemical expression of 8-hydroxy-2′-deoxyguanosine (8-OHdG) in the VCM-induced liver tissue were ameliorated after Zin administration. In addition, Zin reversed the changes in levels and/or activities of inflammatory and apoptotic parameters such as nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), p53, cysteine aspartate specific protease-3 (caspase-3), cysteine aspartate specific protease-8 (caspase-8), cytochrome c, Bcl-2 associated X protein (Bax) and B-cell lymphoma-2 (Bcl-2) in the VCM-induced hepatotoxicity. Significance Collectively, these results reveal probable ameliorative role of Zin against VCM-induced hepatotoxicity.

In this study, the protective effects of chrysin (CR) on lead acetate (PbAc)-induced renal toxicity in Sprague-Dawley rats were investigated with biochemical, histopathological, and immunohistochemical methods. In the study, rats were given orally at 30 mg/kg/body weight (BW) PbAc after CR of 25 and 50 mg/kg/BW was administered to them orally (a total of 7 administrations for 7 days). The results showed that CR reduced urea and creatinine levels by alleviating PbAc-induced kidney damage. It was determined that CR decreases PbAc-induced lipid peroxidation due to its antioxidant properties and increases catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and glutathione (GSH) levels. It was also detected that CR protects DNA from the toxic effects of PbAc and reduces 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels. Biochemical and immunohistochemical findings demonstrated that CR had anti-inflammatory and antiapoptotic effects and reduced nuclear factor kappa-B (NF-κB), interleukin-33 (IL-33), prostaglandin-E2 (PGE-2), tumor necrosis factor-α (TNF-α), p53 levels, and the activities of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), which were increased with PbAc administration. Moreover, CR was found to increase the levels of aquaporin-1 (AQP-1) and nephrine in PbAc-induced kidney tissue. CR decreased the contents of lead (Pb), zinc (Zn), iron (Fe), sodium (Na), and copper (Cu) and increased those of potassium (K) calcium (Ca) in renal tissue. These results indicated that CR considerably alleviates kidney toxicity caused by PbAc.

In this study, the effect of low-dose curcumin on sperm parameters, reproductive hormones, lipid profile, biochemical antioxidant parameters and the histopathological structure of the testis in diabetic male rats were evaluated. In the study, 28 male Wistar albino rats weighing 300-370 g and aged 8-10 weeks were used. Four groups of equal numbers have been created. Diabetes mellitus was induced with 45 mg/kg streptozotocin (STZ) in seven rats. Curcumin was administered to the rats in curcumin and the diabetes + curcumin group by gavage for 15 days at a dose of 10 mg/kg. Then, the rats were sacrificed. Blood samples and testis tissues were obtained, while the rats were under anaesthesia. Glucose, lipid profile, reproductive hormones, sperm parameters, biochemical antioxidant parameters and histopathological examination of the testis were performed. Abnormal sperm ratio, malondialdehyde, glucose, cholesterol, low-density lipoprotein, and triglyceride levels and caspase-3 expression were increased in diabetic rats, while the sperm motility and intensity and reduced glutathione, catalase and testosterone levels were decreased. When low-dose curcumin (10 mg/kg) was administered to diabetic rats, we found that curcumin significantly increased sperm motility and density, and decreased abnormal sperm rate according to the diabetic group. Moreover, curcumin significantly suppressed the lipid profile and increased follicle-stimulating hormone (FSH) and testosterone levels compared to the diabetic group. On testicular damage and decreased reproductive hormones caused by diabetes, curcumin may have a protective effect with indirect effect of glycaemic control by curcumin.

Objective: This study investigated effects of zaprinast and avanafil on angiogenesis, vascular endothelial growth factor (VEGF), bone morphogenic protein (BMP) 2, 4 and 7. Methods: Female rats were randomly divided into four groups (n = 6). Sham; abdomen was approximately 2 cm opened and closed. Ovariectomised (OVX); abdomen was opened 2 cm and the ovaries were cut. OVX + zaprinast and OVX + avanafil groups; after the same procedure with OVX, 10 mg/kg zaprinast and avanafil were orally administered for 2 month, respectively. Angiogenesis and the levels of VEGF, BMP2, 4 and 7 were determined. Results: VEGF, BMP2, 4 and 7 levels in OVX + zaprinast and especially OVX + avanafil groups were higher than the sham and OVX (p < .05). However, only VEGF and BMP2 levels in OVX + zaprinast group were significant according to sham (p < .05). Also, angiogenesis in OVX + zaprinast and OVX + avanafil groups was dominant according to sham and OVX (p < .05). Conclusions: Zaprinast and avanafil induced BMP2, 4 and 7 levels synergistically with increased VEGF and angiogenesis in renal tissue.

This study was aimed to investigate the antihemorrhoidal effects of ethanol (CBE) and water extracts (CBW) of Capsella bursa-pastoris, an edible plant and a precipitant (CBW-1) obtained from the CBW in croton oil (CO)-induced hemorrhoid model in rats. CBW-1 was contain three organic acids, citric acid (36.09%), malic acid (35.56%), and quinic acid (17.73%). Hemorrhoids were evaluated by histopathology of recto-anal tissues and biochemical parameters in plasma and recto-anal tissues of rats. CBW, CBE, and CBW-1 significantly reduced hemorrhagic necrotic enteritis induced by CO. CO also increased the cytokines and lipid peroxidation (LPO) in serum, and myeloperoxidase (MPO) activity and LPO in recto-anal tissues, and reduced the GSH, CAT, GPx, and SOD levels in serum and recto-anal tissues. However, CBE, CBW, and CBW-1 ameliorated the levels of the cytokines, LPO, MPO, and the antioxidants. Our results conclude that the curative effect of Capsella bursa-pastoris is closely related with its organic acids constituents, citric, malic, and quinic acids. PRACTICAL APPLICATIONS: The fresh leaves of Capsella bursa-pastoris are edible, eaten raw or cooked, and also used in salad. It has a widespread traditional usage in the treatment of the hemorrhoids in the Anatolia and in the Middle East Countries. According to our literature survey, any scientific evidence has not been found in the literature that C. bursa-pastoris could be used in the treatment of hemorrhoids. Therefore, in the current study, we aimed to investigate the antihemorrhoidal and antioxidant effects of ethanol and water extracts, and a precipitant (CBW-1) obtained from the CBW of C. bursa-pastoris in croton oil (CO)-induced hemorrhoid model in rats. The current results showed that its water extract and CBW-1 containing three organic acids, citric acid (36.09%), malic acid (35.56%), and quinic acid (17.73%) significantly reduced the hemorrhagic necrotic enteritis induced by CO ameliorating the levels of the cytokines, LPO, MPO, and the antioxidants. Our results conclude that the curative effect of C. bursa-pastoris is closely related with its organic acids constituents, citric, malic, and quinic acids.

This study investigated the effects of rutin against reproductive damage caused by toxic mercury in male rats. Thirty-five Sprague Dawley rats were used. Control group was injected with saline for 7 days. The rutin-100 group received 100 mg/kg/b.w. rutin for 7 days. Mercuric chloride (HgCl2 ) group received 1.23 mg/kg/b.w. of HgCl2 for 7 days. Mercury chloride + rutin-50 group received 50 mg/kg/b.w. rutin and HgCl2 1.23 mg/kg/b.w. for 7 days. HgCl2 + rutin-100 group received 100 mg/kg/b.w. rutin and HgCl2 1.23 mg/kg/b.w. for 7 days. It was detected that HgCl2 treatment increased malondialdehyde (MDA) levels, tumour necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) expressions, necrosis and degeneration of spermatogonium, dead and abnormal sperm percentages; tubular walls thinning; and decreased antioxidant enzyme activities and sperm motility. It was determined that rutin application reduced testicular damage caused by HgCl2 . In conclusion, rutin administration may treat HgCl2 toxicity in testes.

We sought to determine the effects of selenium (Se) on acrylamide (ACR)-induced nephrotoxicity in rats. In our study, 50 adult male Sprague-Dawley rats weighing 200–250 g were randomly divided into five groups. The control group was given intra-gastric (i.g.) saline (1 mL) for 10 days. The ACR group was given i.g. ACR in saline (38.27 mg/kg titrated to 1 mL) for 10 days. The Se0.5 + ACR and Se1 + ACR groups were administered Se in saline (0.5 and 1 mg/kg, respectively) for 10 days and given i.g. ACR (38.27 mg/kg) one hour after the Se injections. The Se1 group was administered i.g. Se (1 mg/kg) for 10 days. On day 11, intracardiac blood samples were obtained from the rats while they were under anesthesia, after which they were euthanized by decapitation. Urea and creatinine concentrations of blood serum samples were analyzed with an autoanalyzer. Enzyme-linked immunosorbence immunosorbent assay (ELISA) was used to quantify malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), tumor necrosis factor-α (TNF-α), nuclear factor-κB (NF-κB), interleukin (IL)-33, IL-6, IL-1β, cyclooxygenase-2 (COX-2), kidney injury molecule-1 (KIM-1), mitogen-activated protein kinase-1 (MAPK-1), and caspase-3 in kidney tissues. Renal tissues were evaluated by histopathological and immunohistochemical examinations for 8-hydroxylo-2′-deoxyguanosin 8-hydroxy-2′-deoxyguanosine (8-OhDG) and Bax. Serum urea and creatinine levels were higher in the ACR group than in the control, and these ACR-induced increases were prevented by high doses of Se. Additionally, ACR induced the renal oxidative stress, inflammation, apoptosis, and damage to DNA and tissue; likewise, these were prevented by high doses of Se. Taken with ACR, Se confers protection against ACR-induced nephrotoxicity in rats by reducing oxidative stress, inflammation, apoptosis, and DNA damage.

Amaç: Sepsis öldürücü ciddi bir klinik hastalıktır. Sepsis durumunda oksidatif stres inflamasyonda önemli bir rol oynar. Bu nedenle çalışmada oleuropeinin (OLE) ve seftriaksonun (CEFT) sepsis üzerine etkileri denenmiştir. Gereç ve Yöntem: Otuz adet erkek rat Sham, Sepsis, CEFT, OLE-150 ve OLE-300 olmak üzere 5 eşit gruba ayrılarak, model uygulamasından 15 dakika önce 150 mg/kg seftriakson (IP), 150 mg ve 300 mg OLE (PO), uygulandı. Uygulamadan 24 saat sonra kan, akciğer ve kalp dokuları alındı. Serumda kreatin kinaz (CK) ve laktat dehidrojenaz (LDH) düzeyleri ölçülürken, kalp ve akciğer dokularında lipit peroksidasyonu (LPO) ve glutatyon (GSH), süperoksit dismutaz (SOD) ve katalaz (KAT) düzeyleri tespit edildi. Ayrıca, patolojik ve immünohistokimyasal olarak akciğerde interlökin (IL)-8 ve kalpte tümör nekrozis faktör (TNF)-α ekspresyonları belirlendi. Bulgular: Sepsis CK, LDH, LPO, GSH ve kalp CAT aktivitelerinde önemli bir artışa, SOD ve akciğer CAT aktivitesinde ise belirgin azalmaya neden oldu (p, Aim: Sepsis is a fatal serious clinical disorder. The oxidative stress in sepsis plays an important role in the inflammation. Therefore, the effects of oleuropein (OLE) and ceftriaxone (CEFT) on sepsis were investigated in this study. Materials and Methods: Thirty male rats were divided into five equal groups: Sham, Sepsis, CEFT, OLE-150 and OLE-300, The 150 mg/kg of ceftriaxone (i.p.), and 150 and 300 mg/kg OLE (p.o.) were administered to the treatment groups fifteen minutes before the experiment. After 24 hours, blood samples, lungs and hearts tissues were taken. The creatine kinase (CK) and lactate dehydrogenase (LDH) activities in serum, lipid peroxidation (LPO), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels were all determined. In addition, the expressions of the interleukin (IL)-8 in lung and tumor necrosis factor (TNF)-α in heart were pathologically and immunohistochemically were determined. Results: Sepsis caused significant increases in CK, LDH, LPO, GSH and heart CAT activity and caused inhibition of SOD and lung CAT activity (p

Background Diplotaenia turcica has been used traditionally to diabetes treatment. In this study, the effects of D. turcica root extract (DT) on diabetes mellitus induced by streptozotocin (STZ) were investigated. Materials and methods In this study, 78 male rats were used, rats were divided into 9 groups randomly. In diabetic groups, STZ was given a single dose of 45 mg/kg by intraperitoneally. DT (50, 100 and 200 mg/kg) and glibenclamide (5 mg/kg) were given by orally. Blood and pancreas tissue samples were taken for biochemical and pathological tests. Results It was found that glucose levels decreased, and insulin levels increased in the treatment groups compared with the diabetes group. In addition, only in 200 mg/kg DT dose group was found to decrease HbA1c levels. Pancreatic tissue analysis showed that MDA levels decreased and GSH levels and CAT, SOD, GSH-Px and GSH-R activities increased in diabetic rats treated with DT. Histopathological and immunohistochemical examinations of the pancreas showed significant improvements in the treatment with DT. Conclusion These results clearly show the antioxidant property of DT. The findings of this study showed that increased doses of DT may have a therapeutic effect on STZ-induced pancreatic damage.

Objective: This study investigated effect of zaprinast and avanafil on vascular endothelial growth factor (VEGF), bone morphogenic protein (BMP) 4 and 7, and vitamin D-3 levels against the negative effect of dexamethazone. Method: Rats were randomly divided into four groups (n = 6). Control: Empty a syringe was immersed and removed subcutaneously. Dexamethasone (DEX): 120 mu g/kg DEX was injected subcutaneously once a day for 28 days. DEX + zaprinast and DEX + avanafil groups: 10 mg/kg zaprinast and avanafil were administrated to rats in addition to the same procedure in the DEX, respectively. VitaminD(3), VEGF, BMP4 and 7 levels by enzyme linked immunosorbent assay (ELISA) and angiogenesis by histopathological/immunohistochemical were evaluated. Results: BMP4 values in the DEX were lower than the other groups (p < .05). DEX + zaprinast and DEX + avanafil exhibited an increase in all the parameters compared to the control and DEX (p < .05). However, these were not significant for the DEX + zaprinast (p > .05). Also, there was a significant increase in angiogenesis in the DEX + zaprinast and DEX + avanafil. Conclusion: Zaprinast and significantly avanafil induced vitamin D-3, BMP4 and 7 levels by increasing angiogenesis in renal.

Bu çalışmada Cyclophosphamide (CYP) uygulaması yapılan ratlarda karaciğer enzimleri (Aspartat aminotransferaz (AST), Alanin aminotransferaz (ALT), Alkalen fosfataz (ALP) ve histopatolojisi üzerine Naringin’in protektif etkilerinin araştırılması amaçlanmaktadır. Araştırmamızda yaklaşık 200-250 g ağırlığında, 40 adet erkek erişkin Sprague Dawley ırkı rat kullanıldı ve 5 grup oluşturuldu. Karaciğer enzimlerinin analizleri otoanalizörde ve spektrofotometrede yapıldı. Hematoksilen eosin ile boyanan karaciğer doku örnekleri ışık mikroskobunda incelendi. CYP’nin ratlarda hepatotoksiteye yol açtığı ve karaciğer enzimlerini artırdığı görüldü. AST, ALT ve ALP değerleri Kontrol grubunda 58±11, 32±8, 38±6; CYP grubunda 237±42, 168±44, 74±11; Naringin 50+CYP grubunda 223±33, 158±42, 62±9; Naringin 100+CYP grubunda 117±25, 107±24, 48±8; Naringin 100 grubunda ise 54±9, 31±7, 36±6 sırasıyla olarak bulundu. Kontrol grubundan elde edilen değerlere göre CYP verilen gruplarda ki AST, ALT ve ALP değerlerinin tamamında P, In this study, it is aimed to investigate the protective effects of Naringin on liver enzymes (Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT), Alkaline Phosphatase (ALP) and histopathology in CYP-induced rats. In our study, forty male adult Sprague Dawley rat weighing approximately 200-250 g were used and 5 gropus formed. Analyzes of liver enzymes were done in auto analyzer and spectrophotometer. The liver tissue samples stained with hematoxylin eosin were examined by light microscopy. CYP was found to cause hapatotoxicity and showed increased liver enzymes in rats. AST, ALT and ALP values were 58±11, 32±8, 38±6 in the control group; 237±42, 168±44, 74±11 in the CYP group; 223±33, 158±42, 62±9 in the Naringin 50+CYP group; 117±25, 107±24, 48±8 in Naringin 100+CYP group; 54±9, 31±7, 36±6 in the group of Naringin 100 were found respectively. According to the values obtained from the control group, there is an increase of P

Ototoxicity refers to cellular damage or functional disorder developing in the inner ear in association with any therapeutic agent or chemical substance. Cisplatin, one of these agents capable of causing ototoxicity, is a chemotherapeutic used in several malignancies. Ferulic acid (FA) is a phenolic acid with known anti-oxidative and anti-inflammatory properties. The purpose of this study was to perform a biochemical and histopathological investigation of the protective efficacy of FA against cisplatin-induced ototoxicity in rats. Twenty-four Wistar rats were used in this study. Animals were randomly assigned into four groups of six rats each. Rats in the control group received intraperitoneal injection of 1 ml salin for four consecutive days. Rats in the cisplatin group received a single intraperitoneal administration of 10 mg/kg cisplatin. Rats in the FA group received intraperitoneal FA at 100 mg/kg for four days, and rats in the cisplatin+FA group received intraperitoneal FA at 100 mg/kg 1 h after administration of intraperitoneal cisplatin at 10 mg/kg, this procedure being performed for four consecutive days. Rats were sacrificed 24 h after the final drug administration. Cochlear tissues were removed for biochemical and histopathological analysis. MDA levels were significantly higher in cochlear tissues of the rats receiving cisplatin compared to the control group. MDA levels in rats receiving cisplatin and treated with FA were significantly lower than those in the cisplatin group. Activities of SOD and GPx decreased significantly in the cochleas of rats administered cisplatin compared to the control group. Both SOD and GPx activities were significantly higher in rats administered FA and cisplatin in combination compared to the cisplatin only. Histopathological evaluation of cochleas of the rats revealed significant protection of FA against cisplatin induced ototoxicity. This study, the first in the literature, shows that FA exhibits a protective effect against cisplatin-induced ototoxicity. [Med-Science 2018; 7(3.000): 528-31]

Vancomycin (VCM) is a glycopeptidic broad-spectrum antibiotic against methicillin-resistant Staphylococcus aureus, though it has some adverse effects, including nephrotoxicity, that limit its usefulness. Zingerone (ZO), a component of dry ginger root, has several pharmacological activities due to its antioxidant, anti-inflammatory and antiapoptotic properties. The aim of this study was to determine the therapeutic efficacy of ZO against VCM-induced oxidative stress, inflammation, apoptosis and kidney aquaporin 1 (AQP1) levels in rats. Intraperitoneal administration of VCM (200 mg/kg body weight) for seven days increased kidney lipid peroxidation and decreased antioxidant enzyme activities, including kidney superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). VCM increased serum creatinine and urea levels and induced histopathological changes while causing a decrease in AQP1 protein level. VCM also increased the levels of the inflammatory markers nuclear factor kappa B (NF-κB), B-cell lymphoma-3(Bcl-3), interleukin-1β (IL-1β), interleukin-33 (IL-33), tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), myeloperoxidase (MPO) and cyclooxygenase-2 (COX-2). Moreover, it activated the apoptotic pathway by increasing the expression levels of p53, Bcl-2 associated X protein (Bax), cysteine aspartate specific protease-3 (caspase-3) and 8-hydroxy-2′-deoxyguanosine (8−OHdG), which is a marker of oxidative DNA damage. Treatment with ZO (25 and 50 mg/kg body weight) at both doses prevented nephrotoxicity by ameliorating the histopathological alterations, oxidative stress, inflammation, apoptosis, oxidative DNA damage and renal AQP1 levels. The findings of the present study suggested that ZO attenuates VCM-induced nephrotoxicity.

Acrylamide (ACR) is a heat-induced carcinogen substance that is found in some foods due to cooking or other thermal processes. The aim of present study was to assess the probable protective effects of morin against ACR-induced hepatorenal toxicity in rats. The rats were treated with ACR (38.27 mg/kg b.w., p.o.) alone or with morin (50 and 100 mg/kg b.w., p.o.) for 10 consecutive days. Morin treatment attenuated the ACR-induced liver and kidney tissue injury by diminishing the serum AST, ALP, ALT, urea and creatinine levels. Morin increased activities of SOD, CAT and GPx and levels of GSH, and suppressed lipid peroxidation in ACR induced tissues. Histopathological changes and immunohistochemical expressions of p53, EGFR, nephrin and AQP2 in the ACR-induced liver and kidney tissues were decreased after administration of morin. In addition, morin reversed the changes in levels of apoptotic, autophagic and inflammatory parameters such as caspase-3, bax, bcl-2, cytochrome c, beclin-1, LC3A, LC3B, p38α MAPK, NF-κB, IL-1β, IL-6, TNF-α and COX-2 in the ACR-induced toxicity. Morin also affected the protein levels by regulating the PI3K/Akt/mTOR signaling pathway and thus alleviated ACR-induced apoptosis and autophagy. Overall, these findings may shed some lights on new approaches for the treatment of ACR-induced hepatotoxicity and nephrotoxicity.

Fucoidan is a polysaccharide with high viscosity and mucilage, which contains significant proportion of sulphate ester group and L-fucose. It is present in intercellular spaces of brown algae. This study aimed to investigate the effect of fucoidan on some biochemical parameters and kidney tissues in nephrotoxicity induced by GM in rats. The rats used in the study were randomly divided into 4 groups. Each group had 7 rats as control, fucoidan, GM and GM+fucoidan. Blood samples were taken after 24 hours from the end of experiment which lasted eight days. Creatinine, BUN, uric acid, glucose, triglycerides, total cholesterol, VLDL, HDL, total bilirubin levels and ALT, AST, ALP, LDH, CK, amylase activities were assayed by an autoanalyser. The kidney tissues were examined histopathologically. In GM+fucoidan group, creatinine (p, Fucoidan, tüm kahverengi alglerin hücreler arası boşluklarında bulunan yüksek vizkoziteye sahip müsilajımsı, önemli oranda sülfat ester grupları ve L-fukoz içeren bir polisakkarittir. Bu çalışmada ratlarda gentamisin (GM) ile oluşturulan nefrotoksisitede fucoidan kullanılmasının bazı biyokimyasal parametreler ile böbrek dokusu üzerine etkisinin araştırılması hedeflenmiştir. Çalışmada kullanılan ratlar rastgele seçilerek her biri 7 rattan oluşan 4 gruba ayrıldı: Kontrol grubu, fucoidan grubu, GM grubu, GM+fucoidan grubu. Sekiz günlük deneme süresinden 24 saat sonra kan örnekleri alındı. Kreatinin, BUN, ürik asit, glukoz, trigliserit, total kolesterol, VLDL, HDL, total bilirubin düzeyleri ile ALT, AST, ALP, LDH, CK, amilaz aktiviteleri otoanalizörde analiz edildi. Böbrek dokuları histopatolojik açıdan incelendi. GM grubuna göre fucoidan+GM grubunda kreatinin (p

Pomegranate juice (PJ) contains relevant amounts of active biological compounds which alleviate the detrimental effects of chronic heavy metal exposure. This study investigated the protective potential of PJ against lead-induced oxidative stress. A total of forty adult male Sprague Dawley rats were divided into four experimental groups. The animals were fed a standard pellet diet and tap water ad libitum. The rats were divided into four groups (n=10 for each group): control, lead asetat (2000 ppm), low-treated PJ- a daily dose of 2.000 ppm lead plus 30µl pomegranate juice (included 1.050 µmol total polyphenols, gallic acid equivalent), and high-treated PJ- a daily dose of 2.000 ppm lead plus 60µl pomegranate juice (included 2.100 µmol total polyphenols, gallic acid equivalent). The treatments were delivered for 5 weeks. After the treatment period, the tissues samples (kidney, liver, heart and testis) were collected. Tissue lead (Pb) and mineral amounts (copper, zinc, and iron), tissues lipid peroxidation level and antioxidant status, and tissues histopathological changes were determined. The results showed that the highest rate lead loading was in the kidney and the testis. Pomegranate juice was decreased the lead levels of soft tissues examined; increased Zn amounts in tissues of which the lead accumulation was higher (kidney and the testis); decreased the copper, zinc and the iron levels of the liver and heart tissues, without creating a weakness in antioxidant capacity of these tissues, restricted the oxidative stress by decreasing lipid peroxidation, improved both of the activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalaz (CAT), and the level of glutathione (GSH) in all the tissues examined in lead-treated groups. As histopathological findings, the cellular damage induced by lead in the tissues of the kidney, liver and the heart were observed to have been partially prevented by PJ treatment. The protective effect of PJ was more pronounced in the testis compared to those others.

The current systemic treatments of the various solid tumors involve Cisplatin (CIS)-based chemotherapy. Due to its cytotoxicity, this approach is limited. Moreover, the safety of CIS is only discussed especially in breast and stomach cancers. Therefore, we, for the first time, explored the restorative efficacy of oleuropein (OLE), in stomach and lung injuries induced by CIS. Sprague-Dawley rats were divided into eight groups: control CIS, OLE and CIS + OLE. Single dose of (7 mg/kg) CIS was administered intraperitoneally to CIS and CIS + OLE groups. After 24 h, 50, 100 and 200 mg/kg OLE was given for three consecutive days to OLE and CIS + OLE groups. The 8-OH-dG, total oxidative/antioxidant status (TOS/TAS) and malondialdehyde (MDA) levels were evaluated and histopathological analyses were performed on the studied tissues. The results indicated that CIS significantly increased 8-OH-dG, MDA and TOS levels and caused severe tissue damages. However, high dose of OLE induced a significant decrease in the 8-OH-dG, MDA levels, an increase in TAS levels and it restores CIS-induced tissue damages. We hope that the results of this study will provide an impetus for future studies on novel therapeutic strategies including the protective use of oleuropein in gastric and lung cancers due to chemotherapy.

Context: Ferulago angulata (Schlecht.) Boiss. (Apiaceae) (FASB) is used to treat liver diseases and has been used both as food and therapeutics by many cultures for thousands of years because of the natural antioxidant compounds. ABSTRACT Context: Ferulago angulata (Schlecht.) Boiss. (Apiaceae) (FASB) is used to treat liver diseases and has been used both as food and therapeutics by many cultures for thousands of years because of the natural antioxidant compounds. Objective: This study determines antioxidant properties of FASB flowers, the levels of minerals and vitamins, and also, evaluates the hepatoprotective effect of flowers against N-nitrosodimethylamine (NDMA) induced on liver tissue by assessing antioxidant enzymes and histopathological parameters in Wistar albino rats. Materials and methods: In the study, the rats were divided into six groups of ten. Control, untreated animals were given 0.9% NaCl. Rats were intraperitoneally given NDMA (10mg/kg) for the first 7 days. FASB methanol extract (150 and 300mg/kg) was administered orally for 21 days. Results: a-Tocopherol, retinol, ascorbic acid, total antioxidant activity, phenolic and flavonoid contents of FASB were 0.70±0.13, 0.29±0.03lg/g, 139.32±7.06lg/100g, 171.61±6.05mM ascorbic acid/g, 90.47±4.11mg GA/g and 37.39±2.85mg QE/g. DPPH and hydroxyl radical scavenging activity was obtained IC50 67.34±4.14 and 64.87±4.68lg/mL, respectively. Discussion and conclusion: The results of the study indicated that FASB flowers contain high levels of vitamins, minerals, total antioxidant activity, phenolics and flavonoids. Due to the positive effect on significant changes in antioxidant enzymes of liver tissue and histopathological examination, it is thought that the plant could be used as a hepatoprotective.

Aim Postoperative pelvic adhesions are significant health care problems causing chronic pelvic pain, infertility and intestinal obstruction after abdominal or pelvic surgery. We investigated the effects of quercetin and Surgicel for the prevention of adhesions after gynecological surgery. Methods A double blind, randomized, controlled experimental study was designed. Forty female Wistar Hannover rats were divided into five groups: control, sham operated, quercetin, Surgicel, and quercetin + Surgicel. The control group received medication used for the surgical procedure only. The sham group received a laparotomy only. The quercetin group received 15 mg/kg quercetin in addition to undergoing the standard surgical procedure, and the injuries in the surgical group were covered with a single, 1 cm2 layer of Surgicel (oxidized regenerated cellulose). The quercetin + Surgicel group received both 15 mg/kg quercetin and a single, 1 cm2 layer of Surgicel. Adhesions were scored 14 days after the first surgical procedure. Results The extent, severity, degree, total adhesion, inflammation and fibrosis scores of the control group were significantly higher than those of the quercetin, Surgicel, and quercetin + Surgicel groups. There was no significant difference between the Surgicel and quercetin groups in degree, but all other parameters were significantly higher in the Surgicel than in the quercetin group. The quercetin + Surgicel group had lower adhesion scores than the quercetin group. Conclusions Quercetin, Surgicel and quercetin + Surgicel treatment may be useful for preventing pelvic adhesions.

The present study was designed to assess the phytochemical content of Ferulago angulata (FA) and possible in vivo nephroprotective effect of FA administration on trace elements, minerals, MDA and GSH in kidney and liver tissue samples, serum vitamin (alpha-tocopherol, retinol, cholecalciferol, phylloquinone), TSA, and LSA in a rat model of DMN-induced nephrotoxicity. In the study, Wistar albino rats were assigned to six groups: Control (0.9% NaCl), (DMN 10 mg/kg), (FA 150 mg/kg), (DMN + FA 150 mg/kg), (FA 300 mg/kg), and (DMN + FA 300 mg/kg). Rats were intraperitoneally given DMN for the first 7 days. Renal injury caused by DMN was proved by the histopathological alterations. The FA (300 mg/kg) treatment significantly normalized Se, Cr, Ca levels in liver and Co level in kidney tissue samples. These observed positive effects are due to the phytochemical content of the plant. The flower extract of FA (300 mg/kg) can be used for the prevention of kidney damage. Practical applications Ferulago angulata flowers are used in traditional medicine for treat kidney and liver digestive system diseases. This species is endemic taxa of the family Apiaceae, which has been used both as food and therapeutics because of their phytochemical composition. In this study, the phenolic characterization of FA flower was used to a new RP-HPLC method, as well as the biological activity of FA flower and possible in vivo nephroprotective effect of FA flowers on trace elements, minerals, MDA and GSH in kidney and liver tissue samples and vitamins, TSA, and LSA in serum samples a rat model of DMN-induced nephrotoxicity. It was found that high level of phenolic compounds (chlorogenic acid, vanillic acid, 2-hydroxycinnamic acid) present in the flower extract of F. angulata has positive effects and antioxidant properties. Due to its phenolic content, FA flower extract could protect for kidney damage and can be used as antioxidants in the food additive and pharmaceutical industry.

This study aimed to investigate the effect of curcumin (CUR) on doxorubicin (DOX)-induced testicular damage in male rats. Thirty-five adult male Wistar rats were used. Control group was received saline for 7 days. CUR group received CUR for 7 days. DOX group received single dose DOX on the 5th day. DOX+ CUR-100 group received 100 mg/kg/day CUR for 7 days and DOX injection on the 5th day. DOX + CUR-200 group received 200 mg/kg/day CUR for 7 days and DOX injection on the 5th day. DOX treatment decreased in sperm motility rate, live sperm percentages, cellular antioxidants, and increased malondialdehyde (MDA) levels, necrosis, degenerations, and slimming in seminiferous tubules, and DNA damages in testes by inducing oxidative stress. CUR treatment mitigated significantly these side effects when compared with DOX group in a dose-dependent manner. In conclusion, CUR treatment can be used in the mitigation of DOX-induced testicular toxicity.

The present study aims to examine the possible beneficial effects of gallic acid (GA) against doxorubicin-induced cardiotoxicity in the experimental model. Rats were weighed and divided into groups. Groups as following; control, gallic acid (GA), doxorubicin (DOX) and GA + DOX groups. At the end of the experiment, rats were sacrificed and heart tissue removed. The tissues were analysed in terms of biochemical (MDA, SOD, CAT, GSH, GPx), pathological (hyaline degeneration, Zenkerin necrosis, hyperaemia) and immunohistochemical (TNF-alpha, Cox-2). MDA level decreased and antioxidant enzyme activities increased in GA + DOX group compared to doxorubicin group. TNF-alpha, Cox-2 expression levels were severe in the DOX group. Also, pathologic tissue damage in heart tissue increased due to doxorubicin. Additionally, pathologic tissue damage and TNF-alpha, Cox-2 expression levels decreased in GA + DOX group. According to our findings, GA has protective effect against doxorubicin-induced cardiotoxicity.

Deltamethrin (DMN) exposure causes severe damage to the gill and liver tissues of aquatic organisms, as well as neurotoxic effects and metabolic disorders. The goal of the present study was to assess the impacts of DMN toxicity on blood biochemistry, malondialdehyde (MDA) levels, catalase (CAT) levels, behavior disorder, acetylcholinesterase (AChE) activity, histopathology and 8-hydroxy-2-deoxyguanosine (8 OHdG) of brown trout (Salmo trutta fario). Acute concentrations (1.0 and 2.0 mu g/L) of DMN caused behavioral disorder such as rapid swimming, loss of balance, aggressiveness and increasing in the surface activity and inactivity in brown trout. A significant increase in malondialdehyde (MDA), aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, and a significant decrease in CAT, AChE, blood albumin, and blood total protein content were observed. Histopathologically, both doses of DMN have caused steatosis, necrosis, and degeneration in hepatocytes and hyperemia in the liver. Also, they led to inflammation, adhesion and fusion depending on severe hyperplasia in secondary lamellae, hyperemia and lamellar edema in gill tissues when compared to control group. Additionally, 8-hydroxy-2-deoxyguanosine (8 OHdG) levels at 2.0 mu g/L dose of DMN in liver tissues were more severe according to 1.0 mu g/L dose of DMN. Finally, different concentrations of DMN led to changes of the histopathology, 8 OHdG, the CAT levels, plasma AChE activity, and the serum metabolites, as well as behavioral disorder in brown trout.

This study was carried out to determine vit. E, Se, vit. A, malondialdehyde (MDA), 8-hydroxy-2-deoxyguanosine (8-OHdG), and ubiquinone-10 (CoQ10) levels and histopathological changes in sheep with white muscle disease (WMD). A total of 30 sheep were used; 20 sheep with WMD were brought to our clinic for diagnosis and treatment at various times, and 10 healthy sheep were in the control group. The Se, vit. E, vit. A, MDA, 8-OHdG, and CoQ10 values of the healthy and WMD sheep were as follows: 0.917 +/- 0.037, 0.790 +/- 0.067; 1.190 +/- 0.011, 1.090 +/- 0.021; 5.400 +/- 0.275, 5.200 +/- 0.173; 1.602 +/- 0.264, 2.636 +/- 0.576; 0.656 +/- 0.197, 1.485 +/- 0.271; and 0.280 +/- 0.044, 1.753 +/- 0.551 respectively (p

Testicular dysfunction or damage is among the critical side effects of chemotherapeutic drugs like cisplatin. This study was mapped out to assess the possible therapeutic effect of eugenol on cisplatin-induced testicular damage. In this experimental study, a single dose of cisplatin (15 mg/kg) was given intraperitoneally. After 72 hr of cisplatin injection, rats were sacrificed and testis tissues were removed. Tissues were examined by biochemical, histopathological and immunohistochemical methods. While tissue lipid peroxidation product and apoptotic marker levels increased, antioxidant enzyme activities of testis tissue were decreased in the cisplatin group. Additionally, histopathological damage was also determined in testis tissue. Contrary to all these results, the severity of damage in the tissue was reduced histopathologically owing to eugenol treatment. The lipid peroxidation decreased and antioxidant enzyme activities increased in the eugenol treatment group. It has been determined that eugenol has a therapeutic effect on oxidative stress and apoptosis against cisplatin-induced testicular damage. © 2019 Blackwell Verlag GmbH