Effects on sister chromatid exchange frequency of polymorphisms in DNA repair gene XRCC1 in smokers

Yu Chen Lei, Shing J. Hwang, Chuen-Chau Chang, Hsen W. Kuo, Jiin Chyuan Luo, M. J W Chang, Tsun J. Cheng

Research output: Contribution to journalArticle

100 Citations (Scopus)

Abstract

The association between metabolic polymorphisms and cigarette smoking-induced cancers has been documented. However, the role of DNA repair polymorphism in carcinogenesis is less clear. To investigate if the polymorphisms of metabolic traits and DNA repair modulate smoking-related DNA damage, we used sister chromatid exchange (SCE) as a marker of genetic damage to explore the relationship of microsomal epoxide hydrolase (mEH), glutathione S-transferase M1 (GSTM1), and X-ray cross-complementing group 1 (XRCC1) and cigarette smoking-induced SCE. Sixty-one workers without significant exposure to mutagens were recruited. Questionnaires were completed to obtain detailed occupational, smoking, and medical histories. SCE frequency in peripheral lymphocytes was determined using a standard cytogenetic assay and GSTM1, mEH (exons 3 and 4), XRCC1 (codon 399) genotypes were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR/RFLP). Smokers had higher SCE frequency than non-smokers (8.4 versus 7.1, P

Original languageEnglish
Pages (from-to)93-101
Number of pages9
JournalMutation Research - Genetic Toxicology and Environmental Mutagenesis
Volume519
Issue number1-2
DOIs
Publication statusPublished - Aug 26 2002
Externally publishedYes

Keywords

  • Cigarette smoking
  • DNA repair
  • Glutathione S-transferase M1
  • Metabolism
  • Microsomal epoxide hydrolase
  • Polymorphism
  • Sister chromatid exchange
  • X-ray cross-complementing group 1

ASJC Scopus subject areas

  • Genetics
  • Health, Toxicology and Mutagenesis

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