Journal
TOXICOLOGY
Volume 160, Issue 1-3, Pages 11-18Publisher
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0300-483X(00)00433-9
Keywords
alcohol, alcoholism and the breast; alcohol biotransformation and breast cancer; breast ethanol metabolism; ethanol, acetaldehyde and breast; ethanol promotion of breast cancer; free radicals and breast cancer; purines, alcohol and breast cancer; purines, xanthine oxidase and breast cancer
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Epidemiological evidence links alcohol intake with increased risk in breast cancer. Not all the characteristics of the correlation can be explained in terms of changes in hormonal factors. In this work. we explore the possibility that alcohol were activated to acetaldehyde and free radicals in situ by xanthine dehydrogenase (XDh) and xanthine oxidase (XO) and/or aldehyde oxidase (AO). Incubation of cytosolic fraction with xanthine oxidoreductase (XDh + XO) (XOR) cosubstrates (e.g. NAD(+), hypoxanthine, xanthine, caffeine, theobromine, theophylline or 1,7-dimethylxanthine) significantly enhanced the biotransformation of ethanol to acetaldehyde. The process was inhibited by allopurinol and not by pyrazole or benzoate or desferrioxamine and was not accompanied by detectable formation of 1HEt. However, hydroxylated aromatic derivatives of PEN were detected, suggesting either that hydroxyl free radicals might be formed or that XOR might catalyze aromatic hydroxylation of PEN. No bioactivation of ethanol to acetaldehyde was detectable when a cosubstrate of AO such as N-methylnicotinamide was included in cytosolic incubation mixtures. Results suggest that bioactivation of ethanol in situ to a carcinogen, such as acetaldehyde, and potentially to free radicals, might be involved in alcohol breast cancer induction. This might be the case, particularly also in cases of a high consumption of purine-rich food (e.g. meat) or beverages or soft drinks containing caffeine. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
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