Alcohol and Colorectal Cancer

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Seitz HK, Arslic-Schmitt T and Mueller S

Centre of Alcohol Research (CAR), University of Heidelberg and Department of Medicine, Salem Medical Centre, Heidelberg, Germany

Chronic alcohol consumption is a risk factor for colorectal cancer. The mechanisms by which ethanol exerts its carcinogenic effect on the colorectal mucosa are not clear and may include among others the action of acetaldehyde (AA) and oxidative stress. Colonic AA from mucosal or bacterial ethanol metabolism result in cellular hyperregeneration and an extension of the proliferative compartment of the colonic crypt, a precancerous condition. AA accelerates colorectal carcinogenesis in rats. An increased production of AA by alcohol dehydrogenase (ADH) 1C1*1 is associated with an increased risk for colorectal cancer following chronic ethanol consumption. In addition to AA, oxidative stress with the action of reactive oxygen species (ROS) generated through ethanol metabolism via cytochrome P-4502E1 (CYP2E1) may lead to carcinogenic etheno DNA adducts. ROS may also induce apoptosis. However, the effect of chronic ethanol consumption on CYP2E1, etheno DNA-adducts as well as anti-apoptotic proteins in the colorectal mucosa of heavy drinkers without colorectal inflammation is still not known. Therefore, rectal biopsies from 32 alcoholics (>6og ethanol/day) and from 12 controls (

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