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BioMed Research International
Volume 2014, Article ID 140165, 10 pages
Review Article

Superoxide Dismutase 1 Loss Disturbs Intracellular Redox Signaling, Resulting in Global Age-Related Pathological Changes

1Department of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan
2Department of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan
3Department of Orthopaedics, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-0033, Japan

Received 23 April 2014; Revised 29 July 2014; Accepted 6 August 2014; Published 8 September 2014

Academic Editor: Chi-Feng Hung

Copyright © 2014 Kenji Watanabe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aging is characterized by increased oxidative stress, chronic inflammation, and organ dysfunction, which occur in a progressive and irreversible manner. Superoxide dismutase (SOD) serves as a major antioxidant and neutralizes superoxide radicals throughout the body. In vivo studies have demonstrated that copper/zinc superoxide dismutase-deficient (Sod1−/−) mice show various aging-like pathologies, accompanied by augmentation of oxidative damage in organs. We found that antioxidant treatment significantly attenuated the age-related tissue changes and oxidative damage-associated p53 upregulation in Sod1−/− mice. This review will focus on various age-related pathologies caused by the loss of Sod1 and will discuss the molecular mechanisms underlying the pathogenesis in Sod1−/− mice.