EFFECTS OF CAPSAICIN ON LIVER MICROSOMAL METABOLISM OF THE TOBACCO-SPECIFIC NITROSAMINE NNK

Chemically-induced mutagenesis and carcinogenesis is modulated by vari ous plant products, some of which are present in the human diet. 4-(me thylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a potent carcinogen i n tobacco and tobacco smoke, is activated by microsomal enzymes. In th is study, we investigated the effects of capsaicin on the in vitro met abolism of NNK. Capsaicin is the principal component of Capsicum fruit s used widely by humans as a food additive. Liver microsomes from sali ne-injected, phenobarbital-induced and beta-naphthoflavone-induced ham sters were used. Microsomes from phenobarbital and beta-naphthoflavone -induced animals expressed decreased NNK reduction and enhanced pyridi ne-N-oxidation, but did not significantly alter alpha-carbon hydroxyla tion of NNK. Capsaicin (0.5 mM) inhibited the formation of all metabol ites of NNK by all microsomal fractions and inhibited alpha-hydroxylat ion by phenobarbital-induced microsomes more than by either of the oth er two treatments. Our results suggest that capsaicin, as a naturally occurring dietary constituent, possesses antimutagenic and anticarcino genic properties through the inhibition of xenobiotic metabolizing enz ymes.