Oxidative Stress and Apoptosis in Benzo[a]pyrene-Induced Neural Tube Defects.

摘要: Neural tube defects (NTDs) are among the most common and severe congenital malformations result from incomplete closure of neural during early development. Maternal exposure to polycyclic aromatic hydrocarbons (PAHs) has been suggested be a risk factor for NTDs previous studies imply that mechanism underlying association between PAH may involve oxidative stress apoptosis. The objectives this study were investigate whether there is direct effect maternal benzo[α] pyrene (BaP) on in mice, examine mechanisms by combining animal experiments human subject studies. We found intraperitoneal injection BaP embryonic day 7 at dose 250 mg kg-1 induced (13.3% frequency) ICR mice. significantly increased expression genes associated with stress, Cyp1a1, Sod1 Sod2, while repressing Gpx1. Elevated apoptosis higher protein cleaved caspase-3 neuroepithelium treated embryos observed. Pre-treatment vitamin E, added food, protected against BaP-induced (1.4% (P < 0.05). Vitamin E also partly normalized related gene excess BaP-treated embryos. Examination tissues revealed levels carbonyl PAHs NTDs. Collectively, these results suggest could induce apoptosis, have protective effect.