Objective Although the etiopathogenesis of preeclampsia (PE) is unknown,
evidence suggests that it may be associated with increased oxidative stress.
Studies have shown that oxidative stress can affect DNA fragments called
telomeres. However, the interactions of PE, oxidative stress, and telomere
length are not clearly known. This study aims to evaluate the
oxidative/anti-oxidative stress balance in the placenta and umbilical
cord and examine the effect of oxidative stress on telomeres.
Materials-Method Cord blood and placental samples were collected from 27
pregnant women with severe PE
(280/7–336/7 gestational
weeks) and 53 healthy pregnant women. Telomere length (TL) was measured by
real-time PCR in the cord blood and placenta tissue. Total antioxidant status
(TAS) and total oxidant status (TOS) levels were measured in the cord blood and
placenta tissue using a colorimetric method.
Results No significant differences were found between groups regarding
age, BMI, gravida, parity, and newborn gender (p>0.05). Cord blood and
placental TL of PE patients were significantly shorter than the control group,
while cord blood and placental TAS and TOS levels were higher (p<0.05).
The results of a multivariate logistic regression analysis showed that the level
of placental TOS in PE patients (OR=1.212, 95%
CI=1.068–1.375) was an independent risk factor affecting PE.
Conclusion This study found that oxidative stress is an independent risk
factor in the development of PE and shortens TL in both placental and umbilical
cord blood. Future research on telomere homeostasis may offer a new perspective
for the treatment of PE.