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OXIDATIVE STRESS INDUCES CELL DEATH IN CD-1 MOUSE CRANIAL NEURAL CREST CELLS IN VITRO
Citation:
Smith, J., E S. Hunter III, AND K. K. Sulik. OXIDATIVE STRESS INDUCES CELL DEATH IN CD-1 MOUSE CRANIAL NEURAL CREST CELLS IN VITRO. Presented at Research Society on Alcoholism, Montreal, Quebec, Canada, June 23-28, 2001.
Description:
OXIDATIVE STRESS INDUCES CELL DEATH IN CD-1 MOUSE CRANIAL NEURAL CREST CELLS IN VITRO. J.B. Smith, K.K. Sulik, E.S. Hunter III. University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.
The induction of craniofacial defects by ethanol exposure is mediated in part by damage to the cranial neural crest cells (NCCs). In the embryo ethanol exposure increases reactive oxygen species (ROS) and induces cell death of NCCs. Antioxidants ameliorate the cell death and dysmorphogenesis that result from ethanol exposure. Since NCCs are a critical target of ethanol-induced effects, we determined if oxidative stress would induce cell death in primary cultures of NCCs from ethanol-resistant CD-1 mice. Cranial neural folds were removed from day 8 (plug day = 0) CD-1 mouse embryos, grown in culture for 24 hours, and then exposed to ethanol or hydrogen peroxide (H2O2) for an additional 24 hours. Exposure of NCCs to 50-200 millimolar ethanol (250-1000 mg/dL) did not increase the incidence of cell death beyond that observed in control cultures. Treatment of NCCs with 100 or 500 micromolar H2O2 resulted in a concentration dependent increase in cell death compared to control cultures. These results indicate that oxidative damage will induce cell death in the NCCs from an ethanol-resistant embryo. This suggests that the mechanisms necessary for ROS generation from ethanol are not present in the NCCs from CD-1 mouse embryos at this stage of differentiation.
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Supported by NIAAA/AA11605.