The role of mitochondrial superoxide anion (O<sub>2</sub>-) on physiological aging in C57BL/6J mice

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  • MIYAZAWA Masaki
    Department of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine
  • ISHII Takamasa
    Department of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine
  • YASUDA Kayo
    Department of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine
  • NODA Setsuko
    Department of Nursing, Tokai University School of Health Science
  • ONOUCHI Hiromi
    Department of Ophthalmology, Tokai University School of Medicine
  • HARTMAN Philip S.
    Department of Biology, Texas Christian University, Fort Worth
  • ISHII Naoaki
    Department of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine, Tokai University School of Medicine

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タイトル別名
  • The Role of Mitochondrial Superoxide Anion (O2-) on Physiological Aging in C57BL/6J Mice
  • The role of mitochondrial superoxide anion (O2−) on physiological aging in C57BL/6J mice

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<p>Much 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.

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