Abstract:

The aim of this study was to evaluate the role of antioxidant enyzmes, lipid peroxidation products and free radicals which involve in the etiopathogenesis of the hypoxic damage. The experimental animals were assigned to 5 groups. Group 1: Hypoxia group (n=9), Group II: Hypoxia + melatonin group (n=9), Group III: Control group (n=7). Blood was taken for analysing the levels of basal serum troponin I, creatine kinase-MB (CKMB), lactate dehydrogenase(LDH), plasma glutation peroxidase (GSH-Px), superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) before inducing the hypoxia. In the experimental animals of groups I, II, the hypoxia was induced by leaving the animals to breathe in belljar, containing 10 per cent oxygen-nitrogen mixture, for 10 minutes at 5 liter velocity. After inducing the hypoxia melatonin (10 mg/kg/daily & intraperitoneal) was administered to the animals of second group during 5 days. The levels of serum CKMB, LDH and troponin I, plasma NO, MDA, SOD and GSHPx were analysed at the end of the treatment. After sacrificing the experimental animals, tle levels of myocardial NO, MDA, SOD, GSH-Px were analysed and myocardial tissue was examined histopathologically with haematoxylin - eosin stain. The levels of serum-CMKB, LDH and troponin I were found increased; whereas the levels of plasma SOD and GSH-Px were found decreased in the hypoxia-induced group and a heavy cardiomyopathy associated with swelling in myocardial flaments, interstitial edema, disorganization and necrosis was determined. There was a meaningful increase in the levels of plasma SOD but a meaningful decrease in the levels of tissue NO and MDA and a mild and intermediate cardiomyopathy associated with swelling, interstitial edema and disorganization was shown histopathologically in the second group (hypoxia and melatonin). It is shown that the melatonin can protect the hypoxic cardiac damage by being activated as an antioxidant

Keywords: