RESUMO
The substantial increase in the number of elderly people in our societies represents a challenge for biology and medicine. The societies of the industrialized countries are subject to a progressive aging process that translates into an increase in the cardiovascular risk of the population. In the present work, the activity of catalase and superoxide dismutase was evaluated, as well as markers of oxidative stress (concentration of nitric oxide and total lipoperoxidation in its main components: malondialdehyde and 4-hydroxyalkene) in cardiomyocytes during the aging process in rats treated with resveratrol. Rats were divided into 4 groups according to the following categories: control (without treatment), negative control group (administered with physiological solution with 10% ethanol), positive control group (administered with vitamin E, 2 mg/kg/day), and group administered with resveratrol (10 mg/kg/day); these groups in turn were divided into 2, 4, 6, and 8 months of treatment. The analysis of nitric oxide showed a decreased level in the cardiac tissue in the groups treated with resveratrol; the same occurs when total lipoperoxidation is analyzed. The enzymatic activity studied (catalase and superoxide dismutase) did not present significant changes with respect to the controls. It is concluded that the cardioprotective effect of resveratrol is due to the antioxidant effect and other antiaging effects and not to the activation of the enzymes catalase and superoxide dismutase.
Assuntos
Miócitos Cardíacos/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Estilbenos/uso terapêutico , Envelhecimento , Animais , Masculino , Ratos , Ratos Wistar , Resveratrol , Estilbenos/farmacologiaRESUMO
The elevated expression of stress proteins is considered to be a universal response to adverse conditions, representing a potential mechanism of cellular defense against disease and a potential target for novel therapeutics. Exposure to arsenicals either in vitro or in vivo in a variety of model systems has been shown to cause the induction of a number of the major stress protein families such as heat shock proteins (Hsp). Among them are members with low molecular weight, such as metallotionein and ubiquitin, as well as ones with masses of 27, 32, 60, 70, 90, and 110 kDa. In most of the cases, the induction of stress proteins depends on the capacity of the arsenical to reach the target, its valence, and the type of exposure, arsenite being the biggest inducer of most Hsp in several organs and systems. Hsp induction is a rapid dose-dependent response (1-8 h) to the acute exposure to arsenite. Thus, the stress response appears to be useful to monitor the sublethal toxicity resulting from a single exposure to arsenite. The present paper offers a critical review of the capacity of arsenicals to modulate the expression and/or accumulation of stress proteins. The physiological consequences of the arsenic-induced stress and its usefulness in monitoring effects resulting from arsenic exposure in humans and other organisms are discussed.