Apoptosis in alcoholic liver disease and cytochrome P4502E1 and the relationship between oxidative stress.docVIP

 PAGE \* MERGEFORMAT 8 Apoptosis in alcoholic liver disease and cytochrome P4502E1 and the relationship between oxidative stress [Abstract] alcoholic liver apoptosis and cytochrome P4502E1 (CYP2E1), and oxidative stress are closely related. Recent studies found that alcohol-induced liver CYP2E1 is to promote the main mechanism of apoptosis, and reactive oxygen species by the liver cells caused by pathological factors such as oxidative stress-induced liver cell apoptosis is an important trigger mechanism. In this paper, alcohol-induced liver cell apoptosis and oxidative stress of CYP2E1 status are reviewed. [Keywords:] liver disease; Alcohol; apoptosis; CYP2E1; oxidative stress Alcoholic liver disease (ALD) is caused by drinking large quantities of chronic liver disease, a higher prevalence in Europe and America, is one of the Western developed countries, common liver disease. In recent years, with the improvement of living standards in China, alcoholics increased, ALD was the incidence of an upward trend year by year, alcohol has become a post-viral cause liver damage following the second largest cause of [1]. The liver is an important site of alcohol metabolism, alcohol intake of over 90% of the body metabolism in the liver. Of ethanol in the liver, primarily by three enzymes oxidized: (1) the cytoplasm of the alcohol dehydrogenase (ADH); (2) microsomal ethanol oxidation system of cytochrome P4502E1; (3) in peroxisome peroxidase [2]. 1 Apoptosis and ALD Removal of apoptotic cells and apoptosis of liver function is to ensure that the key factors [3]. Ethanol in the liver alcohol dehydrogenase was cytoplasmic fluid, microsomal cytochrome P4502E1-based microsomal ethanol oxidizing system, as well as peroxisomal catalase in the decomposition of acetaldehyde, chronic habitual alcohol consumption who, CYP2E1 activity is relatively high, has a strong oxidation activity, so that oxidation of ethanol-hydroxyethyl roots, liver cells of reactive oxygen species and l