Our objective was to demonstrate the protective effect of glycine (Gly) and vitamin E (VE) on a model of ethanol-induced acute liver injury during the early phase of liver regeneration after partial hepatectomy (PH) in rats. Fifty male Wistar rats (body weight (b.w.), 240 - 280 g) were divided into four groups (n = 10, each, respectively) as follows: 1) control partial hepatectomy (PH), 70%; 2) PH + ethanol (EtOH) at 1.5 g/kg b.w; 3) PH + Gly (0.6 g/kg b.w) + EtOH, and; 4) PH + VE (400 International units [IU]) + EtOH. Twenty four h after surgery, animals were killed and liver damage and oxidative stress parameters were measured. Ethanol caused a decrease in serum albumin (2.27 vs 3.12 g/dL; p < 0.05), cholesterol (31.4 vs 48.0 mg/dL; p < 0.05), Aspartate aminotransferase (AST, 70 vs 380 UI; p< 0.05), and alanine aminotransferase (ALT, 110 vs 170 UI; p < 0.05) in comparison with the PH control group, but these decreases were reverted with either Gly or VE administration. Furthermore, Gly and VE administration decreased (p < 0.05) Thiobarbituric acid reactive (TBARS) levels, stimulated superoxide dismutase (SOD) activity, and a significant restitution of liver weight was observed. Our results suggested a protective effect against liver injury with glycine and VE supplementation. Treatment with either Gly or VE causes an elevation in total SOD activity and a decrease in TBARS levels, showing a protective effect in liver regeneration on a model of ethanol-induced acute liver injury after PH in rats. Key words: Antioxidants, ethanol-induced liver injury, free radicals, glycine, liver regeneration, vitamin E.
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