Abstract
Background & Aims: One mechanism by which alcoholic liver disease (ALD) progresses from pure fatty liver to fibrosis and cirrhosis is oxidative stress and the generation of reactive oxygen species (ROS), predominantly due to the induction of cytochrome P-4502E1 (CYP2E1). Experimental data underline the key role of CYP2E1 since ALD could be partially prevented in rats by the administration of the specific CYP2E1 inhibitor chlormethiazole. Since CYP2E1 is responsible for the formation of carcinogenic etheno DNA-adducts in man and since CYP2E1 inhibition in rats results in a significant reduction of hepatic adenomas, a causal role of alcohol induced CYP2E1 in hepatocarcinogenesis has been recognized. The purpose of this study was to investigate CYP2E1 induction in ALD and to correlate CYP2E1 with various DNA lesions and histological parameters including hepatic fat, inflammation, fibrosis.
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