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Mol. Hum. Reprod. Advance Access published online on August 6, 2004

Molecular Human Reproduction, doi:10.1093/molehr/gah095
© 2004 by Oxford University Press
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Received March 27, 2004
Revised June 2, 2004
Accepted July 11, 2004

Article

Glutathione S-transferase M1 *null genotype but not myeloperoxidase promoter G-463A polymorphism is associated with higher susceptibility to endometriosis

Yao-Yuan Hsieh 1, Chi-Chen Chang 2, Fuu-Jen Tsai 3, Cheng-Chieh Lin 4, Jiun-Ming Chen 3, Chang-Hai Tsai 3*

1 Department of Obstetrics and Gynecology, China Medical University Hospital, Taichung, Taiwan; Department of Biological Science and Technology, National Chiao Tung University, Hsinchu, Taiwan
2 Department of Obstetrics and Gynecology, China Medical University Hospital, Taichung, Taiwan
3 Department of Pediatrics and Medical Genetics, China Medical University Hospital, Taichung, Taiwan
4 Department of Family Medicine, China Medical University Hospital, Taichung, Taiwan,

* To whom correspondence should be addressed. E-mail: d0704{at}www.cmuh.org.tw.


   Abstract

Glutathione S-transferase M1 (GSTM1), one member of the GST family, is responsible for metabolism of xenobiotics and carcinogens. Myeloperoxidase (MPO) plays an important role in the oxidation and activation of carcinogens and nitric oxide. Allelic variants of GSTM1 and MPO gene polymorphisms might impair detoxification function and increase the susceptibility to endometriosis. We aimed to investigate if these polymorphisms are useful markers for predicting endometriosis susceptibility. Women were divided into two groups: (i) endometriosis (n=150); (ii) non-endometriosis (n=159). Polymorphisms for GSTM1 and MPO were amplified by polymerase chain reaction and detected by electrophoresis after restriction digestion. The relative frequencies of the GSTM1*wild (+/+,+/0)/null (0/0) genotypes and MPO-463*G/A gene polymorphisms between both groups were compared. The distribution of GSTM1 polymorphisms was significantly different between the two groups. Proportions of GSTM1*wild/null alleles in both groups were: (i) 36.7/63.3%; (ii) 95/5% (P=0.001). In contrast, MPO-463 genotypes were not significantly different between the two groups. Proportions of MPO*A homozygote/heterozygote/G homozygote in both groups were: (i) 2.7/17.4/79.9% and (ii) 1.9/17/81.1% (P> 0.05). We conclude that the GSTM1*null genotype is associated with a higher risk of endometriosis development. MPO-463*G/A gene polymorphism is not related to the susceptibility of endometriosis.

Keywords: endometriosis; gene polymorphism; glutathione S-transferase (GSTM1); myeloperoxidase (MPO).
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