Antioxidant defence of L-glutamine on mitochondrial function in experimentally induced myocardial infarction in rats

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 isoprenalineinduced 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.

Potential Deleterious Effects of L-Citrulline Supplementation in Isoproterenol-Induced Myocardial Infarction: Focus on Nitrosative Stress

“…All induced groups were significantly different from the normal group (p<0.05). This result was in accordance with the study conducted by Anandan, et al, (2015) where isoproterenol caused a decrease in blood pressure and protection against AMI was represented as an amelioration in this decrease. However, the decrease of blood pressure in both the low and high dose groups contradicted the supposed cardioprotective effect of L-citrulline against AMI.…”