Genetic Polymorphism of ADH1B and Risk of Colorectal Adenoma in Middle-aged Japanese Men
نویسندگان
چکیده
Alcohol consumption is a conclusive risk factor of colorectal adenocarcinoma among men (WCRF/ AICR, 2007). The increased risk might be caused by acetaldehyde, the first metabolite in ethanol catabolism, which has a carcinogenic effect in animals (Seitz et al., 1990; Feron et al., 1991) and in humans (Seitz et al., 1996). Additionally, the effects of alcohol may be mediated through the low folate concentration in blood, because alcohol and acetaldehyde disturb the absorption of folate (Giovannucci, 2004). Ethanol is oxidized to acetaldehyde by alcohol dehydrogenase (ADH), and further metabolized to acetate by aldehyde dehydrogenase (ALDH). Human ADH has several isoenzymes, whose functional polymorphisms are known for ADH1B and ADH1C genes (Yoshida et al., 1991). ADH1B Arg47His polymorphism (rs1229984) affects the enzyme activity substantially; the 47His (alternatively ADH2*2) is an allele with faster ethanol oxidation. ADH1C Ile349Val polymorphism (rs698) also
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