Prenatal exposure to decabrominated diphenyl ether impairs learning ability by altering neural stem cell viability, apoptosis, and differentiation in rat hippocampus.

Research paper by Y-H YH Chen, Z-H ZH Li, Y Y Tan, C-F CF Zhang, J-S JS Chen, F F He, Y-H YH Yu, D-J DJ Chen

Indexed on: 26 Feb '14Published on: 26 Feb '14Published in: Human & experimental toxicology


Background:Polybrominated diphenyl ether (PBDE) levels in children and teenagers were higher than those of the adults and the highest levels were found in infants and toddlers. 2,2',3,3',4,4',5,5',6,6'-Decabrominated diphenyl ether (BDE-209) readily crosses the placental barrier and produces toxicity in the developing fetus, particularly to the developing brain.Objectives:This present study aims to investigate the potential effects of prenatal BDE-209 exposure on regulation of neurogenesis and learning function in an experimental rat model.Methods:Pregnant rats received BDE-209 (10, 30, or 50 mg kg(-1) day(-1)) or vehicle (arachis oil) through gastric gavage from gestation day 1 to 14 (n = 10 per group). The embryonic hippocampal neural stem cells (NSCs) from five pregnant rats in each group were collected on day 14 and cultured in vitro to determine the cell viability, apoptosis, and differentiation of NSCs using cell counting kit 8 assay, flow cytometry, and immunofluorescence staining, respectively. In total, 20 male offspring on postnatal day 25 from each group were chosen to evaluate learning ability using a Morris water navigation task assay.Results:The data showed that prenatal exposure to BDE-209 decreased cell viability and differentiation of NSCs but promoted apoptosis in a dose-dependent manner. Prenatal BDE-209 exposure also impaired rat-learning acquisition in a dose-dependent manner.Conclusions:Prenatal BDE-209 exposure impairs rat-learning acquisition, possibly by affecting neurogenesis in the hippocampus during embryonic development.