Induction of apoptosis by antimycin A in differentiated PC12 cell line

Abstract

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 Ca(2+) increased in the early stage of cell apoptosis induced by AMA treatment. All of Ca(2+) chelators, L-type Ca(2+) channel blockers and inhibitors of Ca(2+) released from endoplasmic reticulum and ROS scavenger, were used in this experiment. It was found that the Ca(2+) 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 Ca(2+).