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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.

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