The role of lysosomes in BDE 47-mediated activation of mitochondrial apoptotic pathway in HepG2 cells

Our results showed that reactive oxygen species production was an initial response of HepG2 to BDE 47 exposure, followed by a decreased membrane potential; a loss of MMP caused additional ROS generation which acted to induce lysosomal membrane permeability; an increased LMP resulted in a release of cathepsin B which aggravated the loss of MMP leading to release of cytochrome C and caspase 3 and subsequent apoptosis

Xiaohui Liu; Jian Wang; Chengquan Lu; Chunyan Zhu; Bo Qian; Zhenwei Li; Chang Liu; Jing Shao; Jinsong Yan

2014

Scholarcy highlights

  • Polybrominated diphenyl ethers are a group of widely used flame retardants
  • Lysosomes and mitochondria may communicate through feedback interactions
  • While the mitochondrial–apoptotic pathway has been suggested in PBDEs-induced apoptosis, the role of lysosomes is yet to be understood
  • HepG2 cells were exposed to BDE 47 at various concentrations and durations to establish the causal and temporal relationships among various cellular events, such as cell viability, reactive oxygen species, mitochondrial membrane potential, apoptosis, and expression of cytochrome C and caspase 3
  • Our results showed that ROS production was an initial response of HepG2 to BDE 47 exposure, followed by a decreased MMP; a loss of MMP caused additional ROS generation which acted to induce lysosomal membrane permeability; an increased LMP resulted in a release of cathepsin B which aggravated the loss of MMP leading to release of cytochrome C and caspase 3 and subsequent apoptosis
  • Our data indicate that lysosomes might be involved in BDE 47-mediated mitochondrial–apoptotic pathway in HepG2 cells, possibly through feedback interactions between mitochondria and lysosomes

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