Journal
EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
Volume 2013, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2013/575287
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Funding
- Priority Research Centers Program through the National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2011-0031403]
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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) mu M) was present in cultures of embryos exposed to nicotine, these parameters improved significantly. These findings indicate that beta carotene effectively protects against nicotine-nduced teratogenesis in mouse embryos through its antioxidative, antiapoptotic, and anti-inflammatory activities.
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