z-logo
Premium
Effects of the XRCC1 gene‐environment interactions on DNA damage in healthy Japanese workers
Author(s) -
Weng Zuquan,
Lu Yuquan,
Weng Huachuan,
Morimoto Kanehisa
Publication year - 2008
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/em.20421
Subject(s) - xrcc1 , dna repair , genotype , genetics , allele , dna damage , biology , base excision repair , xrcc3 , mutagen , gene , dna , single nucleotide polymorphism
X‐ray repair crosscomplementing group 1 ( XRCC1 ) has a central role in base excision repair (BER) and single‐strand break repair (SSBR). XRCC1 gene polymorphisms (codons 194, 280, and 399) have been identified, and in some cases have been reported to contribute to variations in DNA repair capacity and susceptibility to cancer. To further characterize the effects of XRCC1 gene polymorphisms and their possible interactions with environmental factors on individual levels of DNA damage, we investigated the XRCC1 genotypes of 222 healthy Japanese workers and analyzed data with respect to smoking, drinking habits, age, and health practice index (HPI). Our results showed that poor HPI would associate with a higher level of tail moment (TM). Individuals with one or two XRCC1 R280H variant alleles exhibited significantly higher TM values, and these differences were enhanced by alcohol consumption and aging, whereas smoking and poor HPI may cover up the differences. On the other hand, using a stratified analysis, we found that the XRCC1 R194W variant was associated with a higher TM value in the 40–50 year‐old age group, and the XRCC1 R399Q variant was associated with a lower TM value in the ≤20 pack‐years group or in the 40–50 year‐old age group. These data suggest that XRCC1 polymorphisms could influence individual DNA repair capacity by interacting with lifestyle factors, and specifically, the data indicated that the XRCC1 R280H allele may be more important than codon 194 or 399 alleles. Environ. Mol. Mutagen., 2008. © 2008 Wiley‐Liss, Inc.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here