Kingston, Ontario -- Researchers have shown that carbon monoxide may prevent the placental cell death caused by oxidative stress injury, possibly averting the risks of pre-eclampsia. The report by Bainbridge et al., "Carbon monoxide inhibits hypoxia/reoxygenation-induced apoptosis and secondary necrosis in syncytiotrophoblast," appears in the September issue of The American Journal of Pathology.
Pre-eclampsia, a form of pregnancy-associated hypertension, affects 5-7% of pregnancies and poses serious risks for both mother and child. If maternal blood vessels at the placental barrier fail to remodel and adapt to the changing nutrient/oxygen needs of the growing fetus, the maternal blood pressure rises in an effort to improve nutrient delivery. This leads to oxidative stress and damage to the placenta, specifically to the syncytiotrophoblast. When syncytiotrophoblast cells die, they are released into the maternal circulation, initiating a cascade of inflammation that can damage maternal organs.
Interestingly, mothers who smoke cigarettes during pregnancy have a 33% decreased risk of developing pre-eclampsia compared to nonsmokers. New research questions whether the carbon monoxide found in cigarette smoke, and subsequently carried in a smoking mother's blood, may be the cause. Carbon monoxide, which is produced naturally by the body at low levels, possesses vessel-relaxing and cytoprotective activities that may prevent syncytiotrophoblast cell death and the resulting injury to fetus and mother.
Dr. Graeme Smith and colleagues examined this hypothesis using tissue from term human placentas obtained following elective caesarian section from nonsmoking, low-risk women. When cultured tissues were exposed to oxidative stress (hypoxia and re-oxygenation), syncytiotrophoblast cell death occurred. However, when tissues were treated with carbon monoxide, at levels similar to those found in blood of smoking mothers, cell death was significantly r
Contact: Audra Cox
American Journal of Pathology