Maternal Thrombophilia Disrupts Fetal Redox Homeostasis.

Abstract

Considering that the fetal redox homeostasis is a key factor for normal prenatal development, this study researched the effects of maternal thrombophilia on fetal redox homeostasis by assessing the redox profile of amniotic fluid cells and amniotic fluid during the second trimester of pregnancy. Concentration of redox biomarkers (superoxide anion, O₂.^-; hydrogen peroxide, H₂O₂; nitric oxide, NO; peroxynitrite, ONOO^-; lipid peroxides, LPO, micronuclei, reduced glutathione, GSH; oxidized glutathione, GSSG) were assayed in the amniotic fluid cells and amniotic fluid of healthy pregnant women and pregnant women with thrombophilia gestational age from 16 to 18 weeks. Results of this study indicate that pregnant women with thrombophilia have significantly higher concentrations of O₂.^-, NO, ONOO^-, and LPO but lower concentrations of H₂O₂, GSH, and GSSG in the amniotic fluid cells, as well as a higher concentration of GSSG in the amniotic fluid. No difference is shown in concentration of O₂.^-, H₂O₂, NO, ONOO^-, LPO, and GSH in the amniotic fluid, as well as in frequency of micronuclei in the amniotic fluid cells among investigated groups of pregnant women. The present study provides the first evidence that babies born to mothers with thrombophilia in the second trimester of intrauterine life experience intense oxidative stress characterized by overproduction of O₂.^-, NO, ONOO^-, and LPO, as well as GSH depletion.