Prenatal nicotine exposure tied to oxidative stress and vascular dysfunction in male rat offspring
FRIDAY, July 22 (HealthDay News) -- Prenatal nicotine exposure in rats can increase the production of reactive oxygen species (ROS) resulting in vascular hypertensive reactivity in male offspring, according to an experimental study published online July 21 in the British Journal of Pharmacology.
DaLiao Xiao, Ph.D., from the Loma Linda University School of Medicine in California, and colleagues investigated the effects of prenatal nicotine exposure on ROS production and vascular reactivity in male rat offspring. A total of 25 pregnant Sprague-Dawley rats were randomly assigned to receive nicotine or saline water subcutaneously through osmotic mini-pumps throughout the gestation period. Oxidative damage in the vascular tissue of 5-month-old male offspring was determined by measuring malondialdehyde concentrations, and superoxide dismutase (SOD) activity. Angiotensin II was used for contraction study, and acetylcholine for relaxation.
The investigators found that the angiotensin II-induced contractions of the aorta in the offspring increased significantly after antenatal nicotine exposure, and were inhibited by both apocynin and tempol in a concentration-dependent manner. Acetylcholine-induced relaxations were impaired in these aortas. The nicotine treatment significantly increased malondialdehyde, superoxide, and nitrotyrosine protein levels in the vascular wall, and decreased the SOD activity. The protein expression of nicotinamide adenine dinucleotide phosphate-oxidase (Nox)2/gp91 in the aorta, but not that of Nox4, was significantly enhanced by antenatal nicotine exposure.
"The present investigation provides evidence in a rat model that prenatal nicotine exposure increases vascular superoxide production via an upregulation of angiotensin II/angiotensin II type 1 receptor-mediated Nox2 signaling in adult offspring. The increased superoxide production and peroxynitrite formation play an important role in developmental programming of vascular hypertensive reactivity, supporting the concept of heightened oxidative stress in fetal programming of cardiovascular disease," the authors write.
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