Objectives: Ceramide (Cer), known as apoptotic markers, increases with prenatal ethanol (EtOH) exposure, resulting in neuroapoptosis. Whether maternal nutrition can impact Cer concentrations in brain, via altering plasma and brain fatty acid compositions have not been examined. This study compared a standard chow with a formulated semi-purified energy dense (E-dense) diet on fatty acid composition, Cer concentrations, and apoptosis in plasma and brain regions (cortex, cerebellum, and hippocampus) of pups exposed to EtOH during gestation. Methods: Pregnant Sprague-Dawley rats were randomized into four groups: chow (n = 6), chow + EtOH (20% v/v) (n = 7), E-dense (n = 6), and E-dense + EtOH (n = 8). At postnatal day 7, representing the peak brain growth spurt in rats, lipids, and apoptosis were analyzed by gas chromatography and a fluorometric caspase-3 assay kit, respectively. Results: Maternal E-dense diet increased total fatty acid concentrations (p < 0.0001), including docosahexaenoic acid (DHA) (p < 0.0001) in plasma, whereas DHA concentrations were decreased in the cerebellum (p < 0.03) of pups than those from chow-fed dams. EtOH-induced Cer elevations in the hippocampus of pups born to dams fed chow were reduced by an E-dense diet (p < 0.02). No significant effects of maternal diet quality and EtOH were observed on caspase-3 activity. No significant correlations existed between plasma/brain fatty acids and Cer concentrations. Discussions: Maternal diet quality affected fatty acid compositions and Cer concentrations of pups with prenatal EtOH exposure, differently. Maternal nutrition has the potential to prevent or alleviate some of the adverse effects of prenatal EtOH exposure.
Keywords: Prenatal ethanol exposure; apoptosis; ceramides; fatty acid composition; maternal diet.