Abstract
Myocardial infarction is a major public health concern and the leading cause of death all over the world. A better understanding of the processes involved in myocardial infarction has stimulated the search for biomolecules, which could limit the myocardial injury. We determined the protective activity of L-glutamine on mitochondrial function in isoprenaline-induced myocardial infarction in rats, an animal model of myocardial infarction in man. Oral pre-treatment with glutamine significantly inhibited the isoprenaline-induced changes in the levels of troponin T and homocysteine in the plasma. It conserved the activities of tricarboxylic acid cycle enzymes (isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase) and respiratory marker enzyme (NADH dehydrogenase) and the level of myocardial ATP content at levels comparable to that of normal controls. It also attenuated isoprenaline-induced oxidative stress in rat mitochondria and preserved the antioxidant defence system at near normal. The results indicate that the cardioprotective effect of glutamine can be correlated directly with its ability to activate the energy status and antioxidant defence system.Keywords: isoprenaline
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