Effects of capsaicin on liver microsomal metabolism of the tobacco-specific nitrosamine NNK
Chemically-induced mutagensis and carcinogenesis is modulated by various plant products, some of which are present in the human diet. 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a potent carcinogen in tobacco and tobacco smoke, is activated by microsomal enzymes. In this study, we investig...
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Published in | Cancer letters Vol. 75; no. 1; pp. 45 - 52 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Shannon
Elsevier Ireland Ltd
30.11.1993
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Chemically-induced mutagensis and carcinogenesis is modulated by various plant products, some of which are present in the human diet. 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a potent carcinogen in tobacco and tobacco smoke, is activated by microsomal enzymes. In this study, we investigated the effects of capsaicin on the in vitro metabolism of NNK. Capsaicin is the principal component of
Capsicum fruits used widely by humans as a food additive. Liver microsomes from saline-injected, phenobarbital-induced and β-naphthoflavone-induced hamsters were used. Microsomes from phenobarbital and β-naphthoflavone-induced animals expressed decreased NNK reduction and enhanced pyridine-
N-oxidation, but did not significantly alter α-carbon hydroxylation of NNK. Capsaicin (0.5 mM) inhibited the formation of all metabolites of NNK by all microsomal fractions and inhibited α-hydroxylation by phenobarbital-induced microsomes more than by either of the other two treatments. Our results suggest that capsaicin, as a naturally occurring dietary constituent, possesses antimutagenic and anticarcinogenic properties through the inhibition of xenobiotic metabolizing enzymes. |
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ISSN: | 0304-3835 1872-7980 |
DOI: | 10.1016/0304-3835(93)90206-O |