PBDE-209 exposure damages learning and memory ability in rats potentially through increased autophagy and apoptosis in the hippocampus neuron

Environ Toxicol Pharmacol. 2017 Mar:50:151-158. doi: 10.1016/j.etap.2017.02.006. Epub 2017 Feb 4.

Abstract

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.

Keywords: Autophagy; Hippocampus; PBDE-209; Pregnancy.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Autophagy / drug effects
  • Caspase 3 / metabolism
  • Cells, Cultured
  • Female
  • Gene Expression Regulation / drug effects
  • Halogenated Diphenyl Ethers / toxicity*
  • Hippocampus / cytology
  • Hippocampus / embryology*
  • Maze Learning / drug effects*
  • Memory / drug effects*
  • Neurons / drug effects*
  • Poly(ADP-ribose) Polymerases / metabolism
  • Pregnancy
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Halogenated Diphenyl Ethers
  • Poly(ADP-ribose) Polymerases
  • Casp3 protein, rat
  • Caspase 3
  • decabromobiphenyl ether