SOD2 Overexpression Affects Mouse Hepatic OXPHOS Complex Integrity

Reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, are produced as byproducts of cellular respiration and can damage DNA, proteins, and lipids within a cell. To combat the production of superoxide, cells express superoxide dismutase 2 (SOD2), an antioxidant enzyme which converts superoxide into hydrogen peroxide. Mice that overexpress SOD2 were used to examine tissue‐specific ROS‐responsive genes. Microarray data indicates a disruption in genes encoding proteins that function in oxidative phosphorylation in SOD2 mice. BN‐PAGE analysis confirms the defect, but kinetic analysis of complexes 2 and 5 show no significant difference. We propose that the overexpression of SOD2 may destabilize assembled OXPHOS complexes, rendering them more sensitive to detergent. Current research is being conducted to test the stability of SOD2 oxidative phosphorylation complexes against oxidative stress, as well during aging. Support or Funding Information ASU Office of Student Research ASU Department of Chemistry This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .