Preventive effect of betaine on ethanol-induced membrane lipid composition and membrane ATPases

Cell Stress and Chaperones

Lakshmanan

2011

Stress can be defined as physical and psychological modifications that disrupt the homeostasis and the balance of organisms. Stress is known as one of the most important reasons of several diseases. In the present study, the anti-stress effect of betaine was evaluated with reference to its antioxidant property. Wistar albino rats were divided into four groups such as control, betaine, restraint stress (6 h/day for 30 days), and betaine+restraint stress. The oxidative damage was assessed by measuring the protein and corticosterone in plasma, lipid peroxidation, nonenzymic (reduced glutathione), and enzymic antioxidants (glutathione peroxidase, glutathione-S-transferase, catalase, and superoxide dismutase) in the lymphoid organs of thymus and spleen. Followed by the induction of restraint stress, the non-enzymic and enzymic antioxidants were significantly decreased with concomitant increase observed in the levels of corticosterone and lipid peroxidation. Oral pretreatment with betaine (250 mg/kg body weight daily for a period of 30 days) significantly (P<0.001) prevented the restraint stress-induced alterations in the levels of protein and corticosterone in plasma of experimental groups of rats. It counteracted the restraint stress-induced lipid peroxidation and maintained the antioxidant defense system in the lymphoid tissues at near normal. The findings suggest that betaine possesses significant anti-stress activity, which may be due to its antioxidant property.

Section: Resultsmentioning

confidence: 99%

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

Cell Stress and Chaperones

Lakshmanan

2011

“…49) Reports by Kim and Kim 7) indicated that betaine supplementation was effective in prevention of lipopolysaccharide-induced necrotic damage in liver by inhibiting Kupffer cell activation and behaving as an antioxidant. Earlier reports 6,50,51) indicated that betaine had a potent reducing effect on the production of free radicals in rats exposed to cytotoxicity. Feeding SH-generating substances such as methionine or non-enzymic antioxidants such as glutathione have been reported to protect cellular and subcellular membranes from toxic free radical metabolites.…”

Section: Discussionmentioning

confidence: 96%

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

Rajesh

JOURNAL OF HEALTH SCIENCE

et al. 2007

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.

“…Betaine supplementation was effective in the prevention of lipopolysaccharide-induced necrotic damage in liver by inhibiting Kupffer cell activation and behaving as an antioxidant (Kim et al 1998). Subsequent reports indicated that betaine had a potent reducing effect on the production of free radicals in rats exposed to cytotoxicity (Balkan et al 2004;Kanbak et al 2001). Feeding SH-generating substances such as methionine or nonenzymatic antioxidants such as glutathione have been reported to protect cellular and subcellular membranes from toxic free radical metabolites (Selvam and Kannabiran 1993).…”

Section: Resultsmentioning

confidence: 99%

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

Cell Stress and Chaperones

2009

Myocardial infarction is one of the most common manifestations of cardiovascular disease. In the present study, we investigated the protective effect of betaine, a potent lipotropic molecule, on changes in the levels of lysosomal enzymes and lipid peroxidation in isoprenalineinduced myocardial infarction in Wistar rats, an animal model of myocardial infarction in man. Male albino Wistar rats were pretreated with betaine (250 mg/kg body weight) daily for a period of 30 days. After the treatment period, isoprenaline (11 mg/100 g body weight) was intraperitoneally administered to rats at intervals of 24 h for 2 days. The activities of lysosomal enzymes (β-glucuronidase, β-galactosidase, β-glucosidase, and acid phosphatase) were significantly (p<0.05) increased in plasma with a concomitant decline in the activities of these enzymes in heart tissue of isoprenaline-administered rats. Also, the level of lipid peroxidation was higher in heart lysosomes of isoprenaline-injected rats. Pretreatment with betaine daily for a period of 30 days to isoprenaline-induced rats prevented the changes in the activities of these lysosomal enzymes. Oral treatment with betaine (250 mg/kg body weight) to normal control rats did not show any significant effect in all the biochemical parameters studied. Thus, the results of our study show that betaine protects the lysosomal membrane against isoprenaline-induced myocardial infarction. The observed effects might be due to the free radical-scavenging and membrane-stabilizing properties of betaine.