EFFECTS ON SISTER CHROMATID EXCHANGE FREQUENCY OF POLYMORPHISMS IN DNA REPAIR GENE XRCC1 IN SMOKERS
Resource
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS v.519 n.1-2 pp.93-101
Journal
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS
Journal Volume
v.519
Journal Issue
n.1-2
Pages
93-101
Date Issued
2002
Date
2002
Author(s)
LEI, YU-CHEN
HWANG, SHIN-JEN
CHANG, CHUN-CHAO
KUO, HSIEN-WEN
LUO, JIIN-CHYUAN
CHANG, MING, J., W.
CHENG, TSUN-JEN
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/PFLP). Smokers had higher SCE frequency than non-smokers (8.4 versus 7.1, P < 0.05). Among workers who had smoked equal to or greater than 10 cigarettes each day, those with XRCC1 Arg/Gln + Gln/Gln had higher SCE frequency than those with XRCC1 Arg/Arg after adjusting for potential confounders (9.0 versus 7.9, P < 0.05). The interaction of XRCC1 and cigarettes smoked per day on SCE frequency was also observed (P = 0.02). There was no significant interaction between cigarettes smoked per day with GSTM1 and mEH on SCE frequency. Our results support previous epidemiological studies that XRCC1 may play a role in cigarette smoking-induced lung cancer. (C) 2002 Elsevier Science B.V. All rights reserved.
Subjects
microsomal epoxide hydrolase
X-ray cross-complementing group 1
glutathione S-transferase M1
sister chromatid exchange
cigarette smoking
polymorphism
SDGs
Type
journal article
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