2021-01-152021-01-152009-01-01https://repository.tcu.edu/handle/116099117/43071https://academic.oup.com/jrr/article/50/1/73/921119Much attention has been focused on the mitochondrial superoxide anion (O2-), which is also a critical free radial produced by ionizing radiation. The specific role of the mitochondrial O2- on physiological aging in mammals is still unclear despite wide-spread evidence that oxidative stress is involved in aging and age-related diseases. The major endogenous source of O2- is generated as a byproduct of energy metabolism from mitochondria. In order to better understand how O2-relates to metazoan aging, we have comprehensively examined age-related changes in the levels of oxidative damage, mitochondrial O2- production, mitochondrial antioxidant enzyme activity and apoptosis induction in key organs of an inbred mouse strain (C57BL/6J). Oxidative damage accumulated and excess apoptosis occurred in the brain, oculus and kidney with aging, but comparatively little occurred in the heart and muscle. These rates are correlated with O2- levels. Mitochondrial O2- production levels increased with aging in the brain, oculus and kidney, and did not significantly increased in the heart and muscle. In contrast to O2- production, mitochondrial SOD activities increased in heart and muscle, and remained unchanged in the brain, oculus and kidney with aging. These results suggest that O2- production has high organ specificity, and oxidative damage by O2- from mitochondria mediated apoptosis can lead to organ atrophy and physiological dysfunction. In addition, O2- from mitochondria plays a core role in physiological aging.en-UShttps://academic.oup.com/journals/pages/self_archiving_policy_cMitochondrial superoxide anion (O2-)Mitochondrial SODOxidative damageApoptosisPhysiological agingArticleOxford University Press and the Journal of Radiation Research are the original place of publication. Authors of open access articles are entitled to deposit their original version or the version of record in institutional and/or centrally organized repositories and can make this publicly available immediately upon publication, provided that the journal and OUP are attributed as the original place of publication and that correct citation details are given. Authors should also deposit the URL of their published article, in addition to the PDF version.https://doi.org/10.1269/jrr.08097