GSTM1 genotype influences the susceptibility of men to sperm DNA damage associated with exposure to air pollution
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem, Research Support, U.S. Gov't, Non-P.H.S.
PubMed
17714740
DOI
10.1016/j.mrfmmm.2007.05.012
PII: S0027-5107(07)00278-3
Knihovny.cz E-zdroje
- MeSH
- delece genu MeSH
- dospělí MeSH
- fragmentace DNA MeSH
- genotyp MeSH
- glutathiontransferasa genetika MeSH
- látky znečišťující vzduch toxicita MeSH
- lidé MeSH
- poškození DNA genetika MeSH
- spermie účinky léků metabolismus MeSH
- znečištění ovzduší škodlivé účinky analýza MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mužské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Geografické názvy
- Česká republika MeSH
- Názvy látek
- glutathione S-transferase M1 MeSH Prohlížeč
- glutathiontransferasa MeSH
- látky znečišťující vzduch MeSH
Previous studies have provided evidence for an association between exposure to high levels of air pollution and increased DNA damage in human sperm. In these studies DNA damage was measured using the sperm chromatin structure assay (SCSA) wherein the percentage of sperm with abnormal chromatin/fragmented DNA is determined and expressed as % DNA fragmentation index (%DFI). Here we extend these observations to address the following hypothesis: men who are homozygous null for glutathione-S-transferase M1 (GSTM1-) are less able to detoxify reactive metabolites of carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) found in air pollution. Consequently they are more susceptible to the effects of air pollution on sperm chromatin. Using a longitudinal study design in which men provided semen samples during periods of both low (baseline) and episodically high air pollution, this study revealed a statistically significant association between GSTM1 null genotype and increased SCSA-defined %DFI (beta=0.309; 95% CI: 0.129, 0.489). Furthermore, GSTM1 null men also showed higher %DFI in response to exposure to intermittent air pollution (beta=0.487; 95% CI: 0.243, 0.731). This study thus provides novel evidence for a gene-environment interaction between GSTM1 and air pollution (presumably c-PAHs). The significance of the findings in this study with respect to fertility status is unknown. However, it is biologically plausible that increases in %DFI induced by such exposures could impact the risk of male sub/infertility, especially in men who naturally exhibit high levels of %DFI.
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