Galactosamine-induced acute liver injury in rats reduces hepatic α-tocopherol transfer protein production

Abstract

The liver plays the main role in the secretion of food-derived α-tocopherol into the circulation through the functioning of α-tocopherol transfer protein (α-TTP). However, the effect of liver disease on α-TTP level and α-tocopherol metabolism has not been clarified. We examined the amount of liver α-TTP and its effect on serum α-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, α-tocopherol concentrations, and hepatic α-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 α-TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the α-TTP protein level had begun to decrease. Lipid and α-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 α-tocopherol concentration was unchanged. These results show that galactosamine-induced liver injury decreases hepatic α-TTP synthesis in rats. Serum α-tocopherol concentration was not directly affected by the acute change in hepatic α-TTP level, suggesting that the chronic changes in α-TTP activity would be necessary to regulate serum α-tocopherol concentration.