Effect of chronic ethanol feeding on plasma and liver α- and γ-tocopherol levels in normal and vitamin E-deficient rats: Relationship to lipid peroxidation

Abstract

The effects of chronic ethanol intake on the levels of α-tocopherol and γ-tocopherol in serum and liver of both vitamin E-deficient and normal rats were studied. An intragastric feeding rat model was used. Both normal and vitamin E-deficient animals were fed a liquid diet and ethanol for 1 month. In pair-fed animals, dextrose was isocalorically replaced by ethanol. The blood ethanol level in the ethanol-fed animals was between 150 and 250 mg/dL. Liver peroxidation was determined by measuring thiobarbituric acid reactive substances (TBARS). Plasma alanine aminotransferase (ALT) was increased by 3-fold in vitamin E-deficient ethanol-fed rats compared with normal ethanol-fed rats. Plasma α- and γ-tocopherol were decreased in the normal ethanol-fed rats by 22.3 and 65%. respectively (P < 0.01). Liver α- and γ-tocopherol were also decreased by 51.7 and 76%, respectively (P < 0.01). Vitamin E-deficient animals had significantly lower mean plasma α-tocopherol (5670 vs 530 ng/mL, P < 0.01), and ethanol feeding did not decrease the levels any further. However, ethanol feeding decreased liver α-and γ-tocopherol by 58.5 and 56.5% (P < 0.01), respectively, beyond the already low levels observed in this group. There was an inverse correlation between liver TBARS and liver α-tocopherol ( r = − 0.59, P < 0.05) and γ-tocopherol ( r = −0.65, P < 0.02). Also of significance is that ethanol feeding decreased the plasma and liver γ-tocopherol more than the α--tocopherol in both normal and vitamin E-deficient animals. In conclusion, ethanol feeding markedly decreased both α- and γ-tocopherol in livers of normal and vitamin E-deficient rats, but it only decreased plasma levels of tocopherols in normal rats. The higher ALT in vitamin E-deficient animals and the inverse correlation between TBARS and α- and γ-tocopherol suggest that enhanced lipid peroxidation is associated with greater severity of liver injury induced by ethanol in vitamin E-deficient rats.