Effects of capsaicin on liver microsomal metabolism of the tobacco-specific nitrosamine NNK

Cancer Lett. 1993 Nov 30;75(1):45-52. doi: 10.1016/0304-3835(93)90206-o.

Abstract

Chemically-induced mutagenesis 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 beta-naphthoflavone-induced hamsters were used. Microsomes from phenobarbital and beta-naphthoflavone-induced animals expressed decreased NNK reduction and enhanced pyridine-N-oxidation, but did not significantly alter alpha-carbon hydroxylation of NNK. Capsaicin (0.5 mM) inhibited the formation of all metabolites of NNK by all microsomal fractions and inhibited alpha-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.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Benzoflavones / pharmacology
  • Capsaicin / pharmacology*
  • Carcinogens / metabolism*
  • Cricetinae
  • Enzyme Induction
  • Hydroxylation
  • In Vitro Techniques
  • Male
  • Mesocricetus
  • Microsomes, Liver / metabolism*
  • Nitrosamines / metabolism*
  • Oxidation-Reduction
  • Phenobarbital / pharmacology
  • beta-Naphthoflavone

Substances

  • Benzoflavones
  • Carcinogens
  • Nitrosamines
  • beta-Naphthoflavone
  • 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone
  • Capsaicin
  • Phenobarbital