An increased accumulation of intracellular levels of reactive oxygen species with time may play an important role in the process of ageing. The antioxidant properties of resveratrol are dependent upon the up-regulation of endogenous cellular antioxidant systems. We evaluated whether resveratrol has protective antioxidant effects on ovarian damage related to oxidative stress in a rat model. Twenty-four female rats were randomly divided into three groups and were given saline (group 1: control); intraperitoneal cisplatin, 4.5 mg/kg, two weekly doses in total (group 2); or cisplatin, 4.5 mg/kg plus intraperitoneal resveratrol 10 mg/kg/day, 24 h before the administration of cisplatin (group 3). Serum anti-Müllerian hormone (AMH) concentrations were significantly lower in group 2 than in group 3 (P < 0.01 and P = 0.04, respectively). The evaluation of the atretic and antral follicle counts revealed statistically significant differences between the groups (P = 0.04 and P < 0.01, respectively). A statistically significant difference was observed in the follicle count positive for AMH between the groups (P = 0.01). Oxidative stress plays an important role in the process of ovarian ageing. Because of its natural antioxidant properties, resveratrol may be an effective option in protecting ovarian tissue against oxidative damage.
Energy drinks (ED) are containing large doses of metabolic stimulants and its use with ethanol has increased dramatically among young adults. In this study, we examined the effects of ED exposure either alone or in combination with ethanol on oxidative stress parameters including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and lipid peroxidation parameter malondialdehyde (MDA) in rat. Some histopathological findings were also evaluated. ED exposure led to a dose-dependent increase in liver MDA compared to the control indicating oxidative damage. Histopathological findings also revealed that ED alone may generate liver damage. Ethanol exposure increased MDA level and SOD, CAT, and GSH-Px activity in both the brain and the liver. The combination of ethanol and ED produced greater damage which is considered by further increases in SOD and GSH-Px activity in the brain. Similar results for MDA were observed in both the liver and brain as well. Our findings suggest that ED consumption alone or combination with ethanol may represent a significant public health concern.
Apart from its effect on the regulation of reproductive function, recent studies indicate that kisspeptin may play roles in the antioxidant defense system. The antioxidant defense system and oxidative stress contribute to the etiology and pathogenesis of neuronal cell death after brain injury. We have investigated the postacute effect of kisspeptin-10 on brain injury induced by L-methionine. DNA fragmentation, malondialdehyde (MDA), reduced glutathione levels, and superoxide dismutase (SOD) activities were analyzed. Our results showed that methionine treatment increases apoptotic cell death. Kisspeptin alone showed no side effect on apoptotic cell death. However, kisspeptin treatment reversed the proapoptotic effect of methionine associated with reduced MDA and increased glutathione levels. Furthermore, SOD activity was completely depleted in methionine-treated animals. In conclusion, our results revealed that delayed kisspeptin-10 treatment reduces neuronal cell death by activation of SOD activity.
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