Abstract
The mechanism of increased srum mGOT levels in patients with alcoholic liver disease was studied, using Wistar male rats fed with nutritionally adequate liquid diets containing ethanol as 36% of the total calories. After 6 weeks feeding, mGOT activity in the whole liver and in the liver mitochondoria was significantly elevated in etanol-fed rats compared with control-fed rats. In light microscopic immunohistochemistry, the intensity of mGOT stain was increased in hepatocytes in the centri-lobular area of ethanol-fed rats. In electron microscopic immunohistochemistry, reaction products of mGOT were observed in the mitochondoria both in control-fed and ethanol-fed rats, but they were more prominent in ethanol-fed rats. In vitro study revealed that mGOT leakage from isolated hepatocytes with mildly damaged plasma membrane was increased in ethanol-fed rats than in control-fed rats. These results suggest that the increased serum mGOT level in alcholic liver disease was resulted from the excessive production of mGOT in hepatocytes and the increased leakage across the plasma membrane.
