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GST M1 GENOTYPE INFLUENCES THE SUSCEPTIBILITY OF MEN TO SPERM DNA DAMAGE ASSOCIATED WITH EXPOSURE TO AIR POLLUTION
Citation:
Rubes, J., S G. Selevan, R. Sram, D. P. Evenson, AND S P. Darney. GST M1 GENOTYPE INFLUENCES THE SUSCEPTIBILITY OF MEN TO SPERM DNA DAMAGE ASSOCIATED WITH EXPOSURE TO AIR POLLUTION. Presented at American Society of Andrology, Baltimore, MD, April 17-20, 2004.
Description:
GSTM1 GENOTYPE INFLUENCES THE SUSCEPTIBILITY OF MEN TO SPERM DNA DAMAGE ASSOCIATED WITH EXPOSURE TO AIR POLLUTION. J. Rubes1, SG Selevan2, R. Sram3, DPEvenson4, SD Perreault5. 1VRI, Brno, CR; 2US EPA/ORD/NCEA, Washington, DC; 3IEM AS CR, Prague, CR; 4SDSU, Brookings, SD; 5US EPA/ORD/NHEERL, RTP, NC.
Exposure to episodic air pollution in the Czech Republic has been associated with abnormal semen quality and sperm DNA damage (Environ Health Perspect 108:887;2000). A follow-up longitudinal study evaluated semenfrom 36 men sampled up to 7 times over 2 years during periods of both low and high air pollution. As before, exposure was significantly associated with increased DNA fragmentation index (DFI) as detected by the Sperm Chromatin Structure Assay?. It is biologically plausible that metabolites of polycyclic aromatic hydrocarbons (PAH) in the air pollution could form DNA adducts in sperm, with adverse consequences. Because PAH metabolites are detoxified by glutathione s-transferase M1, we hypothesized that men lacking the gene for this enzyme, GST M1(-),might be more susceptible to effects of air pollution on sperm DNA. To test this hypothesis, GSTM1 genotyping was performed on DNA isolated from WBC. As expected, about half (17/37) of the men were GSTM1(-).The relationship between pollution and DFI was then re-examined with and without genotype in the model, adjusted for smoking. For exposure and DFI (without genotype), ? (CI) = 0.175 (0.006, 0.345); for genotype and DFI (without exposure), ? = 0.251 (0.030, 0.473); and, for the interaction (exposure x genotype) and DFI, ? = 0.427 (0.157, 0.697). Although DFI was associated with both exposure and genotype, the interaction between genotype and exposurewas even more significant. This novel gene-environment interaction supports the hypothesis that GST M1(-)men may be at increased risk for sperm DNA damage per se and may be more susceptible than GST M1 men to the adverse reproductive effects of air pollution. Supported byUSEPA R820968 and CRMinistry of Environment VaV/340/02/00. This abstract does not reflect EPA policy.