Exploring the Associations of Maternal and Neonatal eNOS Gene Variant rs2070744 with Nitric Oxide Levels, Oxidative Stress and Adverse Outcomes in Preeclampsia: A Study in the Bangladeshi Population

Research has shown that endothelial dysfunction due to low nitric oxide (NO) bioavailability is one of the primary causes of preeclampsia (PE). Variations in the eNOS gene may be implicated in reducing NO levels. This study examined the relationship between eNOS gene variations and NO and malondialdehyde (MDA) levels in preeclamptic women and their neonates in Bangladesh. This study compared 100 healthy pregnant women (controls) with 82 preeclampsia-diagnosed women and their newborns. PCR-RFLP was used to detect eNOS gene variants, while spectrophotometric methods were used to measure NO and MDA levels in plasma. The maternal eNOS gene variant rs2070744 exhibited a significant relationship with PE risk, particularly under the dominant model and allele frequency scrutiny. Similarly, the neonatal eNOS gene variant rs2070744 exhibited a robust association with PE risk across various genetic models. The case‒control comparison of the genotypic distribution of NO and MDA in the studied subjects revealed that although PE mothers with TT genotypes had significantly lower NO levels than did the controls, the neonates of PE mothers with TT and CC genotypes showed a significant decrease in NO levels compared to their control groups. Moreover, the PE group and their neonates with the TT and CT genotypes had significantly greater MDA levels than did the control group. These findings illuminate the profound influence of eNOS gene variants on preeclampsia onset, suggesting a potential mechanism involving altered NO production via heightened oxidative stress among affected mothers and neonates. Consequently, screening for eNOS variants and estimating NO levels in pregnant women could offer early identification of those predisposed to PE, thus enabling timely interventions.