Study Of Ethanol-Induced Chondriosome Injury And Alcoholic Disease

Background: In west countries, alcohol abuse is a leading cause of serious liver disease. The incidence of ALD in our country has increased markedly and alcohol becomes the second reason of hepatic lesion after virus hepatitis in these years. The classical clinical manifestations of ALD are alcoholic fatty liver, alcoholic hepatitis and alcoholic liver fibrosis, which even can become inconvertible alcoholic cirrhosis. So the prevention and cure of ALD become more and more important in medical topic. The study and research of ALD has increasingly increased in world, but most of them are concentrating on the direct toxic action to liver cell by alcohol itself or its metabolic product and the contribution by the changes of nutritional disturbance, liver metabolism abnormality and lipid peroxidation in ALD. Immune reaction, cytogene abnormal regulation and apoptosis taking part in the process of pathological lesion in ALD were found in these years and apoptosis was considered as the major factor in the pathogenesis of ALD. The mechanism of liver cell apoptosis has not been well known, even though some research display that liver cell apoptosis is connected with activation of CYP2E1, addition of iron burden, augment of activity of TNF or TNF receptor, oxidative stress with oxide increasing and anti-oxide decreasing, apoptosis effect induced by myofibroblast and TGF β and other apoptosis factors. Some researches found that hepatocyte mitochondria swelled and its function deteriorated. The usage of chronic alcohol can inhibit the duplication of mtDNA, thus the number of mitochondra in hepatocyte is reduced. The content of GSH in mitochondra of ALD was found decrease obviously in some other studies, just because of the changes in the structure and function of the mitochondra play an...