Selenite-mediated production of superoxide radical anions in A549 cancer cells is accompanied by a selective increase in SOD1 concentration, enhanced apoptosis and Se-Cu bonding

Abstract

Selenite may exert its cytotoxic effects against cancer cells via the generation of reactive oxygen species (ROS). We investigated sources of, and the cellular response to, superoxide radical anion (O2 ·-) generated in human A549 lung cancer cells after treatment with selenite. A temporal delay was observed between selenite treatment and increases in O2 ·- production and biomarkers of apoptosis/necrosis, indicating that the reduction of selenite by the glutathione reductase/NADPH system (yielding O2 ·-) is a minor contributor to ROS production under these conditions. By contrast, mitochondrial and NADPH oxidase O2 ·- generation were the major contributors. Treatment with a ROS scavenger [pol..