In this study, effects of cholesterol and protective effects of vitamin E (vit E) and Selenium (Se) on the morphology of the liver in rats were observed. Cholesterol (Chol) supplemented diet, Chol + vit E, Chol + Se and Chol + vit E + Se were applied to the rats. Portal fibrosis with bile ductal proliferation and an increased inflammatory infiltration were seen in Chol group. In this group, ultrastructurally, granular endoplasmic reticulum (GER) arrangement was seen in irregular shape in hepatocyte cytoplasm. The membranes of GER and mitochondria were not seen clearly. A morphological improvement was seen in the other groups. It has been concluded that the mechanism of the injury may be involved in the accumulation of toxic bile acids or the generation of free radicals from cholesterol oxidation products. In addition it has been realized that the growth factors may be released into the hepatic sinusoids to activate stellate cells and to initiate fibrogenesis.

In this study, effects of cholesterol and protective effects of vitamin E (vit E) and Selenium (Se) on the morphology of the liver in rats were observed. Cholesterol (Chol) supplemented diet, Chol + vit E, Chol + Se and Chol + vit E + Se were applied to the rats. Portal fibrosis with bile ductal proliferation and an increased inflammatory infiltration were seen in Chol group. In this group, ultrastructurally, granular endoplasmic reticulum (GER) arrangement was seen in irregular shape in hepatocyte cytoplasm. The membranes of GER and mitochondria were not seen clearly. A morphological improvement was seen in the other groups. It has been concluded that the mechanism of the injury may be involved in the accumulation of toxic bile acids or the generation of free radicals from cholesterol oxidation products. In addition it has been realized that the growth factors may be released into the hepatic sinusoids to activate stellate cells and to initiate fibrogenesis.