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Superoxide is the anion O2. It is important as the product of the one-electron reduction of dioxygen, which occurs widely in nature.[1] With one unpaired electron, the superoxide ion is a free radical, and, like dioxygen, it is paramagnetic.

Synthesis, basic reactions, and structureEdit

Superoxides are compounds in which the oxidation number of oxygen is -1/2. The O-O bond distance in O2 is 1.33 Å, vs. 1.21 Å in O2 and 1.49 Å in O22−.

The salts CsO2, RbO2, KO2, and NaO2 are prepared by the direct reaction of O2 with the respective alkali metal.[2] The overall trend corresponds to a reduction in the bond order from 2 (O2), to 1.5 (O2), to 1 (O22−).

The alkali salts of O2 are orange-yellow in color and quite stable, provided they are kept dry. Upon dissolution of these salts in water, however, the dissolved O2 undergoes disproportionation (dismutation) extremely rapidly:

2 O2 + 2 H2O → O2 + H2O2 + 2 OH

In this process O2 acts as a strong Brønsted base, initially forming HO2. The pKa of its conjugate acid, hydrogen superoxide (HO2, also known as "hydroperoxyl" or "perhydroxy radical"), is 4.88 so that at neutral pH 7 the vast majority of superoxide is in the anionic form, O2.

Salts also decompose in the solid state, but this process requires heating:

2NaO2 → Na2O2 + O2

This reaction is the basis of the use of potassium superoxide as an oxygen source in chemical oxygen generators, such as those used on the space shuttle and on submarines.

Biology and superoxideEdit

Superoxide is biologically quite toxic and is deployed by the immune system to kill invading microorganisms. In phagocytes, superoxide is produced in large quantities by the enzyme NADPH oxidase for use in oxygen-dependent killing mechanisms of invading pathogens. Mutations in the gene coding for the NADPH oxidase cause an immunodeficiency syndrome called chronic granulomatous disease, characterized by extreme susceptibility to infection. Superoxide is also deleteriously produced as a byproduct of mitochondrial respiration (most notably by Complex I and Complex III), as well as several other enzymes, for example xanthine oxidase.

The biological toxicity of superoxide is due to its capacity to inactivate iron-sulfur cluster containing enzymes (which are critical in a wide variety of metabolic pathways), thereby liberating free iron in the cell, which can undergo Fenton chemistry and generate the highly reactive hydroxyl radical. In its HO2 form (hydroperoxyl radical), superoxide can also initiate lipid peroxidation of polyunsaturated fatty acids. It also reacts with carbonyl compounds and halogenated carbons to create toxic peroxy radicals. Superoxide can also react with nitric oxide (NO) to form ONOO. As such, superoxide is one of the main causes of oxidative stress.

Because superoxide is toxic, nearly all organisms living in the presence of oxygen contain isoforms of the superoxide scavenging enzyme, superoxide dismutase, or SOD. SOD is an extremely efficient enzyme; it catalyzes the neutralization of superoxide nearly as fast as the two can diffuse together spontaneously in solution. Genetic inactivation ("knockout") of SOD produces deleterious phenotypes in organisms ranging from bacteria to mice. The latter species dies around 21 days after birth if the mitochondrial variant of SOD (Mn-SOD) is inactivated, and suffers from multiple pathologies, including reduced lifespan, liver cancer, muscle atrophy, cataracts and female infertility when the cytoplasmic (Cu,Zn-SOD) variant is inactivated.

Superoxide may contribute to the pathogenesis of many diseases, and perhaps also to aging via the oxidative damage that it inflicts on cells. In model organisms (yeast, the fruit fly Drosophila and mice), knocking out CuZnSOD shortens lifespan and accelerates certain features of aging, but the converse, increasing the levels of CuZnSOD, does not seem (except in Drosophila), to consistently increase lifespan.


  1. Sawyer, D. T. Superoxide Chemistry, McGraw-Hill, DOI:10.1036/1097-8542.669650
  2. Holleman, A. F.; Wiberg, E. "Inorganic Chemistry" Academic Press: San Diego, 2001. ISBN 0-12-352651-5.

Further readingEdit

  • McCord, J. M.; Fridovich, I. Superoxide dismutase. An enzymic function for erythrocuprein (hemocuprein). J. Biol. Chem. 244:6049-6055.; 1969.
  • Li, Y. et al. Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase. Nat. Genet. 11:376-381; 1995.
  • Elchuri, S. et al. CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life. Oncogene 24:367-380; 2005.
  • Muller, F. L.; et al. Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy. Free Radic. Biol. Med. 40:1993-2004; 2006.
  • Muller, F. L., Lustgarten, M. S., Jang, Y., Richardson, A. and Van Remmen, H. (2007) Trends in oxidative aging theories. Free Radic. Biol. Med. 43, 477-503

See alsoEdit

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