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Modulation of N-nitrosomethylbenzylamine bioactivation by diallyl sulfide in vivo

B I Ludeke1, F Dominé, H Ohgaki

  • 1Department of Pathology, University of Zürich, Switzerland.

Carcinogenesis
|December 1, 1992
PubMed

Insights

Diallyl sulfide (DAS), a garlic oil component, inhibits N-nitrosomethylbenzylamine (NMBzA) metabolism and DNA methylation in rats. This chemopreventive effect suggests modulation of carcinogen bioactivation contributes to tumor prevention.

Area of Science:

  • Oncology
  • Chemoprevention
  • Toxicology

Background:

  • Diallyl sulfide (DAS), a key component of garlic oil, is recognized for its potential chemopreventive properties against carcinogens.
  • Previous studies indicated DAS can suppress tumorigenesis induced by metabolically activated carcinogens, including N-nitrosomethylbenzylamine (NMBzA).

Purpose of the Study:

  • To investigate the effects of Diallyl sulfide (DAS) on the overall metabolism of N-nitrosomethylbenzylamine (NMBzA).
  • To determine the impact of DAS on the in vivo DNA methylation by NMBzA under conditions relevant to chemoprevention assays.

Main Methods:

  • Male Fischer 344 rats were administered varying doses of DAS followed by [methyl-14C]NMBzA.
  • Carcinogen metabolism was assessed by measuring 14CO2 exhalation.
  • DNA methylation, specifically O6-methyldeoxyguanosine (O6-MEdG) and 7-MEdG, was quantified in various tissues.

Main Results:

  • DAS administration altered NMBzA metabolism, affecting the rate and extent of 14CO2 exhalation.
  • Acute doses of DAS significantly inhibited NMBzA-induced DNA methylation in multiple organs, including the esophagus, nasal mucosa, trachea, lung, and liver.
  • The inhibition of DNA methylation by DAS was dose-dependent across different tissues.

Conclusions:

  • Diallyl sulfide (DAS) effectively modulates N-nitrosomethylbenzylamine (NMBzA) metabolism and significantly reduces its DNA methylation in vivo.
  • These findings support the role of short-term modulation of carcinogen bioactivation in the chemopreventive mechanisms of DAS against nitrosamine-induced tumorigenesis.

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