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PBDE-209 exposure damages learning and memory ability in rats potentially through increased autophagy and apoptosis in the hippocampus neuron.
Environmental Toxicology and Pharmacology 2017 March
This study is to investigate the neurotoxicity of PBDE-209 during pregnancy through autophagy and apoptosis in the fetal hippocampus neuron. The autophagy protein levels of LC3-II and Beclin-1 were significantly higher in hippocampus tissue and neuron, while P62 protein were lower. Apoptosis protein Cleaved Caspase-3 and Cleaved PARP was significantly higher in PBDE dose groups and BCL-2 levels in high PBDE dose groups were significantly lower. During the Morris water maze task, the escape latency times of high PBDE dose groups were significantly longer. PBDE-209-induced autophagy leads to neurons death and inhibition of autophagy reduce PBDE-209-induced apoptotic cell death. These results suggest that exposure of the PBDE-209 during pregnancy increases hippocampal autophagy, decrease neuron viability, and it partly effect apoptosis induced by PBDE-209. All that may contribute to the decline of learning and memory ability in the offspring.
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