Biochemical Studies on the Protective Effect of Betaine on Mitochondrial Function in Experimentally Induced Myocardial Infarction in Rats

Abstract

The present study was designed to examine the cardioprotective effect of betaine on mitochondrial function in isoprenaline-induced myocardial infarction in rats with respect to changes in the mitochondrial energy status and antioxidant defense system. Prior oral treatment with betaine significantly prevented the isoprenaline-induced elevation in the levels of diagnostic maker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)] and homocysteine in plasma of the experimental group of rats. Its administration significantly counteracted the isoprenaline-induced aberrations in the myocardial energy status by maintaining the levels of myocardial ATP and betaine contents and the activities of mitochondrial TCA cycle enzymes [isocitrate dehydrogenase (ICDH), α-ketoglutarate dehydrogenase (α-KDH), succinate dehydrogenase (SDH), and malate dehydrogenase (MDH)] and respiratory marker enzymes (NADH dehydrogenase and cytochrome-c-oxidase) at near normalcy. It also exerted an antioxidant effect against isoprenalineinduced myocardial infarction by blocking the induction of mitochondrial lipid peroxidation (LPO). A tendency to minimize the isoprenaline-induced alterations in the level of reduced glutathione (GSH) and in the activities of glutathione-dependent antioxidant enzymes [glutathione peroxidase (GPx) and glutathione-S-transferase (GST)] and antiperoxidative enzymes [superoxide dismutase (SOD) and catalase (CAT)] in the heart mitochondria was also observed. The results of the present study indicate that the overall cardioprotective effect of betaine is probably related to its ability to maintain the myocardial energy status (ATP) at higher level by maintaining the activities of TCA cycle enzymes and respiratory marker enzymes at near normalcy, and/or to its free radical-scavenging ability against isoprenaline-induced lipid peroxidation, which is primarily responsible for the irreversible necrosis of the myocardial membrane.

Studies on the protective effects of betaine against oxidative damage during experimentally induced restraint stress in Wistar albino rats

“…Glutathione functions by reaction with superoxide radicals, peroxy radicals and singlet oxygen, followed by the formation of oxidized glutathione and other disulphides (Aweda et al 2003). Depletion of GSH results in enhanced lipid peroxidation, and excessive lipid peroxidation can cause increased GSH consumption (Ganesan et al 2007a), as observed in the present study (Figs. 7 and 10).…”

“…Earlier, we reported the protective effect of betaine on mitochondrial function (Ganesan et al 2007a) protein and glycoprotein metabolism (Ganesan et al 2007b) and lipid metabolism (Ganesan et al 2008) and lysosomal function (Ganesan and Anandan 2009) against isoprenaline-induced myocardial infarction in rats. In the present study, an attempt was made to assess the protective effects of betaine against oxidative damage during experimentally induced restraint stress in Wistar albino rats with respect to changes in the levels of lipid peroxidation, antioxidant status (GST, GPx, CAT, SOD activities, and GSH level) in lymphoid organs of thymus and spleen, changes in the adrenal weight, plasma protein, and corticosterone levels.…”

Effect of Solanum surattense seed on the oxidative potential of cauda epididymal spermatozoa

“…The activity level of the enzyme iso-citrate dehydrogenase recorded significant depletion in the extract fed rats when compared with that of the control indicating the deranged oxidative potential in the sperm suspension. ICDH is a specific marker for the mitochondrial density [38] . The sperm motility showed a drastic depletion in the extract fed rats.…”

Protective effect of betaine on changes in the levels of lysosomal enzyme activities in heart tissue in isoprenaline-induced myocardial infarction in Wistar rats

“…It has been shown that betaine regulates erythrocyte (red blood cell) membrane ATPases via conformational changes, which results in cell volume control (Moeckel et al 2002). Earlier, we reported the protective effect of betaine on antioxidant status (Ganesan et al 2008b), mitochondrial function (Ganesan et al 2007a), protein and glycoprotein metabolism (Ganesan et al 2007b), and lipid metabolism (Ganesan et al 2008a) in isoprenaline-induced myocardial infarction in Wistar rats. In the present study, an attempt was made to assess the protective effects of betaine on isoprenaline-induced myocardial infarction with respect to changes in the levels of lysosomal enzymes and lipid peroxidation.…”