Glu298Asp polymorphism of the endothelial nitric oxide synthase gene and plasma concentrations of asymmetric dimethylarginine in Turkish pre-eclamptic women without fetal growth retardation

dc.contributor.authorTuran, Fahri
dc.contributor.authorIlhan, Necip
dc.contributor.authorKaman, Dilara
dc.contributor.authorAtes, Kadir
dc.contributor.authorKafkasli, Ayse
dc.date.accessioned2026-08-12T17:14:20Z
dc.date.issued2010
dc.departmentFırat Üniversitesi
dc.description.abstractAims: Pre-eclampsia (PE) is a leading cause of maternal death worldwide, affecting 3 to 5% of all pregnancies. We analyzed the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene and asymmetric dimethylarginine (ADMA) in 55 Turkish patients with PE without fetal growth retardation (FGR) and in 54 healthy pregnant women. Methods: Restriction fragment length polymorphism analysis of Glu298Asp of the endothelial nitric oxide synthase gene was evaluated by amplification of genomic DNA isolated from whole blood followed by digestion with the restriction enzyme Frio. PE was defined according to the Working Group2000 criteria as high blood pressure (>= 140/90 mmHg after 20 weeks of gestation) and proteinuria (> 300 mg/24 h). We excluded the women with FGR Serum arginine, with only ADMA and symmetric dimethylarginine (SDMA) levels measured by high-performance liquid chromatography. Results: Genotypes were defined as GG, GT and TT according to the presence of the G and T alleles. In this case-control study, we did not find any significant difference in either the genotypic distribution or allelic frequency of Glu298Asp gene polymorphism between the pre-eclamptic patients and healthy pregnant women. Serum ADMA, arginine and SDMA levels were higher in patients with PE compared with healthy pregnant women (respectively, P < 0.0001, P < 0.0001, P < 0.0001). Conclusions: The results suggested a lack of association between the Glu298Asp gene polymorphism and pre-eclampsia without FGR in the Turkish population. But elevated ADMA and SDMA levels suggest that ADMA has a role in the pathogenesis of PE.
dc.identifier.doi10.1111/j.1447-0756.2010.01172.x
dc.identifier.endpage501
dc.identifier.issn1341-8076
dc.identifier.issn1447-0756
dc.identifier.issue3
dc.identifier.orcid0000-0001-9997-0418
dc.identifier.pmid20598027
dc.identifier.scopus2-s2.0-77953335372
dc.identifier.scopusqualityQ2
dc.identifier.startpage495
dc.identifier.urihttps://doi.org/10.1111/j.1447-0756.2010.01172.x
dc.identifier.urihttps://hdl.handle.net/11508/51771
dc.identifier.volume36
dc.identifier.wosWOS:000278563400006
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Obstetrics and Gynaecology Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260511
dc.subjectADMA
dc.subjecteNOS gene polymorphism
dc.subjectpre-eclampsia
dc.titleGlu298Asp polymorphism of the endothelial nitric oxide synthase gene and plasma concentrations of asymmetric dimethylarginine in Turkish pre-eclamptic women without fetal growth retardation
dc.typeArticle

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