dinoprost and Neural-Tube-Defects

Neural tube defects (NTDs) are among the most common and severe congenital malformations. To examine the association between markers of macromolecular oxidative damage and risk of NTDs, we measured levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), protein carbonyl (PC), and 8-iso-prostaglandin F2α (8-iso-PGF2α) in maternal serum samples of 117 women with NTD-affected pregnancies and 121 women with healthy term newborns. We found higher levels of 8-OHdG and PC in the NTD group than in the control group; however, we did not observe a statistically significant difference in 8-iso-PGF2α levels between the NTD and the control groups. NTD risk increased with increasing quartiles of 8-OHdG [odds ratio (OR)=1.17; 95% confidence interval (CI) 0.39-3.51; OR=2.19; 95% CI, 0.68-7.01; OR=3.70; 95% CI, 1.30-10.51, for the second, third, and fourth quartile relative to the lowest quartile, respectively; P=0.009], and with increasing quartiles of PC (OR=2.26; 95% CI, 0.66-7.69; OR=3.86; 95% CI, 1.17-12.80; OR=5.98; 95% CI, 1.82-19.66, for the second, third, and fourth quartile relative to the lowest quartile, respectively; P=0.002]. Serum levels of 8-OHdG were higher in women who did not take folic acid supplements during the periconceptional period. These results suggest that oxidative stress is present in women carrying pregnancies affected by NTDs.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Adult; Biomarkers; Case-Control Studies; China; Deoxyguanosine; Dietary Supplements; Dinoprost; DNA Damage; Female; Folic Acid; Hospitals, Maternity; Humans; Neural Tube Defects; Odds Ratio; Oxidative Stress; Population Surveillance; Protein Carbonylation; Risk

The effect of acetyl salicylic acid (aspirin) on neural tube development in chick embryo was studied, using the chick embryo blastoderm model. Aspirin was injected in four different doses sub-blastodermally into fresh embryonated eggs. The role of PGE1 and PGE2 alpha in the defect induced by aspirin on neural tube development in chick embryo was studied. PGE1 (5 micrograms) given after aspirin (30 micrograms) treatment was found to produce greater defect in development. All the four doses of aspirin used (i.e., 6, 30, 60 and 120 micrograms/embryo) produced significant changes (P < 0.01) in the neural tube development of chick embryo. Pre-treatment with PGE1 did not modify the defect induced by aspirin, whereas pre-treatment with PGF2 alpha prevented neural tube defects induced by aspirin. It appears that aspirin (in the doses used) affects neural tube formation by decreasing PGF2 alpha synthesis in chick embryo blastoderm.

Topics: Alprostadil; Animals; Aspirin; Chick Embryo; Dinoprost; Neural Tube Defects