Preeclampsia and angiotensin converting enzyme (ACE) I/D and angiotensin II type-1 receptor (AT1R) A1166C polymorphisms: association with ACE I/D polymorphism

Background: The aim of the present study was to investigate the association between angiotensin converting enzyme (ACE) insertion/deletion (I/D) and angiotensin II type-1 receptor (AT1R) A1166C polymorphisms with the risk of preeclampsia and lipid peroxidation in preeclamptic women from Western Iran...

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Bibliographic Details
Main Authors: Zohreh Rahimi, Ziba Rahimi, Hadi Mozafari, Abbas Parsian
Format: Article
Language:English
Published: Hindawi - SAGE Publishing 2013-06-01
Series:Journal of the Renin-Angiotensin-Aldosterone System
Online Access:https://doi.org/10.1177/1470320312448950
Description
Summary:Background: The aim of the present study was to investigate the association between angiotensin converting enzyme (ACE) insertion/deletion (I/D) and angiotensin II type-1 receptor (AT1R) A1166C polymorphisms with the risk of preeclampsia and lipid peroxidation in preeclamptic women from Western Iran. Methods: One hundred and ninety-eight preeclamptic women (128 women with mild and 70 with severe forms) and 100 age- and parity-matched controls were enrolled in this case-control study. Results: The presence of D allele of ACE was associated with a 1.8-fold increased risk of preeclampsia ( p =0.002) in total preeclamptic patients. The frequency of AT1R AC+CC genotypes was higher in mild preeclamptic women (32%) compared to controls (27.2%) ( p >0.05). In mild preeclamptic women with ID genotype, the level of total antioxidant capacity (TAC) was significantly decreased compared to those with II genotype. Also, there was a trend toward increasing malondialdehyde (MDA) and decreasing TAC levels in mild and severe preeclamptic women with AT1R AA through CC genotypes. Conclusions: Our study indicates that lipid peroxidation and oxidative stress are involved in the development of preeclampsia that might be influenced by polymorphism in the renin-angiotensin-aldosterone system genes.
ISSN:1470-3203
1752-8976