Mitochondria and lysosomes play a key role in HepG2 cell apoptosis induced by microcystin-LR

Abstract

The aim of the present study was to investigate the toxicological mechanism of microcystin-LR (MC-LR) on HepG2 cells to understand MC-related human hepatitis and primary liver cancer. The results showed that MC-LR induced the time- and concentration-dependent apoptosis of HepG2 cells, and MC-LR exposure promoted the expression of Smac/Diablo in HepG2 cells. In addition, Bad and cleaved-Bid protein levels were also altered. Moreover, MC-LR exposure promoted the expression of Fas and FasL and increased caspase-8 transcription and enzymatic activity, suggesting that the MC-LR-induced apoptosis of HepG2 cells may be mediated via mitochondrial and Fas/FasL pathways in which lysosomal destabilization might play an important role.

Keywords:

• MC-LR
• HepG2
• lysosome
• mitochondria
• apoptosis

Declaration of interest

All authors declare that they have no conflicts of interest.

This research was financially supported by the National Natural Science Foundation of China [Grant No. 31472285], the Innovation Scientists and Technicians Troop Construction Projects of Henan Province, China [Grant No. 16420050001], and the Key Subjects of Biology and Ecology in Henan Province, China.