Chronic prenatal ethanol exposure-induced effects on glutathione, 8-iso-prostaglandin F2alpha, cytochrome C and caspase-3 in the hippocampus and frontal cortex of the term fetal and neonatal guinea pig.

摘要

It is hypothesized that oxidative stress (OS) and apoptosis are key mechanisms of neurodegeneration that occur in the neurobehavioural teratogenicity produced by chronic prenatal ethanol exposure (CPEE). To test this hypothesis, timed pregnant guinea pigs (term, about gestational day (GD) 68) received chronic oral administration of. 4 g ethanol/kg maternal body weight/day, isocaloric-sucrose/pair-feeding or water throughout gestation. At GD 65 (term fetus) and postnatal day (PD) 0 (neonate), individual offspring were euthanized, and the brain was excised and dissected into selected brain regions. Fetal blood, amniotic fluid and placenta were also collected. Reduced glutathione (GSH) was determined in the mitochondrial fraction of homogenate of the hippocampus and frontal cortex. Samples were also analyzed for lipid peroxidation by measuring F2-isoprostanes, a marker for OS. (Abstract shortened by UMI.).