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Superoxide dismutase (SOD, EC 1.15.1.1) is an enzyme that alternately catalyzes the dismutation (or partitioning) of the superoxide (O − 2) anion radical into normal molecular oxygen (O 2) and hydrogen peroxide (H 2 O 2). Superoxide is produced as a by-product of oxygen metabolism and, if not regulated, causes many types of cell damage. [2]
Superoxide dismutase 2, mitochondrial (SOD2), also known as manganese-dependent superoxide dismutase (MnSOD), is an enzyme which in humans is encoded by the SOD2 gene on chromosome 6. [5] [6] A related pseudogene has been identified on chromosome 1. Alternative splicing of this gene results in multiple transcript variants. [5]
SOD1 binds copper and zinc ions and is one of three superoxide dismutases responsible for destroying free superoxide radicals in the body. The encoded isozyme is a soluble cytoplasmic and mitochondrial intermembrane space protein, acting as a homodimer to convert naturally occurring, but harmful, superoxide radicals to molecular oxygen and hydrogen peroxide.
Chronic granulomatous disease (CGD), also known as Bridges–Good syndrome, chronic granulomatous disorder, and Quie syndrome, [1] is a diverse group of hereditary diseases in which certain cells of the immune system have difficulty forming the reactive oxygen compounds (most importantly the superoxide radical due to defective phagocyte NADPH oxidase) used to kill certain ingested pathogens. [2]
Copper deficiency, or hypocupremia, is defined as insufficient copper to meet the body's needs, or as a serum copper level below the normal range. [1] Symptoms may include fatigue , decreased red blood cells , early greying of the hair, and neurological problems presenting as numbness , tingling, muscle weakness, and ataxia . [ 2 ]
Competing with its formation, superoxide is destroyed by the action of superoxide dismutases, enzymes that catalyze its disproportionation: 2 O − 2 + 2H + → O 2 + H 2 O 2. hydrogen peroxide (H 2 O 2) is also produced as a side product of respiration. [4] Peroxynitrite (ONO − 2) results from the reaction of superoxide and nitric oxide.
Manganese superoxide dismutase (MnSOD) is the principal antioxidant in mitochondria. Several enzymes activated by manganese contribute to the metabolism of carbohydrates, amino acids, and cholesterol. [2] A deficiency of manganese causes skeletal deformation in animals and inhibits the production of collagen in wound healing. [3]
Subsequently, superoxide is quickly dismutated to hydrogen peroxide by two dismutases including superoxide dismutase 2 (SOD2) in mitochondrial matrix and superoxide dismutase 1 (SOD1) in mitochondrial intermembrane space. Collectively, both superoxide and hydrogen peroxide generated in this process are considered as mitochondrial ROS. [1]