Published literature revealed that mitochondria from heterozygous (SOD2+/−) mice were partially deficient in MnSOD, showing increased proton leakage, respiratory depression, and mitochondrial oxidative damage, while liver mitochondria from homozygous mutant mice were completely deficient in MnSOD, showing significant respiratory depression and significant sensitization of mitochondrial permeability transition pores [54]. This evidence concerns the gene SOD2 and depressive disorder.