| Growing evidence shows that reactive oxygen species (ROS) play a critical role in the pathogenesis of many cardiovascular diseases. The oxidative injury was mediated by ROS, a group of highly reactive oxygen compounds, which mainly include oxygen free radicals. It is well known that excess generation of ROS or their incessant attack can cause an array damages to cells, which is referred as oxidative stress, including membrane lipid peroxidation, cross-linking and degradation of proteins, and the injury to DNA, resulting in the impairment of cellular integrity and function. At high doses that apparently overwhelm cardiomyocyte antioxidant defense, ROS cause irreversible cell injury and cell death. Lower concentration of ROS especially H202 and 0H have been shown to cause reversible cell injury by activating a variety of intracellular signaling processes. So it is very useful to investigate the effects of lower concentration of ROS, and this can aid the design of more specific interventions with potential clinical utility to the ischemic heart disease patients. H202 is a kind of ROS and is an important tool for studying the effects of ROS. H202 can readily cross the cell membrane and be converted, via the Fenton reaction, to the more toxic OHradicals and 0H radicals can in turn initiate a cascade of radical reactions. In this experiment, H202 was used to simulate the attack of ROS on cardiac myocytes. Melatonin(MT), a hormone secreted mainly by the pineal gland, was recently found to be an effective free radical scavenger and antioxidant as well as other important biological functions. MT production in the organism is gradually lost throughout life. While most studies to date have used pharmacological quantities of melatonin to limit oxidative damage, physiologic concentrations of MT, which are present in aerobic organisms, have also been shown to resist molecular damage inflicted by free radicals. Melatonin reduces oxidative stress by several means. It readily scavenges the most highly toxic free radical, the hydroxyl radical, and it directly detoxifies the peroxynitrite anion, nitric oxide, singlet oxygen. MT inhibits the oxidation of unsaturated lipids. Additionally, melatonin may stimulate some important antioxidative enzymes, including superoxide dismutase, glutathione peroxidase, and glutathione reductase as well as inhibiting the pro-oxidative enzyme, nitric-oxide synthase. Finally, melatonin chelates transition metal ions and prevents the deterioration of cellular membranes. Melatonin is highly effective in reducing nuclear DNA damage and membrane lipid destruction due to toxic free radicals in vivo, This combination of actions may all contribute to melatonin抯 ability to reduce oxidative damage. These findings have implications for disease processes, such as neurodegenerative and cardiovascular diseases, which involve free radicals and for aging itself and which also is related to accumulated oxidative damage. Its lack of toxicity and the ease with which melatonin crosses morphophysiological barriers and enters subcellular compartments are essential features of this antioxidant. In the present study, we used a cell culture model of isolated cardiac cells treated with 100 ~t mol/L H202 and 100 ~i mol/L MT to investigate how the lower concentration of exogenous H202 and evaluate the role of MT in cardiac protection against oxidative injury. The main results of this work were as follows:...
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