Duplications and defects in the CYP2A6 gene: identification, genotyping, and in vivo effects on smoking.

@article{Rao2000DuplicationsAD,
  title={Duplications and defects in the CYP2A6 gene: identification, genotyping, and in vivo effects on smoking.},
  author={Y. Saideswara Rao and Eva Hoffmann and M Ahsan Zia and Laurent Bodin and Miroslav Zeman and Edward M. Sellers and Rachel F. Tyndale},
  journal={Molecular pharmacology},
  year={2000},
  volume={58 4},
  pages={747-55}
}
In humans, 80% of nicotine is metabolized to the inactive metabolite cotinine by the enzyme CYP2A6, which can also activate tobacco smoke procarcinogens (e.g., 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone). Previously, we demonstrated that individuals who are nicotine-dependent and have defective CYP2A6 alleles (*2, *3) smoked fewer cigarettes; however, we recognize that the genotyping method used for the CYP2A6*3 allele gave a high false-positive rate. In the current study we used improved… CONTINUE READING

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