Antiteratogenic Effects of beta-Carotene in Cultured Mouse Embryos Exposed to Nicotine

Contains fulltext : 127284.pdf (publisher's version ) (Open Access)
After maternal intake, nicotine crosses the placental barrier and causes severe embryonic disorders and fetal death. In this study, we investigated whether beta -carotene has a beneficial effect against nicotine-induced teratogenesis in mouse embryos (embryonic day 8.5) cultured for 48 h in a whole embryo culture system. Embryos exposed to nicotine (1 mM) exhibited severe morphological anomalies and apoptotic cell death, as well as increased levels of TNF- alpha , IL-1 beta , and caspase 3 mRNAs, and lipid peroxidation. The levels of cytoplasmic superoxide dismutase (SOD), mitochondrial manganese-dependent SOD, cytosolic glutathione peroxidase (GPx), phospholipid hydroperoxide GPx, hypoxia inducible factor 1 alpha , and Bcl-x L mRNAs decreased, and SOD activity was reduced compared to the control group. However, when beta -carotene (1 x 10(-7) or 5 x 10(-7) muM) was present in cultures of embryos exposed to nicotine, these parameters improved significantly. These findings indicate that beta -carotene effectively protects against nicotine-induced teratogenesis in mouse embryos through its antioxidative, antiapoptotic, and anti-inflammatory activities.