SummaryThe liver plays the main role in the secretion of food-derived ␣ -tocopherol into the circulation through the functioning of ␣ -tocopherol transfer protein ( ␣ -TTP). However, the effect of liver disease on ␣ -TTP level and ␣ -tocopherol metabolism has not been clarified. We examined the amount of liver ␣ -TTP and its effect on serum ␣ -tocopherol concentration in liver injury. Male Wistar rats were injected intraperitoneally with D -galactosamine at 800 mg/kg body weight, and liver and serum lipid concentrations, ␣ -tocopherol concentrations, and hepatic ␣ -TTP mRNA and protein levels were measured at 24, 48, and 72 h after injection. On the basis of body weight changes and serum transaminase activities, the livers were found to be in an injured state 24 and 48 h after galactosamine injection but had recovered by 72 h. The hepatic ␣ -TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the ␣ -TTP protein level had begun to decrease. Lipid and ␣ -tocopherol concentrations in the serum were decreased at 24 and 48 h after injection and increased at 72 h. Liver lipid concentrations were increased at 24 and 48 h after injection, but the liver ␣ -tocopherol concentration was unchanged. These results show that galactosamine-induced liver injury decreases hepatic ␣ -TTP synthesis in rats. Serum ␣ -tocopherol concentration was not directly affected by the acute change in hepatic ␣ -TTP level, suggesting that the chronic changes in ␣ -TTP activity would be necessary to regulate serum ␣ -tocopherol concentration.

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