Abstract
Objective
To assess the influence of oxidative stress on the gene expression of nitric oxide synthases (NOS 3 and NOS 2) and, hence, the cardiovascular responses in preeclampsia.
Methods
This was a case control study in which patients with preeclampsia (PE group) and normal pregnancy controls (NP group) were included according to the guidelines of the American College of Obstetricians and Gynecologists (ACOG). The serum levels of malondialdehyde (MDA), total antioxidant capacity, and nitric oxide (NO) were estimated, and the heart rate andmean arterial pressure were recorded. The gene profiling of NOS3 and NOS2 was performed through real-time polymerase chain reaction (RT-PCR). The statistical analysis was performed using the Student t-test, and values of p<0.05 were considered statistically significant.
Results
The serum levels of malondialdehyde were increased (p<0.0001), and the total antioxidant capacity was reduced in the PE group (p=0.034), indicating oxidative stress. In the PE group, themean arterial pressure was significantly higher (p<0.0001), but the serum levels of NO did not show a statistically significant reduction (p=0.20). The gene expression profiling of NOS3 and NOS2 revealed a down regulation in the PE group by 8.49 and 51.05 times respectively.
Conclusion
Oxidative stress may lead to endothelial dysfunction, which could result in increased mean arterial pressure. Nitric oxide may play a role in this mechanism, but interactions with other vasoactive /biological substances cannot be overlooked, as the gene expression of NOS3 and NOS2 has been reduced.
Keywords:
molecular genetics; preeclampsia/eclampsia; vascular biology
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