Introduction & Objectives: Preeclampsia (PE) is a human pregnancy disorder. Although, the pathogenesis of preeclampsia remain unclear, placental oxidative stress and endoplasmic reticulum stress and genetic variation may all be important. Oxidative stress is known as one of the most important factor that plays a significant role in pathogenesis of preeclampsia. An imbalance between toxic compounds, such as lipid peroxides and oxygen free radicals might be contribute to the pathophysiology of pre-eclampsia. Microsomal epoxide hydrolase (mEH) located primarily in smooth endoplasmic reticulum membrane that contribute to hydrolytic catalyses of reactive epoxides, formed by the action of cytochrome 450. Polymorphisms in coding region of microsomal epoxide hydrolase (EPHX1) gene change enzymes detoxifying activity. So, functional polymorphisms in the EPHX1 gene may produce toxic intermediates that could be involved in development of pre-eclampsia. Materials & Methods: The propose of this study is to investigate polymorphisms of EPHX1 His139Arg between two study groups. Blood sample were collected from100 Iranian women with and 100 whiteout preeclampsia. Genomic DNA was extracted by salting out method to the public. Genotyping were performed by polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) to explore association between genetic polymorphism of EPHX1 A416G and the susceptibility to preeclampsia. Results: AA, AG and GG frequency were not significantly different between two study groups. Therefore, the results indicated that the EPHX1 A416G polymorphism were not associated with the preeclampsia. Conclusion: Based on our analysis, the EPHX1 His139Arg polymorphism was no associated with increased preeclampsia risk in the studied population. Future study using large Sample size will be required to precisely detect genetic variation.
