Prenatal Nicotine Exposure Augments Renal Oxidative Stress in Embryos of Pregnant Rats with Reduced Uterine Perfusion Pressure.

BACKGROUND/AIM Both maternal nicotine (NIC) exposure and placental insufficiency increase oxidative stress in the fetal kidney ensuing fetal programming of renal diseases in adult life. Their combined effects, however, are unknown. We tested the hypothesis that maternal NIC exposure exacerbates renal oxidative stress and injury in fetuses of pregnant rats with placental insufficiency. MATERIALS AND METHODS Fourteen-day-pregnant rats were subjected to sham operation or reduced uterine perfusion pressure (RUPP) that received either nicotine (20 μg/ml in 1% saccharine) or vehicle (1% saccharine) in their drinking water. At gestational age of 21 days, male fetuses were collected by C-section and sacrificed: plasma and renal cotinine content, extent of renal oxidative stress (4-hydroxynonenal [HNE] and HO-1) and injury (KIM-1) were determined together with the weight of the fetal kidney and fetus. RESULTS Prenatal NIC exposure resulted in cotinine accumulation in the plasma and kidney of the fetuses, augmented RUPP-associated increase in renal HNE content and HO-1 expression as well as KIM-1 expression. NIC also enhanced RUPP-induced reduction in fetal and fetal kidney weight. CONCLUSION Prenatal NIC exposure augments the existing renal risk in the growth-restricted fetus, which may contribute to worsening in fetal programming of renal disease.