Antioxidant and methyl donor effects of betaine versus ethanol-induced oxidative stress in the rat liver

Oxidative stress is one hypothesis for the association of ethanol consumption with cardiovascular, cerebrovascular, and liver diseases. Thus, we examined whether oral betaine can act as a preventive agent in ethanol-induced oxidative stress on the rat liver. A total of 32 male Sprague–Dawley rats were divided into four equal groups. The control group received normal saline. The ethanol group was administered ethanol (4 g/kg). The betaine group received betaine [1.5 % (w/w) of the total diet], and the betaine plus ethanol group (Bet. & Eth.) were administered with betaine; after 120 min, the rats received ethanol. All of the treatments were applied for 2 months via gavage. Elevation of glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were observed in the betaine-treated groups. Thiobarbituric acid reactive substances (TBARS, an indicator of lipid peroxidation) concentration also decreased in the betaine-treated rats as compared to the ethanol group. There was also a significant reduction in plasma total homocysteine (tHcy) concentration in the betaine and Bet. & Eth. groups as compared to the ethanol-treated rats. In contrast, ethanol treatment in rats resulted in significant lower antioxidant enzyme activities (GPx and SOD), and indicated lipid peroxidation to the liver, as monitored by the elevation in TBARS level. Administration of ethanol to rats also induced toxicity in their liver, as shown by the histopathological findings, whereas betaine could suppress liver damages in the Bet. & Eth. group. Overall, oral pretreatment with betaine significantly prevented ethanol-induced oxidative stress and hyperhomocysteinemia via increasing antioxidant enzyme activities and decreasing tHcy concentration. Thus, betaine may be recommended as a therapeutic agent for patients with liver damages induced by oxidative stress in various diseases.