Oxidative stress and ischemic myocardial syndromes.

Oxidative stress is a condition in which reactive oxygen species (ROS) or free radicals, namely O2*(-), H2O2, and *OH, are generated extra- or intracellularly and exert toxic effects on cells. The heart is one of the major organs affected by ROS. Recent evidence suggests that oxidative stress is a common denominator in many aspects of cardiovascular diseases. During myocardial oxidative stress, the generation of ROS is enhanced and the defense mechanisms of myocytes are altered. The sources of ROS in cardiac myocytes could be mitochondrial electron transport chain, nitric oxide synthase (NOS), NADPH oxidase, xanthine oxidase, and lipoxygenase/cyclooxygenase and the auto-oxidation of various substances, particularly catecholamines. In acute myocardial infarction (AMI), two distinct types of damage occur to the heart: ischemic injury and reperfusion injury, which lead to mitochondrial dysfunction in heart cells. During ischemia and reperfusion, ROS can be produced by both endothelial cells and circulating phagocytes. Ischemia also causes alterations in the defense mechanisms against ROS. Some proteins, including heat-shock proteins, are overexpressed in conditions of ischemia/reperfusion and can protect from cardiac injury. This article outlines the current understanding of oxidative stress and ROS generation and their role in cardiovascular diseases, including ischemic myocardial syndromes. The following aspects are covered: oxidative stress, mitochondrial dysfunction and pathophysiological mechanisms of atherosclerosis, precipitation of MI, sources of ROS in cardiac myocytes, effects of ROS in the heart, and ischemia and reperfusion injuries and their mechanisms.

Xanthine oxidase as a marker of myocardial infarction.

In the present communication, we report remarkably elevated levels of xanthine oxidase activity in the blood of the patients with myocardial infarction when compared to age and sex matched healthy persons. Highly significant increase of malondialdehyde, serving as an index of lipid peroxidation and thus free radical mediated damage, has also been found in the patients. We propose the measurement of the blood levels of xanthine oxidase, a very simple, reliable and less time consuming method as an indicator of myocardial infarction.

Effect of ascorbic acid supplementation on certain oxidative stress parameters in the post reperfusion patients of myocardial infarction.

Reperfusion injury causes oxidative stress thereby resulting in an imbalance between oxidant-antioxidant systems. In the present communication, the effect of ascorbic acid supplementation has been studied on certain oxidant and antioxidant parameters in the blood of the patients with myocardial infarction before and after thrombolysis. In patients after thrombolysis, the activity of antioxidant enzyme, superoxide dismutase, in the blood was found to be significantly reduced where as the activity of the oxidant enzyme, xanthine oxidase, was found to be significantly increased. Malondialdehyde levels, the index of free radical mediated damage, was also found to be significantly elevated in thrombolysed patients compared to the patients before thrombolysis. Supplementation of vitamin C to the post reperfusion patients restored these parameters back to normal or near normal levels.

Oxidative stress parameters in erythrocytes of post-reperfused patients with myocardial infarction.

The effect of reperfusion of patients with myocardial infarction on the levels of some anti-oxidant enzymes, total thiols, malondialdehyde formation in erythrocytes and plasma ascorbate levels have been investigated. Significantly decreased activities of catalase and superoxide dismutase and decreased levels of total thiols in RBC's and ascorbic acid in plasma suggest that reperfusion of the infarcted myocardium leads to oxidative stress conditions wherein anti-oxidant mechanisms become less effective in coping with the oxidative insult. This view is further supported by the observation that in the post reperfused patients there is a highly significant enhancement in the levels of malondialdehyde.