DOSE-RELATED GROWTH DEFICITS IN LS BUT NOT SS MICE PRENATALLY EXPOSEDTO ALCOHOL

Genetically based alcohol sensitivity may influence the severity of al cohol-related birth defects. To examine this question, measures of gro wth and survival were examined in offspring of the alcohol sensitive L ong-Sleep (LS) and alcohol-resistant Short-Sleep (SS) mouse lines foll owing prenatal ethanol exposure. Pregnant LS and SS mice received an e thanol dose of either 6 or 8 g/kg/day from days 7 through 18 of pregna ncy. Control groups received a maltose-dextrin solution made isocalori c to the 8 g/kg/day dose. Ethanol and maltose-dextrin solutions were a dministered as split doses, 6 h apart, via gavage. Nonintubated lab ch ow control groups were also included for both mouse lines. Offspring w ere fostered at birth to lactating mice of an outbred stock. Pregnancy was longer for ethanol-treated LS darns compared to maltose-dextrin a nd lab chow LS control groups, whereas pregnancy length for ethanol-tr eated SS dams was similar to SS controls. Prenatal ethanol exposure re sulted in dose-related growth deficits in LS but not in SS litters. Li ne differences in postnatal growth deficits in response to prenatal al cohol exposure suggest maternal or fetal alcohol sensitivity influence alcohol-related birth defects.