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Bats are a diverse and ecologically important group of mammals that exhibit remarkable diversity in their feeding habits. These diverse feeding habits are thought to be reflected in the composition and function of their gut microbiota, which plays important roles in nutrient acquisition, immune function, and overall health. Despite the rich biodiversity of bat species in South America, there is a lack of microbiome studies focusing on bats from this region. Such studies could offer major insights into conservation efforts and the preservation of biodiversity in South America. In this work, we aimed to compare the gut microbiota of four bat species with different feeding habits from Southern Brazil, including nectarivorous, frugivorous, insectivorous, and hematophagous bats. Our findings demonstrate that feeding habits can have a significant impact on the diversity and composition of bat gut microbiotas, with each species exhibiting unique metabolic potentials related to their dietary niches. In addition, the identification of potentially pathogenic bacteria suggests that the carriage of microbial pathogens by bats may vary, depending on feeding habits and host-specific factors. These findings provide novel insights into the relationship between bat feeding habits and gut microbiota composition, highlighting the need to promote diverse habitats and food sources to support these ecologically important species.

In this work, we examined the levels of vitamin E in the heart, liver, and kidneys of four species of adult male bats with distinct feeding habits. Our results indicate consistent vitamin E levels in the heart across all four bat species, suggesting the presence of regulatory mechanisms. Additionally, the liver displayed notably higher vitamin E levels in nectarivorous and frugivorous bats, while hematophagous bats exhibited lower levels, indicating a link between dietary intake and liver vitamin E levels. Furthermore, correlation analysis provided additional insights into the relationships between vitamin E and key antioxidant parameters in the livers of bats. On the other hand, no correlation was observed between vitamin E and key antioxidant parameters in the heart. Intriguingly, vitamin E was not detected in the kidneys, likely due to physiological factors and the prioritization of vitamin E mobilization in the heart, where it serves critical physiological functions. This unexpected absence of vitamin E in bat kidneys highlights the unique metabolic demands and prioritization of vitamin mobilization in wild animals like bats, compared to conventional animal models. These findings provide insight into the intricate distribution and utilization of vitamin E in bats, emphasizing the influence of dietary intake and metabolic adaptations on vitamin E levels in different organs.

The aim of this study was to compare the oxidative metabolism of four neotropical bat species with different feeding habits and investigate the relationship between their feeding habits and oxidative status. In terms of oxidative damage, our findings revealed major differences among the four bat species. In particular, hematophagous bats had lower levels of oxidative damage in the heart but higher levels in the liver. Nectarivorous bats had lower levels of carbonyl groups in the kidneys compared to insectivorous and hematophagous bats. The activity of various antioxidant and non-antioxidant enzymes in the heart, liver, and kidney also showed significant differences among the bat species. H 2 O 2 consumption was lower in the heart of hematophagous bats, while insectivorous bats exhibited the highest enzymatic activity in the kidney. SOD activity was lower in the heart of hematophagous bats and lower in nectarivorous bats in the liver. Fumarase activity was higher in the heart of frugivorous/insectivorous and lower in nectarivorous/hematophagous bats. GPx activity was higher in the heart of nectarivorous/insectivorous and higher in the kidney of insectivorous bats. GST activity was higher in the heart of nectarivorous and lower in hematophagous bats. The correlation analysis between oxidative markers and enzymatic/non-enzymatic antioxidants in the heart, liver, and kidney exhibited distinct patterns of correlations due to variations in antioxidant defense mechanisms and oxidative stress responses in different organs. The observed differences in oxidative damage, antioxidant enzyme activities, and correlations between oxidative markers and antioxidants highlight the adaptability and complexity of the antioxidant defense systems in these bats. Each organ appears to have specific demands and adaptations to cope with oxidative stress based on its physiological functions and exposure to dietary components. Our results have major significance for the conservation and management of bats, which are threatened species despite being crucial components of ecosystems. Our study's implications go beyond bat biology and offer valuable insights into comparative oxidative physiology.

Assessing the levels of oxidative stress markers and antioxidant enzymes in the brain is crucial in evaluating its antioxidant capacity and understanding the influence of various dietary patterns on brain well-being. This study aimed to investigate the antioxidant status and oxidative damage in the brain of bat species with different feeding habits to gain insights into their protective mechanisms against oxidative stress and their interspecific variation. The levels of oxidative damage markers and the activities of antioxidants were measured in the brain of four bat species with different feeding habits, namely insectivorous, frugivorous, nectarivorous, and hematophagous. Insectivorous bats showed higher levels of SOD and fumarase compared to the other groups, while hematophagous bats showed lower levels of these enzymes. On the other hand, the activities of glutathione peroxidase and glutathione S-transferase were higher in hematophagous bats and lower in insectivorous bats. The carbonyl groups and malondialdehyde levels were lower in frugivores, while they were similar in the other feeding guilds. Nitrite and nitrate levels were higher in the hematophagous group and relatively lower in all other groups. The GSSG/GSH ratio was higher in the hematophagous group and lower in frugivores. Overall, our results indicate that the levels of oxidative stress markers and the activities of antioxidant enzymes in the brain vary significantly among bat species with different feeding habitats. The findings suggest that the antioxidant status of the brain is influenced by diet and feeding habits.

Unlike most animals, most bats cannot synthesize vitamin C endogenously. Consequently, this vitamin must be obtained from the diet. Among the bat species, there are several food groups, such as frugivorous, nectarivorous, insectivorous, and hematophagous. In this work, we measured and compared vitamin C levels in different organs of four species of bats, all collected in southern Brazil. When analyzing and comparing the levels of vitamin C in the four bat species, (regardless of the organ), no significant differences were observed. However, when analyzing and comparing the levels of vitamin C in the four organs (regardless of the species), significant differences were observed, with the highest concentrations in the heart, followed by the liver and brain, while the lowest concentration was measured in the kidneys. Additional differences in the levels of Vitamin C were only observed when each organ was analyzed according to the species/diet. These results indicate a high degree of metabolic homeostasis in bats despite the marked difference in the type of diet.

Ticks have developed physiological adaptations to transport, store, metabolize and secrete toxic components from the diet and environment. Different classes of enzymes are involved in these processes, however, the role of several of them is not yet characterized in Rhipicephalus microplus. In this context, this work investigated the action of antioxidant and detoxification enzymes, as well as the levels of essential cellular reductants in R. microplus partially engorged females (PEF) and fully engorged females (FEF). Results demonstrated that enzymes transcriptional levels and enzymatic activity from ovary and fat body were higher in PEF than in FEF, except for ovary Glutathione peroxidase (GPx), which was the only enzyme showing highest activity in the FEF stage. These results indicated a higher demand for antioxidant potential in these organs at the initial feeding phase than during egg-laying. In midgut, however, there was more variability in the transcriptional levels and activity of the different enzymes between the PEF and FEF phases. Similar NADPH levels were found in PEF and FEF phases, suggesting a remarkable capacity to maintain a regular supply of reducing power, despite the developmental changes and large intake of heme and iron. However, reduced glutathione (GSH) levels were variable between PEF and FEF when distinct organs were compared. Taken together, our data suggest a higher demand for reducing potential in FEF ticks. The silencing of catalase (CAT) or thioredoxin reductase (TRx) genes in females did not impair feeding, egg-laying capacity, or larvae hatching. CAT-silenced ticks had increased ovary peroxidase activity, a possible compensatory antioxidant mechanism. Altogether, the results shed light on the complexity of the antioxidant and detoxification enzyme system in ticks and its involvement in different physiological mechanisms., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Objectives: The loss of antioxidant protection from estrogen during menopause may lead to oxidative stress in the kidneys. Thus, antioxidant supplementation may potentially decrease the menopause-derived oxidative stress. The aim of this study was to evaluate the effect of α-lipoic acid (LA) and ω-3 long-chain polyunsaturated fatty acids on the redox profile of the kidneys in the ovariectomized rat model of menopause., Methods: We assessed oxidative damage markers and antioxidant defenses in the kidneys of ovariectomized rats supplemented with LA, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA). Animals received 3 mo of dietary supplementation., Results: Ovariectomy did not increase the levels of the damage markers carbonyl and malondialdehyde. EPA supplementation increased carbonyl and malondialdehyde levels. Ovariectomy increased fumarase activity but did not affect the levels of vitamin C, glutathione, and glutathione S-transferase activity. LA, DHA, and EPA supplementation decreased fumarase activity, but increased the levels of vitamin C, glutathione, and glutathione S-transferase activity. Vitamin E, superoxide dismutase, glutathione peroxidase, and peroxide consumption were not affected by ovariectomy or supplementation., Conclusions: The results suggest that ovariectomy did not affect the redox profile in the kidneys. LA, DHA, and EPA supplementation increased certain endogenous antioxidants; however, EPA may have a prooxidant effect on the kidneys., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Menopause occurs as consequence of ovarian senescence that leads to a drop of oestrogen hormone. The decreased oestrogen levels combined with the impairment of the redox system may contribute to the increased risk of postmenopausal cardiovascular disease. Supplementation with antioxidants may be an alternative to reduce cardiovascular risk. The study evaluated the effect of dietary supplementation with docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and α-lipoic acid (LA) for a period of 16 weeks on oxidative stress biomarkers in the hearts of ovariectomized 3-month-old rats. Ovariectomy did not increase the level of the damage markers malondialdehyde and carbonyl, and both were decreased by LA supplementation. Ovariectomy increased the levels of the endogenous antioxidants glutathione, vitamin C and H 2 O 2 consumption, after restoration by DHA, EPA, and LA supplementation. Vitamin E, glutathione peroxidase, glutathione- S -transferase, and superoxide dismutase are not altered by ovariectomy. Lipid and protein damage are not increased after ovariectomy and a portion of the endogenous antioxidants concomitantly increased, suggesting that hearts may be protected by these antioxidants. DHA, EPA, and LA restored these endogenous antioxidants, showing that all evaluated supplements are effective in modulating the antioxidant redox system in the heart. LA showed additional effect on redox markers, decreasing lipid and protein damage markers.

Ischemia-reperfusion (I/R)-induced oxidative stress is one of the main mechanisms of tissue injury after cardiac arrest (CA). A decrease in antioxidant defenses may contribute to I/R injury. The present study aims to investigate the influence of mild therapeutic hypothermia (MTH) on levels of nonenzymatic antioxidants after CA. We investigated antioxidant levels at 6, 12, 36, and 72 hours after CA in central venous blood samples of patients admitted to intensive care. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 hours of MTH (33°C). Erythrocyte glutathione (GSH) levels were elevated by MTH, increasing at 6, 12, 36, and 72 hours after CA in hypothermic patients (mean GSH levels in normothermic patients: 6 hours = 73.89, 12 hours = 56.45, 36 hours = 56.46, 72 hours = 61.80 vs. hypothermic patients: 6 hours = 176.89, 12 hours = 198.78, 36 hours = 186.96, and 72 hours = 173.68 μmol/g of protein). Vitamin C levels decreased significantly at 6 and 12 hours after CA in hypothermic patients (median vitamin C levels in normothermic patients: 6 hours = 7.53, 12 hours = 9.40, 36 hours = 8.56, and 72 hours = 8.51 vs. hypothermic patients: 6 hours = 5.46, 12 hours = 5.44, 36 hours = 6.10, and 72 hours = 5.89 mmol/L), coinciding with the period of therapeutic hypothermia. Vitamin E and nitric oxide levels were not altered by hypothermic treatment. These findings suggest that MTH alters nonenzymatic antioxidants differently, decreasing circulating vitamin C levels during treatment; however, MTH elevates GSH levels, possibly protecting tissues from I/R injury after CA.

Purpose: Nasal polyposis is a chronic inflammatory disease of the mucosa of the nasal cavity and paranasal sinuses. The etiology of nasal polyposis is unclear; however, it may be associated with asthma and intolerance to acetylsalicylic acid, possibly altering the redox profile. The study intends to compare the redox profile in polyps surgically removed from three clinical groups of patients with nasal polyposis who were divided according to the presence of asthma and intolerance to acetylsalicylic acid., Methods: Patients were divided into three groups: nasal polyposis only (n = 30); nasal polyposis and asthma (n = 19); and nasal polyposis, asthma and intolerance to acetylsalicylic acid (n = 10). The following redox evaluations were performed: enzymatic antioxidant activity of superoxide dismutase, glutathione peroxidase, hydrogen peroxide consumption and glutathione S-transferase; non-enzymatic antioxidant levels of vitamin C, vitamin E and glutathione; levels of the oxidative damage biomarkers carbonyl groups (measuring protein damage) and malondialdehyde (measuring lipid peroxidation); and nitrite and nitrate levels., Results: Compared with the polyposis only group, hydrogen peroxide consumption, glutathione S-transferase, vitamin E and malondialdehyde were lower in the asthma group. Total glutathione (0.12 ± 0.01 vs. 33.34 ± 10.48 µmol/mg) and nitrite and nitrate (0.06 ± 0.01 vs. 15.95 ± 1.38 nmol/mg) levels were higher in the nasal polyposis, asthma and intolerance to acetylsalicylic acid group., Conclusions: In patients with nasal polyposis, asthma may alter the redox profile associated with the hydrogen peroxide and lipid damage pathways, whereas asthma and intolerance to acetylsalicylic acid increase nitrite and nitrate and total glutathione levels.

Background: Bilateral ovariectomy is an experimental model used to analyse the effects of menopause and develop strategies to mitigate the deleterious effects of this condition. Supplementation of the diet with antioxidants has been used to reduce potential oxidative stress caused by menopause. The purpose of the study was to analyse the effects of α-lipoic acid (LA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), dietary supplementation on oxidative stress in the livers of ovariectomized rats., Methods: In this study, we evaluated the effect of dietary supplementation with LA, DHA and EPA for a period of 16 weeks on oestrogen levels and oxidative stress biomarkers in the livers of ovariectomized 25 three-month-old rats., Results: Serum oestrogen levels were lower after ovariectomy but were not altered by dietary treatments. LA was capable of acting in the liver, recovering the activity of the antioxidant enzymes superoxide dismutase and glutathione peroxidase, and reducing protein oxidative damage. Moreover, LA supplementation reduced nitrite and nitrate levels. DHA and EPA recovered the antioxidant activity of cytosolic and mitochondrial superoxide dismutase, decreasing protein oxidation. Protection against lipid oxidation differed between treatments. The DHA-treated group showed increased levels of the lipid peroxidation biomarker malondialdehyde compared to the ovariectomized group. However, malondialdehyde levels were not altered by EPA treatment., Conclusions: The results suggest that the antioxidant response varies among evaluated supplementations and all supplements were able to alter enzymatic and non-enzymatic antioxidants in the livers of ovariectomized rats. DHA presented the most evident antioxidant effect, decreasing protein and lipid damage., (Copyright © 2017 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.)

The disposable soma theory postulates that aging might be the result of tradeoffs between early life reproduction and longevity, thereby involving the costs of reproduction in the expected lifespan. It is known that redox biochemistry plays a major role in these processes. To assess long term effects of reproduction, we analyzed redox rates and the testosterone levels at four different ages, and we performed a principal component analysis between redox measures of five different organs followed by a cluster analysis to determine correlations. The correlations among redox measures between organs were influenced more by reproduction than by age. Non breeders showed no alterations along the aging process up to 24 months, at which point differences were seen. Among breeders, however, we saw differences between three age clusters: cluster 1, 6 month old-animals; cluster 2, 12 month old animals, and cluster 3, 3 and 24 month-old animals. The results show differences between male breeders and non breeders, and provide evidence that oxidative stress plays a role in aging, and that reproduction alters the redox profiles of males.

After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 h mild therapeutic hypothermia (33°C), victims of in- or out-of-hospital cardiac arrest. Parameters were assessed at 6, 12, 36, and 72 h after cardiac arrest in the central venous blood samples. Hypothermic and normothermic patients had similar S100B levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and S100B and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases the activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S-transferase while decreasing the activity of serum paraoxonase-1. These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients.

Reproduction is a critical and demanding phase of an animal's life. In mammals, females usually invest much more in parental care than males, and lactation is the most energetically demanding period of a female's life. Here, we tested whether oxidative stress is a consequence of reproduction in the brains of female Wistar rats. We evaluated the activities of glutathione peroxidase, glutathione S-transferase, and superoxide dismutase; H 2 O 2 consumption; protein carbonylation; NO 2 & NO 3 levels; and total glutathione, as well as sex hormone levels in brain tissue of animals at 3, 6, 12, and 24months of age. Animals were grouped according to reproductive experience: breeders or non-breeders. Most of the studied parameters showed a difference between non-breeders and breeders at 12 and 24months. At 24months of age, breeders showed higher superoxide dismutase activity, H 2 O 2 consumption, glutathione peroxidase activity, and carbonyl levels than non-breeders. In 12-month-old non-breeders, we observed a higher level of H 2 O 2 consumption and higher superoxide dismutase and glutathione peroxidase activities than breeders. By evaluating the correlation network, we found that there were a larger number of influential nodes and positive links in breeder animals than in non-breeders, indicating a greater number of redox changes in breeder animals. Here, we also demonstrated that the aging process caused higher oxidative damage and higher antioxidant defenses in the brains of breeder female rats at 24months, suggesting that the reproduction process is costly, at least for the female brain. This study shows that there is a strong potential for a link between the cost of reproduction and oxidative stress., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Dietary restriction increases life span and protects distinct organisms against a series of diseases, among which, those related to oxidative stress, like neurodegenerative diseases. Interferences in the maternal environment are known to reprogram the offspring metabolism response, impacting in the risk of chronic diseases development in adulthood. We aimed to assess the effects of 40% food restriction on reactive species levels, enzymatic and non-enzymatic antioxidant defenses, and oxidative damage parameters in the cerebellum and total cerebral cortex of pregnant rats and their offspring. Dams and pups showed oxidative modulation caused by food restriction in both structures. Dichlorofluorescein oxidation, reflecting reactive species levels, was reduced in the cerebellum of dams and offspring, while the cerebral cortex was not affected. Decreased mitochondrial superoxide levels were found in the cerebellum and cerebral cortex of pups, while nitric oxide was increased in the cortex. We also measured the activities of important antioxidant enzymes responsible by reactive oxygen species elimination. Superoxide dismutase activity was increased in the cerebellum of dams and in both structures of pups, while it was decreased in dams' cerebral cortex. Both brain structures were affected concerning to catalase, glutathione peroxidase, and glutaredoxin activities, which were reduced in pups and dams. Non-enzymatic defenses were decreased in pups, while dams showed an adaptive pattern in the cerebellum and no alteration in the cerebral cortex. Even though the results suggest increased oxidative status, lipids and proteins were not oxidatively affected. Our data suggest that intrauterine food restriction may disrupt oxidative status, impairing the antioxidant network.

Scope: Postmenopausal women are often affected by a group of metabolic disorders related to oxidative stress. Alternative treatments that can improve the quality of life of these women have been the subject of recent studies. The objective of this study was to evaluate the response to oxidative stress in the brains of rats following ovariectomy, and to determine enzymatic and nonenzymatic antioxidant responses when the animals received 3 months of dietary supplementation., Methods and Results: Ovariectomy produced changes in antioxidant profiles characterized by reductions in glutathione S-transferase activity, H2 O2 consumption, superoxide dismutase activity, and vitamin C levels and increases in protein carbonylation. Docosahexaenoic fatty acid (DHA) supplementation restored these parameters to normal values and increased values of other antioxidants (glutathione peroxidase and total glutathione). However, DHA supplementation also increased protein carbonylation and lipid peroxidation. Eicosapentaenoic acid supplementation produced no changes in antioxidants, but decreased lipid peroxidation. Lipoic acid supplementation increased consumption of H2 O2 and decreased protein carbonylation and lipid peroxidation., Conclusion: These results suggest that the antioxidant response to omega-3 varies in different tissues, and in this study DHA treatment had a prooxidant effect in the brain. Lipoic acid treatment, on the other hand, had a protective effect, reducing markers of oxidative damage., (© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

In this study, we assessed the generation of reactive oxygen species (ROS) induced by subinhibitory concentration of fluconazole in susceptible and resistant Candida glabrata strains at stationary growth phase and measured their oxidative responses parameters: glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione-S-transferase (GST), consumption of hydrogen peroxide, and total glutathione, as well as oxidative damage in lipids, proteins, and DNA. Data showed that fluconazole increased generation of ROS and GPx and SOD enzymatic activity in treated cells; however, these enzymatic activities did not differ between resistant and susceptible strains. Susceptible strains exhibited higher GST activity than resistant, and when susceptible cells were treated with fluconazole, GST activity decreased. Fluconazole treatment cause oxidative damage only in DNA. There are a possible participation of ROS, as organic peroxides and O2(•-), in antifungal mechanism of fluconazole, which results in higher GPx and SOD enzymatic activities and oxidative DNA damage in C. glabrata., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Patients undergoing mechanical ventilation (MV) often experience respiratory muscle dysfunction, which complicates the weaning process. There is no simple means to predict or diagnose respiratory muscle dysfunction because diagnosis depends on measurements in muscle diaphragmatic fibre. As oxidative stress is a key mechanism contributing to MV-induced respiratory muscle dysfunction, the aim of this study was to determine if differences in blood measures of oxidative stress in patients who had success and failure in a spontaneous breathing trial (SBT) could be used to predict the outcome of MV. This was a prospective analysis of MV-dependent patients (≥72 hrs; n = 34) undergoing a standard weaning protocol. Clinical, laboratory and oxidative stress analyses were performed. Measurements were made on blood samples taken at three time-points: immediately before the trial, 30 min. into the trial in weaning success (WS) patients, or immediately before return to MV in weaning failure (WF) patients, and 6 hrs after the trial. We found that blood measures of oxidative stress distinguished patients who would experience WF from patients who would experience WS. Before SBT, WF patients presented higher oxidative damage in lipids and higher antioxidant levels and decreased nitric oxide concentrations. The observed differences in measures between WF and WS patients persisted throughout and after the weaning trial. In conclusion, WF may be predicted based on higher malondialdehyde, higher vitamin C and lower nitric oxide concentration in plasma., (© 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)

The tear film comprises a major mechanism for protection of the ocular surface against harmful external agents. Disruption of tear production can lead to dry eye syndrome, causing damage ranging from mild discomfort to scarring of the ocular surface with irreversible vision impairment. The production of tears by the lacrimal gland is influenced by neuroendocrine, hormonal, and immunological factors. Reactive oxygen and nitrogen species play an important role in its regulation. We assessed the effects of oxidative stress on antioxidant defenses in the lacrimal gland and ocular surface in ovariectomized rats supplemented with n-3 polyunsaturated fatty acids (n-3 PUFA) and alpha-lipoic acid (ALP). We found that n-3 PUFA did not measurably influence oxidative stress, but ALP had site-specific pro-oxidant and antioxidant effects, and was an important influence on ocular surface dry eye improvement. As an index of oxidative damage to proteins and lipids, we measured levels of carbonyl and malondialdehyde (MDA), respectively. Enzymatic antioxidant defenses were measured as total superoxide dismutase (tSOD) and glutathione peroxidase (GPx), and non-enzymatic defenses were estimated by vitamin C, total glutathione, and indirect oxide nitric levels. PUFA and ALP treatment restored lacrimal production with resulting improvement in the dry eye Schirmer test in all supplemented groups. The results indicated that reactive oxygen species resulting from oxidative stress in the lacrimal gland did not play an important role in dry eye through reactive oxygen species; however, alpha-lipoic acid altered the metabolism of reactive nitrogen species, causing increased activity of lacrimal peroxidase and improved lacrimal production., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

The free radical theory of aging postulates that an imbalance between reactive oxygen species (ROS) and reactive nitrogen species (RNS) and antioxidant defenses is important in senescence. To address this issue and gain insight into the aging process, we have evaluated the antioxidant defenses and have assessed oxidative damage in testis tissues in aging male rats. In order to relate aging and reproduction, animals with and without reproductive activity were studied. In reproductive animals the results showed a progressive increase in antioxidant enzyme activity until 12 months of age followed by an abrupt fall at 24 months. In non-reproductive animals, antioxidant activity was stable through 12 months of age, but again, fell abruptly at 24 months of age. In addition, increased aconitase activity and increased testosterone levels were found among reproductively active animals. The data demonstrate the existence of metabolic differences in testis of reproductively experienced animals and reproductively naïve animals., (© 2013.)

Reproduction is a costly life process, and the reproductive investment by females appears to be greater than males in many species. We have analyzed the effects of reproductive investment during aging with respect to oxidative stress parameters in female Wistar rats. We measured the activity glutathione peroxidase, glutathione S-transferase, superoxide dismutase, consumption of hydrogen peroxide, protein carbonylation, lipid peroxidation, nitrite and nitrate levels, and Vitamin C (Vit. C) and E levels. We traced oxidative profiles at ages 3, 6, 12, and 24 months. Animals were grouped according to reproductive experience: experienced or naive with respect to reproductive activity. We measured aconitase activity and sex hormone levels. The naive animals exhibited an increase with respect to experienced in most parameters studied at 6 and 24 months, whereas experienced animals exhibited a similar increase at 3 and 12 months. At 6 months of age, during the period that would represent peak reproductive activity, naive animals showed higher levels of MDA, Vit. C, consumption of hydrogen peroxide and GPx, aconitase, and SOD activities. In naive elderly rats, we observed an increase in oxidative damage markers and an increase in enzymatic and non-enzymatic antioxidants, with the exception of consumption of hydrogen peroxide and Vit. C. In the long term, the reproductive investment was not sufficient to interfere with antioxidant capacity, and did not contribute to oxidative damage in kidneys of female Wistar rats.

Introduction: The capacity to overcome the oxidative stress imposed by phagocytes seems to be critical for Candida species to cause invasive candidiasis., Methods: To better characterize the oxidative stress response (OSR) of 8 clinically relevant Candida sp., glutathione, a vital component of the intracellular redox balance, was measured using the 5,5'-dithiobis-(2-nitrobenzoic acid (DTNB)-glutathione disulfide (GSSG) reductase reconversion method; the total antioxidant capacity (TAC) was measured using a modified method based on the decolorization of the 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic) acid radical cation (ABTS*+). Both methods were used with cellular Candida sp. extracts treated or not with hydrogen peroxide (0.5 mM)., Results: Oxidative stress induced by hydrogen peroxide clearly reduced intracellular glutathione levels. This depletion was stronger in Candida albicans and the levels of glutathione in untreated cells were also higher in this species. The TAC demonstrated intra-specific variation., Conclusions: Glutathione levels did not correlate with the measured TAC values, despite this being the most important non-enzymatic intracellular antioxidant molecule. The results indicate that the isolated measurement of TAC does not give a clear picture of the ability of a given Candida sp. to respond to oxidative stress.

Unlabelled: Coronary Artery Disease (CAD) and, Objectives: Sleep Disordered Breathing (SDB) are both oxidative stress disorders. SDB intermittent hypoxia induces oxidative stress, and reduces NO(·) availability, causing endothelial dysfunction. Low-density lipoprotein (LDL) peroxidation is involved in atherosclerosis, and is reported in SDB. Oxidized LDL (ox-LDL) and malondialdehyde (MDA) are lipid peroxidation markers. High-density lipoprotein (HDL) presents antiatherosclerotic properties related to paraxonase-1 (PON-1) activity. PON-1 hydrolyseyses lipid peroxides as ox-LDL. This study compares the relationship of HDL and PON-1, the lipid peroxidation markers ox-LDL and MDA, and 8-OHdG DNA damage marker in the association of SDB and CAD., Design and Methods: 29 controls and 27 cases with CAD (defined as > 30% coronary narrowing) patients were included. The apnea-hypopnea index (AHI), and several lipid and oxidative stress parameters were measured in these patients., Results: AHI is increased in CAD patients, and PON-1 activity and HDL levels are decreased. Regression analyseyses showed that lower PON-1 activity and higher ox-LDL levels are important CAD predictors, compared to HDL or MDA levels and present an age-dependent increase. Nitrites and nitrates, indirect NO(·) markers, are positive vs correlated with PON-1 and are negatively correlated to ox-LDL. SDB is not correlated to PON-1 activity decrease or ox-LDL increase. AHI is inversely correlated to HDL levels., Conclusions: These results indicate that PON-1 and ox-LDL are important predictors of CAD, however they may not be directly related to SDB.

Reproduction alters the male physiology. We performed a comprehensive examination of oxidative stress in the kidneys of male rats with (experienced) or without (naïve) reproductive activity during aging. Oxidative stress was assessed by measuring the activity of catalase, glutathione peroxidase, glutathione S-transferase, and superoxide dismutase, and by measuring protein carbonylation, lipid peroxidation, nitrite and nitrate levels, vitamin C levels, and glutathione (total, reduced, and oxidized forms) levels, and metabolism was accessed by aconitase activity in kidney tissue, as well as testosterone and estradiol levels in serum. Reproductively active animals exhibited increased testosterone levels and altered metabolism. Aging affects tissues and organs and contributes to their functional decline. Elderly naïve rats showed high nitrite and nitrate levels. The experienced rats had less damage in elderly ages, probably because they had higher antioxidant amount and antioxidant enzyme activities at earlier ages, which would have avoided oxidative damage seen in naïve group, and because of the metabolism decline. Glutathione increase in naïve elder rats probably was induced for direct protection against oxidative damage and indirect protection by higher glutathione peroxidase and glutathione S-transferase activities. Linear regression shows that lipid peroxidation levels explained vitamin C levels (B standardized value of 0.42), indicating that vitamin C was properly produced or recruited into kidneys to combat lipid peroxidation. Catalase activity reflected the protein carbonylation and lipid peroxidation levels (B standardized values of 0.28 and 0.48). These results add comprehensive data regarding changes in oxidative stress during aging, and suggest an explanation for the costs of reproduction., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Reproduction alters the male physiology. We performed a comprehensive study to examine oxidative stress in the brains of male rats with (experienced) or without (naïve) reproductive activity during aging. Oxidative stress was assessed by measuring the activity of catalase, glutathione peroxidase, superoxide dismutase, glutathione S-transferase, aconitase, and aconitase reactivated, and by measuring lipid peroxidation, protein carbonylation, nitrite and nitrate levels, vitamin C levels, and glutathione (total, reduced, oxidized forms) levels in brain tissue, as well as testosterone and estradiol levels in serum. Reproductively active animals exhibited increased testosterone levels and aconitase activity, suggesting an increased metabolism. Increased antioxidant enzyme activities and increased levels of antioxidant compounds were observed, yet damage to biomolecules was also observed in experienced rats. During aging changes in oxidative stress were observed. We found higher activities of antioxidant enzymes, higher amounts of antioxidants, and more damage at six months of age among experienced animals than among naïve animals. Similar antioxidant activities and levels, and damage were found between the groups at twenty-four months of age. These results add comprehensive data regarding changes in oxidative stress during aging, and suggest an explanation for the costs of reproduction., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Context/objective: The objective of the study was to evaluate the effects of normalizing glycemia through iv insulin per 24 h on markers of oxidative stress and inflammation in patients with diabetes submitted to percutaneous coronary intervention (PCI) with stent., Patients/methods: This was a prospective, open-label, randomized controlled trial, comparing continuous iv insulin per 24 h targeting glycemia less than 110 mg/dl iv insulin treatment (IIT; n = 35) to standard treatment (ST; n = 35, regular insulin if glycemia was greater than 200 mg/dl). Blood samples for glycemia, glycated hemoglobin, lipids, inflammatory markers [C-reactive protein (CRP), soluble CD40 ligand, IL-6, and endothelin 1 (ET-1)] and oxidative stress (total antioxidant status, carbonyl) were collected immediately after and 24 h after PCI., Results: Seventy patients were included. Mean age was 60.5 ± 10 yr, 60% were men, glycated hemoglobin was 8.1 ± 1.8 (IIT) vs. 7.6 ± 1.6% (ST) (P = 0.39). The intensive insulin group had lower glycemia (P = 0.006) and higher insulinemia (P < 0.001). Insulin did not change CRP [4.5 (2.1-11.7) vs. 6.8 (2.4-10.3), P = 0.35], soluble CD40 ligand [402 (191-843) vs. 610 (230-1200), P = 0.68], IL-6 [6.21 (3.1.-10.4) vs. 10.37 (5.9-15.3), P = 0.09], and ET-1 [1.02 (0.7-1.8) vs. 1.10 (0.7-1.9), P = 0.657]. CRP, IL-6, and ET-1 increased after PCI in both groups (P < 0.05). No change was observed on protein oxidation (carbonyl, P = 0.70; total antioxidant status, P = 0.33). There was a positive correlation between CRP and glycemia (r = 0.29, P = 0.002)., Conclusions: Continuous iv insulin for 24 h increased insulin levels and prevented hyperglycemia. Insulin infusion did not prevent the rise in inflammatory and oxidative stress markers, and no differences were observed between IIT and ST after PCI with a stent.

Resistance to the toxic effects of reactive oxygen species produced by phagocytes and production of hydrolytic enzymes are important aspects of Candida albicans virulence. In this report, we compared twelve C. albicans isolates for their in vitro capacity to resist oxidants-hydrogen peroxide, menadione and paraquat; and to produce hydrolytic enzymes-phospholipase and protease. Different C. albicans isolates showed different degrees of resistance to oxidants as well as differences in production of hydrolytic enzymes. Resistance to oxidative stress did not correlate with production of hydrolytic enzymes. This reinforces the view that C. albicans differentially regulates the expression of virulence factors in response to local environmental conditions.

Sleep disordered breathing (SDB) is related to coronary artery disease (CAD), but the mechanisms are uncertain. SDB is characterized by periods of intermittent hypoxia and free radical formation. This study tested the hypothesis that carbonylation can be the link between SDB and CAD. It included 14 cases with CAD and 33 controls with <50% coronary narrowing. CAD cases have higher erythrocyte carbonyl levels than controls (p = 0.012). Positive correlation was observed between apnea-hypopnea index (AHI) and erythrocyte carbonyl concentration (rho = 0.310; p = 0.027). To predict CAD, including as regressors: AHI, erythrocyte carbonyl, gender, age and body mass index, the significant variables in the Poisson multiple regression model were AHI and erythrocytes carbonyl. An increase of 1 pmol/gHb in erythrocyte carbonyl levels increases by 1.8% the risk of CAD and one unit of AHI increases by 3.8% the risk of CAD. The present findings represent the first evidence in humans that SDB may cause CAD through protein carbonylation.

In the course of an infection, the formation of reactive oxygen species by phagocytes and the antioxidant defense mechanisms of microorganisms play a crucial role in pathogenesis. In this study, isolates representing 8 pathogenic Candida species-Candida albicans, Candida dubliniensis, Candida famata, Candida glabrata, Candida guilliermondii, Candida krusei, Candida parapsilosis and Candida tropicalis-were compared with regard to their resistance to oxidative stress in vitro. We evaluated degree of resistance, induction of oxidative damage, capacity to adapt, and induction of antioxidant enzymes. The species showed variable sensitivity to oxidative attack. C. albicans, C. glabrata, and C. krusei were more resistant to oxidative stress under the conditions tested; C. parapsilosis and C. tropicalis presented medium resistance; and C. dubliniensis, C. famata, and C. guilliermondii were more sensitive. The overall greater resistance to oxidative stress of C. albicans and C. glabrata may provide an advantage to these species, which are the major causative agents of candidiasis.

The free radical theory holds that the senescence is caused by oxidative damage that results from an imbalance between reactive oxygen and nitrogen species (RONS) and antioxidant defences. Hence, it plays an important role in the field of gerontology. We evaluated, in male and female rats, the activities of the antioxidant enzymes catalase (CAT), glutathione peroxidase (GPx), and total superoxide dismutase (tSOD), as well as oxidative protein damage in pulmonary tissue at 3, 6, 12, and 20 months of age. The results show an increase in the activities of all antioxidant enzymes at 12 months of age in female rats, suggesting an association with the reproductive life cycle. Protein damage in female pulmonary tissues did not change significantly throughout the ageing process. In male rats, the activity of GPx in 20 months of age showed an inter-gender increase, while the tSOD and GPx showed higher activities in 20 months of age in the intra-gender analysis. The male lung showed higher protein damage at 6 months of age. These findings suggest that antioxidant enzymatic activity is connected to the reproductive life cycle., ((c) 2009 John Wiley & Sons, Ltd.)

Background & Aims: Oxidative stress plays a crucial role in the sickle cell disease. Alpha-lipoic acid (ALA) is a potent antioxidant that is employed in the treatment of several diseases. The objective of this study was to test the ALA effect in the sickle cell disease (SCD) treatment., Methods: Sixty subjects were selected and divided into groups according to the hemoglobin profile: AA (normal), AS (SCD trait subject) and SS (SCD patient). Patients were randomized into a placebo-controlled trial and treated with either ALA (200 mg) or vehicle. Blood samples were collected before supplementation and after 3 months of treatment. Catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities and total antioxidant status (TAS) were evaluated as measure of antioxidant defense. Lipid and protein damages were quantified by malondialdehyde (MDA) and carbonyl assays, respectively., Results: CAT activity significantly increased in the AS group after ALA treatment and GPx activity presented significant decrease in all groups. SOD activity was not different in any group. Data on MDA and carbonyl levels showed significant reduction in the AA group with ALA treatment. TAS decreased in the same group., Conclusion: ALA treatment protected AA individuals from oxidative damage to lipids and proteins. In SCD subjects, the dose applied was not effective to prevent the oxidative damage.

Sickle cell anemia (SCA) is a hereditary disorder with higher potential for oxidative damage due to chronic redox imbalance in red cells. We measured antioxidant enzymes including catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD). We also determined oxidative damage of proteins in hemolysate of red blood cells (RBCs) and plasma (carbonyl assay). We characterized the membrane damage in terms of lipid peroxidation by accumulation of malonaldehyde (MDA) by HPLC in 30 healthy controls and 20 SCA patients in steady-state condition. Twenty (9 males/11 females) adult SCA patients and 30 healthy controls were studied. All patients and control subjects had antioxidant (CAT, GPx, SOD, carbonyl and MDA) and hematological parameters done. Our data show that SCA patients had significant higher GPx and SOD activities than healthy controls. Carbonyl assay was noted in plasma but not in hemolysate. An enhanced production of MDA was observed in the serum of SCA patients. Our data support the growing evidence that patients with SCA are subjected to chronic oxidative stress and are able to oxidative damage in biological macromolecules such as proteins and lipids.

Background: S100B is a calcium-binding protein expressed and secreted by astrocytes; serum and cerebrospinal fluid (CSF) S100B elevation has been proposed as an index of brain damage. However, other tissues are shown to produce this protein and the clinical significance of serum S100B elevation has been discussed., Methods: We investigated the levels of serum and CSF S100B in fasting Wistar rats. Animals were divided into two groups, control and fasting for 48 h, and S100B levels in serum and CSF were determined by ELISA. S100B secretion in dissociated epididymal fat cells was investigated in the presence of epinephrine., Results: We observed a significant >2-fold increase of S100B levels in serum of fasting rats, without changes in its CSF content. Moreover, we demonstrated in vitro epinephrine stimulated S100B release from fat cells., Conclusions: Present results reinforce that extracerebral sources of S100B, particularly adipocytes, contribute to its serum levels and support the idea that caution is needed when interpreting serum S100B increase as a clinical marker of brain damage.

The theory of free radicals and accumulation of damages suggests that the reactive species of oxygen play a key role in the context of aging. Thus, for the best understanding of the aging process, the study of antioxidant defenses has to be considered as part of gerontology. The present work evaluated the enzymatic activity of the enzymes catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), and measured the amount of oxidative damage in proteins (carbonyl groups) in brains of rats of both sexes in the ages of 3-, 6-, 12- and 20-months. The results suggest that the patterns of activity and accumulation of damages can be sex-specific and related to the cycle of reproductive life of the organism.

Saccharomyces cerevisiae mutants deficient in superoxide dismutase genes (sod1delta, sod2delta and the double mutant) were subjected to H2O2 stress in the stationary phase. The highest sensitivity was observed in the sod2delta mutant, while the sod1deltasod2delta double mutant was not sensitive. Sod mutants had lower catalase activity (44%) than wild-type cells, independent of H2O2 stress. Untreated cells of sod1deltasod2delta double mutants showed increased glutathione peroxidase activity (126%), while sod1delta had lower activity (77%) than the wild type. Glutathione levels in sod1delta were increased (200-260%) after exposure to various H2O2 concentrations. In addition, the highest malondialdehyde levels could be observed without H2O2 treatment in sod1delta (167%) and sod2delta (225%) mutants. In contrast, the level of malondialdehyde in the sod1deltasod2delta double mutant was indistinguishable from that of the wild type. These results suggest that resistance to H2O2 by sod1deltasod2delta cells depends on the induction of glutathione peroxidase and is independent of catalase, and that glutathione is a primary antioxidant in the defense against H2O2 in stationary phase sod1delta mutants.

The hsp60 expression pattern and catalase activity in the freshwater planarian Dugesia schubarti exposed to copper under laboratory conditions were investigated. In the hsp60 induction experiments, planarians were exposed to a range of copper concentrations (0-960 microgCu/L) for 4 or 24h, to concentrations of 50 or 100 microgCu/L for 2, 4, 8, and 24h at 19 degrees C, and to heat shock at 27 degrees C for 24h. The concentrations of hsp60 in whole-body homogenates were determined immunochemically by Western blotting. Stress protein induction was detected only after 24h treatment at 27 degrees C. The tissue concentration of hsp60 remained unaltered in Cu-exposed planarians under the experimental conditions used. Catalase activity was significantly induced at concentrations of 40, 80, and 160 microgCu/L after 24h exposure. Our results suggest that catalase levels in planarians could represent biomarkers of interest for the estimation of copper effects in freshwater ecosystems.

Recent intervention studies revealed that supplementation with retinoids resulted in a higher incidence of lung cancer. Recently the causal mechanism has begun to be clarified. We report here that retinol caused cellular oxidative stress and modulated superoxide dismutase, catalase and glutathione peroxidase activities. Retinol (7 microM) significantly increased TBARS, conjugated dienes, and hydroperoxide-initiated chemiluminescence in cultured Sertoli cells. In response to retinol treatment superoxide dismutase, catalase and glutathione peroxidase activities increased. TBARS content and catalase activities were decreased by a free radical scavenger. These findings suggest that retinol may induce oxidative stress and modulate antioxidant enzyme activities in Sertoli cells.

Recent intervention studies revealed that supplementation with retinoids resulted in a higher incidence of lung cancer. Recently the causal mechanism has begun to be clarified. We report here that retinol caused cellular DNA damage probably involving cellular iron accumulation. Retinol (7 microM) significantly induced DNA single strands breaks, DNA fragmentation and production of 8-oxo-7, 8-dihydro-2'-deoxyguanosine in cultured Sertoli cells. In contrast, lower doses seemed not to induce single-strands break in this experimental model. The breaks in DNA were inhibited by an iron scavenger; and 7 microM retinol treatment modulated iron turnover leading to iron accumulation, suggesting that iron ions were required for the retinol cellular effects. These findings suggest that retinol-induced DNA damage was associated with the modulation of iron turnover, and these characteristics could be responsible for the increased incidence of lung cancer associated with retinoids supplementation.

Oxidative stress has been implicated in a variety of acute and chronic neurologic conditions, including epilepsy. Both the kainic acid and pilocarpine are useful models of temporal lobe epilepsy in rodents. As an index of lipid peroxidation the level thiobarbituric acid reactive substances (TBARS) was measured after the status epileticus induced by pilocarpine or kainic acid. In hippocampus there was a slight enhancement in the TBARS levels measured 12-14 h after the end of status epileticus induced by pilocarpine and kainic acid. The TBARS levels in pilocarpine treated animals was significantly decreased late after status epileticus and in kainic acid model the TBARS returned to basal levels. These results indicating a putative role of reactive oxygen species in kainic acid and pilocarpine induced epilepsy.

We investigated retinol effects in ornithine decarboxylase activity in Sertoli cells. We also tested the hypothesis that free radical scavengers and iron chelators may attenuate the effect of retinol. Sertoli cells isolated from 15-day-old Wistar rats were previously cultured for 48 h and then treated with retinol by 24 h with or without mannitol (1 mM) or 1,10 phenanthroline (100 microM). We measured ornithine decarboxylase and catalase activities and malondialdehyde concentrations in response to retinol treatment. In response to 7 microM retinol treatment ornithine decarboxylase activity increased 30%. Retinol-induced ornithine decarboxylase activity was significantly decreased by addition of free radical scavenger (mannitol) or iron chelator (1,10 phenanthroline). In addition the same effect was observed in catalase increased activity and in malondialdehyde concentrations. These results suggest that retinol treatment induced ornithine decarboxylase and catalase activity and increased malondialdehyde concentration. These effects appear to be mediate by ROS.

The E. coli recA gene was introduced into the pso4-1 mutant of S. cerevisiae and transformants were treated with 8-MOP+UVA and 254-nm UV light. The results showed that the recA gene increased the resistance to the toxic effect of 8-MOP+UVA and restored the frequency of reversion of the pso4-1 mutants after both treatments. The presence of the recA gene stimulated expression of the small subunit of the ribonucleotide reductase (Rnr2) in the pso4-1 mutants. Thus the E. coli recA gene is functional in yeast. Moreover, it was shown that the pso4-1 mutant is epistatic to pso1-1 and rad6-1, which belong to a mutagenic repair pathway. We propose here that the PSO4 gene has some role in the control of mutagenic repair in yeast.

The mutant allele pso3-1 of Saccharomyces cerevisiae confers sensitivity to treatment with UV365nm (UVA) light-activated mono- and bi-functional psoralens. When pso3-1 is combined in double mutants with selected rad and pso mutant alleles and subjected to 8-MOP + UVA treatment, epistatic interaction with regard to survival is observed with pso1, pso2, and rad3. With the same treatment the combination of pso3-1 with rad6 and rad52 leads to synergistic interaction. For the monofunctional agent 3-carbethoxypsoralen (3-CPs) the analysis of double mutants yields the same results as with the bifunctional 8-methoxypsoralen (8-MOP) with the exception of the pso1-1pso3-1 double mutant. Here we find an additive interaction, i.e., the sensitivities of both parental strains are summed in the double mutant, which indicates a different substrate specificity of the repair activity encoded by the PSO1 and PSO3 genes.