TARGETS OF OXIDATIVE STRESS IN CARDIOVASCULAR-SYSTEM

Although oxidants such as superoxide (O-2(.)) and hydrogen peroxide (H 2O2) play a role in host-mediated destruction of foreign pathogens yet excessive generation of oxidants may lead to a variety of pathologica l complications in the cardiovascular system. An important mechanism b y which oxidants cause dysfunction of the cardiovascular system appear s to be due to the increase in intracellular free Ca2+ concentration. Oxidants cause cellular Ca2+ mobilization by modulating activities of a variety of regulators such as Na+/H+ and Na+/Ca2+ exchangers, Na+/K ATPase and Ca2+ ATPase and Ca2+ channels that are associated with Ca2 + transport in the plasma membrane and the sarco(endo)plasmic reticula r membrane of myocardial cells. Recent research have suggested that th e increase in Ca2+ level by oxidants plays a pivotal role in inducing several protein kinases such as protein kinase C, tyrosine kinase and mitogen activated protein kinases, Oxidant-mediated alteration of diff erent signal transduction systems and their interations eventually reg ulate a variety of pathological conditions such as atherosclerosis, ap optosis and necrosis in the myocardium.