Protective Effect of Vitamin E in Rats with Acute Liver Injury

We have previously shown that supplemental vitamin E has a cytoprotective effect in the liver of rats with chronic CCL 4 ‐induced liver cirrhosis. In this study, we hypothesized that vitamin E would have a protective effect in acute liver injury induced by D‐galactosamine. D‐Galactosamine‐induced injury has been thought to be due to a synergistic direct toxic effect and presence of intestinal bacteria and/or endotoxins. D‐Galactosamine was used to induce acute “hepatitis” (1.5–2.0 g/Kg body weight, ip). Rats were placed on either standard chow or the same chow supplemented with vitamin E (300 mg DL‐alpha‐tocopherol/Kg diet) and 6 days later were given D‐galactosamine. There was significantly improved early (5‐day) survival and late (14‐day) survival in the vitamin E‐supplemented group. The vitamin E beneficial effect was manifested also by decreased liver fat and collagen content and decreased SGPT level. Because bacterial endotoxins have been implicated as playing a role in the pathogenesis of D‐galactosamine hepatitis, the same experiment was carried out using germ‐free and conventional rats. There was significantly improved survival in both the germ‐free and conventional vitamin E‐supplemented groups both at 5 and 14 days. There was no significant difference between conventional and germ‐free rats with or without vitamin E supplementation. In summary (a) vitamin E improves the early fat and collagen accumulation in the liver, decreases SGPT level, and improves survival in the D‐galactosamine experimental model of acute liver injury in both conventional and germ‐free rats; and (b) D‐galactosamine toxicity is probably not mediated through intestinal bacteria and/or endotoxins. (Journal of Parenteral and Enteral Nutrition 10:184–187,1986)