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Human mitochondrial complex II is an intriguing enzyme, which has been the focus of medical research during the past few decades since it contributes to pathogenesis of mitochondrial diseases as well as a target for chemotherapy. Reactive oxygen species (ROS) produced by this enzyme has been implicated in both these conditions. While ROS produced from mutated mitochondrial complex II has been implicated in pathogenesis of mitochondrial diseases, ROS produced from pharmacologically inhibited mitochondrial complex II has been implicated in cancer cell death. In this chapter, we show that inhibition of mitochondrial complex II in human cancer cells with atpenin A5 produces detectable levels of ROS while normal cells do not. Thus, this enzyme may be used as a potential target for developing new anticancer drugs to trigger ROS-mediated selective death of cancer cells.

Differential Effect of Atpenin A5 on ROS Production from Wild- Type Mitochondrial Complex II in Human Cancer Cells and Normal Cells