Taurine Protects the Liver against Lipid Peroxidation and Membrane Disintegration during Rat Hepatocarcinogenesis

Abstract

The purpose of this study was to determine the effects of taurine supplementation on both hepatic morphological changes and the extent of hepatic lipid peroxidation and membrane disintegration during rat hepatocarcinogenesis. Sprague Dawley rats were fed high fat diets containing 15% corn oil and were maintained on drinking water with or without 1% taurine. Two weeks after the appropriate feeding regimen, hepatocarcinogenesis was induced by a modification of the Solt and Farber method. This involved a 8 week protocol, including diethylnitrosamine initiation, 3 weeks of 2-acetylaminofluorene feeding and finally a 70% partial hepatectomy. Morphological changes of the hepatocyte were observed by transmission electron microscopy (TEM). Hepatocytes of the carcinogen-treated rat not exposed to taurine contained normal nuclei, but the endoplasmic reticulum (ER) and the mitochondria (Mi) were almost destroyed. By contrast, although the hepatocytes from the taurine supplemented group contained some irregular contour nuclei, the ER and Mi were normal. In the carcinogen-treated groups, lipid peroxidation was decreased because of the activation of several detoxifying enzymes. Glutathione S-transferase (GST) activity increased in the carcinogen-treated groups but less so in the group supplemented with taurine before treatment with the carcinogen. In the group supplemented with taurine prior to treatment with the carcinogen, glutathione peroxidase (GPx) activity was higher than in the carcinogen-treated group lacking taurine exposure. Consistent with the severe destruction to the membrane in the carcinogen-treated rats, hepatic glucose-6-phosphatase (G6Pase) activity, an index of membrane stability, was also decreased. However, both the fall in G6Pase activity and the degree of membrane damage was reduced in the carcinogen-treated animals receiving oral taurine. These results suggest that taurine appears to inhibit lipid peroxidation, to alter the activity of the defense enzymes and to protect the liver against membrane disintegration during rat hepatocarcinogenesis.