title: Maternal supplementation of nucleotides improves the behavioral development of prenatal ethanol-exposed mice.
abstract: Maternal ethanol consumption during pregnancy can induce learning deficits in the offspring. The objective of this study was to assess whether supplementation of exogenous nucleotides during pregnancy and lactation would ameliorate prenatal ethanol-induced learning and memory deficits in the offspring of mice, and to explore the possible mechanisms. In the present study, pregnant C57BL/6J mice were exposed to ethanol (5 g/kg body weight) intragastrically from gestational day (GD) 6 to GD15. The dams in exogenous nucleotide intervention groups were fed with feed containing 0.01%, 0.04%, or 0.16% nucleotide powder, with control and ethanol groups receiving normal feed. The dams were allowed to deliver naturally and to breast feed their offspring. After weaning, behavioral tests were carried out in the offspring of each group. Serum oxidation indexes were analyzed, and the hippocampus of each offspring was collected and detected for acetyl cholinesterase (AChE) activity and the expression of p-CREB, CREB, and BDNF. The results showed that maternal supplementation with exogenous nucleotides during pregnancy could ameliorate prenatal ethanol-induced learning and memory deficits in the offspring of mice, through improving their antioxidant capacity, reversing hippocampus AChE levels, and allowing the expression of some proteins related to learning and memory. However, different sensitivities were found between the two sexes.
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing, China.
authors.forename: Wenhong
authors.initials: W
authors.lastname: Dong
authors.forename: Zhenghao
authors.initials: Z
authors.lastname: Wu
authors.forename: Linlin
authors.initials: L
authors.lastname: Xu
authors.forename: Yuehui
authors.initials: Y
authors.lastname: Fang
authors.forename: Yajun
authors.initials: Y
authors.lastname: Xu
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight; D002492:Central Nervous System Depressants / Q000097:blood / Q000633:toxicity*; D002658:Developmental Disabilities / Q000097:blood / Q000209:etiology* / Q000517:prevention & control*; D004924:Escape Reaction; D000431:Ethanol / Q000097:blood / Q000633:toxicity*; D005106:Exploratory Behavior; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood; D006624:Hippocampus / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018782:Maze Learning; D051379:Mice; D008810:Mice, Inbred C57BL; D009711:Nucleotides / Q000008:administration & dosage*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D002492:Central Nervous System Depressants; D009711:Nucleotides; D000431:Ethanol; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000110:Acetylcholinesterase