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Mol. Hum. Reprod. Advance Access originally published online on August 6, 2004
Molecular Human Reproduction 2004 10(10):713-717; doi:10.1093/molehr/gah095
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Molecular Human Reproduction vol. 10 no. 10 © European Society of Human Reproduction and Embryology 2004; all rights reserved

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

Yao-Yuan Hsieh1,4, Chi-Chen Chang1, Fuu-Jen Tsai2, Cheng-Chieh Lin3, Jiun-Ming Chen2 and Chang-Hai Tsai2,5

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

5 To whom correspondence should be addressed at: Department of Pediatrics and Medical Genetics, China Medical University Hospital, No.2 Yuh-Der Road, Taichung, Taiwan. Email: d0704{at}www.cmuh.org.tw

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.

Key words: endometriosis/gene polymorphism/glutathione S-transferase (GSTM1)/myeloperoxidase (MPO)


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