Effect of vitamin E on the platelet xanthine oxidase and lipid peroxidation in the patients of myocardial infarction

Abstract

Platelets play important role in precipitating ischaemic myocardial syndromes in many ways. One of the consequences of ischaemic diseases is excessive generation of oxygen derived free radicals that have numerous pathophysiological consequences. Platelet pro-oxidant enzyme, xanthine oxidase is one of the sources of generation of free radicals. In the present paper, we report the effect of administration of vitamin E along with aspirin on the levels of platelet xanthine oxidase and extent of free radical mediated damage in the patients reperfused after myocardial infarction.Our findings show that administration of 400 mg. vitamin E for six days along with 80 mg. aspirin has an excellent anti-oxidant effect as evidenced by reduced platelet xanthine oxidase activity and lowering of malondialdehdye (MDA) levels which is an index of the extent of free radical mediated damage.

Status of some free radical scavenging enzymes in the blood of myocardial infarction patients

“…Damage of the existing enzymes so as to exhibit reduced activities by the high levels of free radicals generated during reperfusion appears to be more probable. This view is further supported by the observation that administration of anti-oxidants such as vitamin E and C for a short time to the patients significantly restores the decreased levels of the enzymes back to near normal values and decreases the levels of MDA generation [27,28].…”

Xanthine oxidase as a marker of myocardial infarction

“…During ischemic conditions, the adenosine nucleotide pool is degraded to hypoxanthine and xanthine, along with conversion of xanthine dehydrogenase to xanthine oxidase (6,7). Xanthine oxidase acts on xanthine and hypoxanthine with the resultant production of oxygen free radicals.…”

“…Under ischemic conditions, there is depletion of ATP and subsequent loss of membrane Ca 2+ gradient. Increased Ca 2+ levels activates Ca 2+ dependent proteases which cause selective proteolysis of the dehydrogenase to convert it into xanthine oxidase which acts both on hypoxanthine and xanthine at the expense of molecular oxygen to produce superoxide ion (6,7). Thus xanthine oxidase in ischemic conditions of the heart, as in myocardial infarction, may play an important role in contributing free radical mediated damage.…”

Oral Administration of L‐Arginine in Patients With Angina or Following Myocardial Infarction May Be Protective By Increasing Plasma Superoxide Dismutase and Total Thiols With Reduction in Serum Cholesterol and Xanthine Oxidase

“…The second line of defense to ROS is provided by antioxidant compounds present in the body such as thiols, or taken from outside such as α-tocopherol, β-carotenoids, flavonoids and L-arginine. We have earlier shown that administration of vitamin C10,11 and vitamin E12,13 to the patients of ischemic myocardial syndromes lower lipid per-oxidation, increase the activities of free radical scavenging enzymes, which are decreased in these patients, and lower the activity of pro-oxidant enzyme which are elevated in the patients. Oxidized low density lipo-proteins are involved in the progression of atherosclerotic lesions14 which can be prevented by L-arginine administration.…”