Transgenerational Impacts of Oxidative Damage Induced by Prenatal Ethanol Exposure on Spatial Learning/Memory and BDNF in the Hippocampus of Male Rats

Background: and Aim: Alcohol use during pregnancy causes damage to normal fetal development and induces oxidative stress (OS), and intervenes in the expression of neurotrophic factors (NTFs). Materials and Methods A rat model of fetal alcohol spectrum disorder (FASD) was initially generated to reflect on the deficits in the first generation, and then those transmitted via the male germline to the unexposed male ones. The pregnant rats were thus divided into four groups, namely, the control group (CTRL) receiving only distilled water, and three groups being exposed to ethanol (20%, 4.5 g/kg) by oral gavage, during the first 10-days gestation (FG), the second 10-days gestation (SG), and the entire gestation (EG) periods. Half of the male offspring were then subjected to the Morris water maze (MWM) test on the 30 postnatal days. The other half was further recruited to evaluate the activity of the antioxidant enzymes, including glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA), in the hippocampus. Ultimately, the qRT-PCR was practiced to measure the BDNF gene expression. Results Prenatal ethanol exposure caused spatial learning/memory deficits during the SG and EG in both generations. The elevated MDA levels, along with the decreased GPx and SOD activity and BDNF gene expression occurred all through the SG and EG of the first filial generation (F1), and the reduction in the GPx and SOD activity together with the BDNF gene expression was only observed in the EG of the second filial generation (F2) of the male rats. Conclusion OS could play a leading role in the diminished BDNF gene expression as well as the spatial learning/memory decline induced by prenatal ethanol exposure.