Volume 10, Issue 1 (7-2012)                   IJRM 2012, 10(1): 23-28 | Back to browse issues page

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Seifati S M, Parivar K, Aflatoonian A, Dehghani Firouzabadi R, Sheikhha M H. No association of GSTM1 null polymorphism with endometriosis in women from central and southern Iran. IJRM. 2012; 10 (1) :23-28
URL: http://journals.ssu.ac.ir/ijrmnew/article-1-257-en.html
1- Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran , seifati@yahoo.com
2- Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
3- Research and Clinical Center for Infertility, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Abstract:   (639 Views)
Background: Endometriosis is one of the most common gynecologic disorders. It is a complex trait and both genetic and environmental factors have been implicated in its pathogenesis. There is growing evidence indicating that exposure to environmental contaminants is a risk factor for endometriosis. Glutathione-S-Transferase M1 (GSTM1) is one of the genes involved in detoxification of endogenous and exogenous compounds.
Objective: Several studies have indicated an association between GSTM1 null mutation and endometriosis. In this study, the possible association between the GSTM1 gene null genotype and susceptibility to endometriosis in woman from central and southern Iran was investigated.
Materials and Methods: One hundred and one unrelated premenopausal women with endometriosis and 142 unrelated healthy premenopausal women without endometriosis were enrolled in the study. Genomic DNA was extracted from Peripheral blood in all subjects. GSTM1 null genotyping was performed by polymerase chain reaction (PCR).
Results: There was no significant difference between frequencies of GSTM1 null genotype in case and control groups (50.5% Vs. 52.1%, p=0.804). Furthermore, this genotype was not associated with severity of endometriosis in our sample (p=0.77).
Conclusion: further studies involving gene-environment and gene-gene interactions, particularly combination of GSTM1 and other GST gene family polymorphisms are needed.
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Type of Study: Original Article |

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