Effects of Chronic Ethanol Consumption on Brain Synaptosomes and Protective Role of Betaine

Abstract

To evaluate the cytotoxic effects of chronic ethanol consumption on brain cerebral synaptosomes and preventive role of betaine as a methyl donor and S-adenosylmethionine precursor, 24 male Wistar rats were divided into three groups: control, ethanol (8 g/kg/day) and ethanol plus betaine(0.5% w/v) group. Animals were fed 60 ml/diet per day for two months, then sacrificed. Malondialdehyde (MDA), protein carbonyl contents and adenosine deaminase (ADA) activities were determined in synaptosomal/mitochondrial enriched fraction isolated from rat cerebral cortexes. When compared to controls, ethanol containing diet significantly increased MDA levels (P < 0.05), also increased protein carbonyl levels and adenosine deaminase activities. But these were not statistically significant (P > 0.05). However, adding betaine to ethanol containing diet caused a significant decrease in MDA, protein carbonyl levels and adenosine deaminase activities (P < 0.05). These results indicate that betaine may appear as a protective nutritional agent against cytotoxic brain damage induced by chronic ethanol consumption.

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

“…The unpaired electron present in the hydroxyl free radical, which is mainly responsible for the restraint stress-induced oxidative damage to the lymphoid tissues might have been trapped and subsequently dismuted by betaine. Earlier reports (Pourahmad et al 2005;Kanbak et al 2008) indicated that betaine had a potent reducing effect on the production free radicals in rats exposed to cytotoxicity. The protective effect of betaine against restraint stress-induced oxidative stress observed in this study may also be associated with the restoration of SAM, which contributes to an increase in the supply of substrate needed for the synthesis of GSH that protects the cell from reactive metabolites and reactive oxygen species.…”

Betaine prevents ethanol-induced oxidative stress and reduces total homocysteine in the rat cerebellum

“…Chronic and excessive ethanol consumption is associated with various biochemical and physiological changes in the central nervous system (CNS). The most affected brain regions seem to be superior frontal association complex, hypothalamus, and cerebellum [35].…”

“…Indeed, brain tissues have unique characteristics that make them especially susceptible to damage due to low levels of antioxidant defenses [10]. Lipid peroxidation is one of the consequences of oxidative stress induced by metabolism of ethanol [35]. In this regard, a previous study demonstrated that chronic gestational exposure to alcohol caused a decrease in the membrane integrity while increasing oxidative stress in cerebellar neurons [48].…”

The investigation of the prenatal and postnatal alcohol exposure-induced neurodegeneration in rat brain: protection by betaine and/or omega-3

“…Betaine, also being a molecular chaperone, protects the cells against oxidative stress and mitohondrial damage. In another study, it was shown that betaine might protect lysosomal membranes with a 30-day pretreatment study [29]. Kim et al found that betaine supplementation is protective against necrotic damage [30].…”