RESUMEN
This article briefly reviews biochemistry of oxygen free radical production, physiological mechanisms of anti-free radical tissue protection and the pathological processes which, at least partly, depend on free radical production and lipid peroxidation. Special accent is put on therapeutic implications of numerous experimental findings in this scientific field. The aim of this paper is to call attention of the physicians to the entirely new concept of pathogenesis of many serious diseases, which affords new therapeutic opportunities.
Asunto(s)
Especies Reactivas de Oxígeno , Animales , Radicales Libres/metabolismo , Radicales Libres/farmacología , Humanos , Especies Reactivas de Oxígeno/química , Especies Reactivas de Oxígeno/metabolismo , Especies Reactivas de Oxígeno/farmacología , Especies Reactivas de Oxígeno/uso terapéuticoRESUMEN
It has been suggested that in the genesis of isoprenaline-induced myocardial necrosis in rats, along with the intracellular calcium homeostasis and energy production breakdown, the mechanism of cytotoxic oxygen free radical generation is also included. The effects of dimethylsulphoxide, a hydroxyl radical scavenger, on the appearance of isoprenaline-induced myocardial necrosis in rats, were investigated. The verification of the efficacy of such pretreatment was based upon the monitoring of changes in plasma activity of enzymes creatine kinase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase, and upon the heart muscle sample light microscopy. The results have shown that the total plasma activity of all the observed enzymes was six hours after isoprenaline application several times increased, as compared with the control values. Histopathological changes in unprotected animals were evident and consisted of coagulation necrosis and myocytolysis. In both dimethylsulphoxide and isoprenaline treated groups of rats only a statistically insignificant increase in enzyme plasma activity was observed, while heart histopathological changes showed considerable reduction both in extensity and intensity of the tissue damage. The evident efficiency of dimethylsulphoxide in the prevention of the extent of myocardial necrosis in rats after the administration of the toxic dose of isoprenaline suggests that the generation of hydroxyl anion radicals, probably via autooxidation of isoprenaline, is a possible mechanism of the tissue injury in this experimental model.