• antimycin A;
  • ROS;
  • apoptosis;
  • PC12 cells;
  • Ca2+;
  • mitochondria


Antimycin A (AMA) is an inhibitor of mitochondrial electron transport chain via binding to mitochondrial complex III. This inhibition increases the production of reactive oxygen species (ROS). The aim of the present study was to investigate the effect of AMA on PC12 cells in vitro. Results of the nuclear morphology and the flow cytometer indicated that AMA efficiently induced PC12 cell apoptosis. Moreover, the levels of ROS and Ca2+ increased in the early stage of cell apoptosis induced by AMA treatment. All of Ca2+ chelators, L-type Ca2+ channel blockers and inhibitors of Ca2+ released from endoplasmic reticulum and ROS scavenger, were used in this experiment. It was found that the Ca2+ chelators and ROS scavengers, in particular, could delay AMA-induced PC12 cell apoptosis. In conclusion, the present study found that AMA induced PC12 cell apoptosis through ROS and Ca2+. Copyright © 2013 John Wiley & Sons, Ltd.