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Introduction: One of the markers of aging is oxidative stress, a condition characterized by an increase in free radicals concomitant with a reduction in antioxidant defenses. Within this, resveratrol is a compound that has been shown to act as a potent antioxidant. However, few studies highlight the cellular signaling pathways that are activated or inhibited during aging and that are responsible for this biological effect. Aim: To verify the antioxidant profile of resveratrol (5 μM) in leukocytes from donors in different age groups. Methods: The project was approved by the Ethics Committee. Individuals were divided into three groups: 20–39, 40–59, and 60–80 years old. After separating the leukocytes, assays were performed to evaluate the AMPK (AMP‐activated protein kinase) and Nrf2 (erythroid nuclear factor 2‐related factor 2) pathways. In addition, luciferase assay and enzyme‐linked immunosorbent assay were performed to evaluate transcription factor activation and Nrf2 expression, respectively. The analysis between age and treatment was performed using Pearson correlation (*P < 0.05). Results: There was a reduction in the antioxidant effect of resveratrol during the aging process. In leukocytes from donors over 60 years of age, the AMPK pathway was silenced. Nrf2 was active at all ages. There was an increase in the activation of the transcription factor and phosphorylated protein in all age groups. Conclusions: Nrf2 is an important biochemical mechanism responsible for the antioxidant effect of resveratrol. This effect diminishes with aging but is still observed. Geriatr Gerontol Int 2024; 24: 954–961. [ABSTRACT FROM AUTHOR]

A study was conducted to compare health status of male adult Wistar rats from two Experimental Animal Houses of UFMG with literature data of SPF (free from specific pathogens) and conventional rats. The animals were divided into two groups: Group I (n=10), rats from the experimental animal houses of FAFICH and Group II (n=10) from ICB and following aspects were studied: a) evident clinical signs (behavior modification, hair loss (alopecia), b) leukocyte counts, c) feces exam and d) histological study of the lungs. The rats did not show clinical signs. However, when compared with SPF and conventional rats, both the groups showed a significant increase (p

The aim of this study was to investigate the possible effects of captopril as a promoter in modulating the oxidant-antioxidant balance in rats with type 1 diabetes, and the influence of protein kinase C (PKC) pathways in the production of reactive oxygen species (ROS) induced by bradykinin in type 1 diabetic rats. This study evaluated the redox status in both the cardiac tissue and at the cellular level (neutrophils). Two concentrations of captopril were utilized: (i) 5 mg x [(kg body mass).sup.-1], which was considered a therapeutic dose; and (ii) 10 mg x [(kg body mass).sup.-1]. Body mass, plasma glucose, and serum insulin were evaluated. To investigate the redox status of the cardiac tissue, we analyzed lipid peroxidation, concentration of carbonylated protein, catalase activity, and the concentration of glutathione. For a more accurate assessment of the possible antioxidant effect of captopril, we also analyzed ROS in neutrophils (in vivo), and ROS production induced by bradykinin and the influence of the PKC pathway in this production (in vitro). Our data show that the hearts of diabetic animals have increased oxidative damage, exemplified by the increased concentration of carbonylated protein and thiobarbituric acid reactive substances (TBARS). However, animals treated with captopril at both concentrations showed lower concentrations of carbonylated protein compared with untreated diabetic animals. We found an increase of catalase activity in the heart of diabetic rats, which was reversed by captopril treatment at both of the dosages tested. Our data showed that captopril was able to reduce ROS production in the neutrophils of diabetic rats at a dose of 10 mg captopril x [(kg body mass).sup.-1]. However, the antioxidant effect of captopril is independent of bradykinin. Diabetes induces oxidative stress, and these results suggest that captopril has an antioxidant effect and can modulate the production of ROS in circulating neutrophils. Key words: diabetes, captopril, oxidative stress, bradykinin, PKC. La presente etude a eu pour but d'examiner, chez des rats presentant un diabete de type 1, les effets possibles du captopril en tant que promoteur de la modulation de l'equilibre oxydant-antioxydant ainsi que l'influence de la voie de la proteine kinase C (PKC) dans la production d'especes reactives de l'oxygene (ROS) induite par la bradykinine. Nous avons evalue l'etat redox dans le tissu cardiaque et au niveau cellulaire (neutrophiles). Nous avons utilise deux concentrations de captopril : une dose de 5 mg x [kg.sup.-1], consideree comme therapeutique, et une dose de 10 mg x [kg.sup.-1]. Nous avons evalue le poids, le glucose plasmatique et l'insuline serique. Pour examiner l'etat redox du tissu cardiaque, nous avons analyse la peroxydation lipidique, la concentration des proteines carbonylees, l'activite de la catalase et la concentration de glutathion. Pour une meilleure evaluation de l'effet antioxydant possible du captopril, nous avons aussi analyse le taux de ROS dans les neutrophiles (in vivo), ainsi que la production de ROS induite par la bradykinine et l'influence de la voie PKC dans cette production (in vitro). Nos resultats montrent que le coeur des rats diabetiques subit une plus fort dommage oxydatif, illustre par l'augmentation de la concentration des proteines carbonylees et des substances reactives a l'acide thiobarbiturique (TBARS). Toutefois, les animaux traites au captopril, aux deux concentrations utilisees, ont montre de plus faibles concentrations de proteines carbonylees que les rats diabetiques non traites. Nous avons observe une augmentation de l'activite catalase dans le co ur des rats diabetiques, qui a ete renversee par le traitement au captopril, aux deux doses analysees. Nos resultats ont montre que le captopril a ete capable de reduire la production de ROS dans les neutrophiles des rats diabetiques lors du traitement avec la dose 10 mg x [kg.sup.-1]. Toutefois, l'effet antioxydant du captopril est independant de celui de la bradykinine. Le diabete induit un stress oxydatif, et ces resultats laissent a penser que le captopril a un effet antioxydant et qu'il peut moduler la production de ROS dans les neutrophiles circulants. Mots-cles : diabete, captopril, stress oxydatif, bradykinine, PKC. [Traduit par la Redaction], Introduction In 1997, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus defined Type 1 Diabetes Mellitus as an autoimmune disease characterized by inflammation of the Langerhans islets, [...]

BACKGROUND: Diabetic patients are exposed to increased oxidative stress due to several mechanisms, mainly hyperglycaemia. Pathological processes, such as those in type 1 diabetes, include diminished activity of the antioxidant defense system(s) or excessive oxidative generation resulting in an oxidative/antioxidant imbalance and development of oxidative stress. METHODS: The purpose of this study was to evaluate the production of reactive oxygen species (ROS) (chemiluminescence) and reduction capacity (MTT dye reduction), the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits, superoxide dismutase and catalase using quantitative reverse-transcriptase polymerase chain reaction, and the levels of cytokines [interleukin (IL)-6, tumour necrosis factor-[alpha], IL-8, IL-10 and IL-4] by sandwich enzyme-linked immunosorbent assay in mononuclear cells from non-diabetic and diabetic donors treated with a vitamin complex (ascorbic acid, [beta]-carotene and [alpha]-tocopherol) in two different concentrations ([A] = ascorbic acid = 0.08 uM, [alpha]-tocopherol = 0.04 uM, [beta]-carotene = 0.0008 uM and [20A] = ascorbic acid = 1.6 uM, [alpha]-tocopherol = 0.82 uM, [beta]-carotene = 0.016 uM). RESULTS: Concentration [A] was antioxidant reducing ROS production, expression of NADPH oxidase subunits and pro-inflammatory cytokines while raising the expression of antioxidant enzymes and reducing pro-inflammatory cytokines in both groups. Concentration [20A] was pro-oxidant by raising ROS production, NADPH oxidase subunits and pro-inflammatory cytokines and reducing antioxidant enzymes and anti-inflammatory cytokines in the non-diabetic group but antioxidant in cells of type 1 diabetic patients by raising antioxidant enzymes and anti-inflammatory cytokines and reducing pro-inflammatory cytokines. CONCLUSION: The vitamin complex has a dual effect, pro-oxidant and antioxidant, being also dose dependent with different profiles of cells of non-diabetic and type 1 diabetic patients. Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Background Diabetic patients are exposed to increased oxidative stress due to several mechanisms, mainly hyperglycaemia. Pathological processes, such as those in type 1 diabetes, include diminished activity of the antioxidant defense system(s) or excessive oxidative generation resulting in an oxidative/antioxidant imbalance and development of oxidative stress. Methods The purpose of this study was to evaluate the production of reactive oxygen species (ROS) (chemiluminescence) and reduction capacity (MTT dye reduction), the expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits, superoxide dismutase and catalase using quantitative reverse-transcriptase polymerase chain reaction, and the levels of cytokines [interleukin (IL)-6, tumour necrosis factor- α, IL-8, IL-10 and IL-4] by sandwich enzyme-linked immunosorbent assay in mononuclear cells from non-diabetic and diabetic donors treated with a vitamin complex (ascorbic acid, β-carotene and α-tocopherol) in two different concentrations ([A] = ascorbic acid = 0.08 µM, α-tocopherol = 0.04 µM, β-carotene = 0.0008 µM and [20A] = ascorbic acid = 1.6 µM, α-tocopherol = 0.82 µM, β-carotene = 0.016 µM). Results Concentration [A] was antioxidant reducing ROS production, expression of NADPH oxidase subunits and pro-inflammatory cytokines while raising the expression of antioxidant enzymes and reducing pro-inflammatory cytokines in both groups. Concentration [20A] was pro-oxidant by raising ROS production, NADPH oxidase subunits and pro-inflammatory cytokines and reducing antioxidant enzymes and anti-inflammatory cytokines in the non-diabetic group but antioxidant in cells of type 1 diabetic patients by raising antioxidant enzymes and anti-inflammatory cytokines and reducing pro-inflammatory cytokines. Conclusion The vitamin complex has a dual effect, pro-oxidant and antioxidant, being also dose dependent with different profiles of cells of non-diabetic and type 1 diabetic patients. Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Acetaminophen is a common analgesic and antipyretic compound which, when administered in high doses, has been associated with significant morbidity and mortality, secondary to hepatic toxicity. Although this may be due to a direct interaction of reactive acetaminophen metabolites with hepatocyte proteins, recent studies have suggested that reactive species produced by neutrophils also contribute to the pathophysiological process. Researches on the chemical composition of B. trimera show that this plant has bioactive compounds such as flavonoids, related to the organism's protection against free radicals. Therefore, in the present study, using Fischer rats, the effect of B. trimera on the antioxidant defense system, the production of nitric oxide (NO) and on the expression of nitric oxide synthase (iNOS), superoxide dismutase (SOD), catalase (CAT) and of the subunits of the NADPH oxidase in neutrophils was evaluated in a model of phagocytosis induced by zimosan (ZC3b) and in a model of inflammation induced by acetaminophen. The results show that the treatment with B. trimera improves the defense system of antioxidant and restores the balance ROS / NO that is altered in the inflammatory process induced by APAP. In conclusion, B. trimera extracts exert antioxidant properties by scavenging ROS and decrease the expression of genes responsible by reactive species production in neutrophils.