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

@article{Miller1993EffectsOC,
  title={Effects of capsaicin on liver microsomal metabolism of the tobacco-specific nitrosamine NNK.},
  author={C. H. Miller and Z L Zhang and S. M. Hamilton and Robert W. Teel},
  journal={Cancer letters},
  year={1993},
  volume={75 1},
  pages={
          45-52
        }
}

Inhibitory Effect of Capsaicin against Carcinogen-induced Oxidative Damage in Rats

The results show that capsaicin may function as a free radical scavenger against chemical carcinogen-induced oxidative cellular damage in vivo and may play an important role in the process of chemoprevention.

In vitro antimutagenicity of capsaicin toward heterocyclic amines in Salmonella typhimurium strain TA98.

Whether capsaicin showed anti-mutagenic effects toward HCA-induced mutagenesis in Salmonella typhimurium TA98 when incubated with 0.5 mg liver S9 protein from rat, hamster and human is looked at.

Reactive intermediates produced from the metabolism of the vanilloid ring of capsaicinoids by p450 enzymes.

It is demonstrated that Capsaicin and structurally similar analogues are converted to reactive intermediates by certain P450 enzymes, which may partially explain conflicting reports related to the cytotoxic, pro-carcinogenic, and chemoprotective effects of capsaicinoids in different cells and/or organ systems.

Modulatory Effects of Capsaicin on N-diethylnitrosamine (DEN)-induced Mutagenesis in Salmonella typhimurium YG7108 and DEN-induced Hepatocarcinogenesis in gpt Delta Transgenic Rats

it reduced the number of liver neoplasms, especially liver cell adenomas, in a dose-dependent manner although the reduction in hepatocellular carcinoma was statistically insignificant, suggesting that chemopreventive effect of capsaicin against DEN-induced hepatocarcinogenesis is slight and that the effect is not due to antimutagenesis.

Capsaicin alleviates the imbalance in xenobiotic metabolizing enzymes and tumor markers during experimental lung tumorigenesis

It is unraveled that capsaicin can effectively detoxify the carcinogens which discloses its anti-carcinogenic effect during experimental lung cancer.

Chemopreventive task of capsaicin against benzo(a)pyrene-induced lung cancer in Swiss albino mice.

A voluminous number of evidence suggests that an increased consumption of fruits and vegetables is a relatively easy and practical strategy to reduce significantly the incidence of cancer. The

Effect of capsaicin on glucose metabolism studied in experimental lung carcinogenesis

Histochemical analysis by periodic acid Schiff's staining confirmed the biochemical findings that highlighted the chemopreventive action of CAP during B(a)P-induced experimental lung tumourigenesis.

Cytochrome P450-Dependent Modification of Capsaicinoids: Pharmacological Inactivation and Bioactivation Mechanisms

This chapter provides as review of the enzymatic processes that appear to be critical in the clearance of capsaicinoids from cells in the human body, with an emphasis on Cytochrome P450-dependent processes.

References

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Effects of pregnancy and ethanol treatment on the metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone by hamster liver and lung microsomes.

Pregnancy decreased the alpha-carbon hydroxylation (activation) of NNK, whereas it increased both the pyridine N-oxidation and carbonyl reduction of N NK in liver microsomes, but not in the lung.

Capsaicin as an in vitro inhibitor of benzo(a)pyrene metabolism and its DNA binding in human and murine keratinocytes.

The results indicate that the substance P inhibitor, capsaicin, is also an inhibitor of epidermal BP metabolism and DNA binding of its metabolites, and may represent a new category of compound with anti-carcinogenic effects.

Metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in mouse lung microsomes and its inhibition by isothiocyanates.

Investigation of the enzymes involved in the metabolism of NNK in lung microsomes and the mechanisms of inhibition of N NK metabolism by isothiocyanates revealed a mixed type of inhibition, and the potency of the inhibition increased with the increase in chain length.

Metabolism in the F344 rat of 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone, a tobacco-specific carcinogen.

The metabolism of the tobacco-specific carcinogen, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), was studied in the F344 rat, in which it induces tumors of the nasal cavity, liver, and

Perinatal metabolism of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in C57BL mice.

Results indicate that NNK and NNAI have the capacity to cross the placental barrier and to be activated in fetal tissues and suggest that exposure of C57BL mice to NNK during the last stage of fetal development or during neonatal life could possibly result in development of tumors.

Dietary effects on cytochromes P450, xenobiotic metabolism, and toxicity

The effects of selected non‐nutritive dietary chemicals, macronutrients, micronut nutrients, and ethanol on cytochromes P450 and xenobiotic metabolism are reviewed in the light of the current understanding of the multiplicity and substrate specificity of cytochrome P450 enzymes.

A tobacco smoke-derived nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, is activated by multiple human cytochrome P450s including the polymorphic human cytochrome P4502D6.

The 2D6/Hol cell line, in conjunction with the control cell line and other isogenic cell lines expressing other human cytochrome P450 cDNAs provides a useful system for the examination of the role of the polymorphic CYP2D6 in human procarcinogen activation and drug metabolism.

Identification of a common chemical signal regulating the induction of enzymes that protect against chemical carcinogenesis.

Structural-activity studies on the induction of quinone reductase and glutathione S-transferases have revealed that many anti-carcinogenic enzyme inducers contain a distinctive and hitherto unrecognized chemical feature (or acquire this feature after metabolism) that regulates the synthesis of these protective enzymes.