A superoxide, also known by the obsolete name hyperoxide, is a compound that possesses the superoxide anion with the chemical formula O2−. The systematic name of the anion is dioxide(1−). It is important as the product of the one-electron reduction of dioxygen O2, which occurs widely in nature. With one unpaired electron, the superoxide ion is a free radical, and, like dioxygen, it is paramagnetic.
The salts CsO2, RbO2, KO2, and NaO2 are prepared by the direct reaction of O2 with the respective alkali metal. 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 Brønsted base, initially forming the radical HO2·. But 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:
- 2 NaO2 → 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. Superoxides are also used in firefighters' oxygen tanks in order to provide a readily available source of oxygen.
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, especially catalase positive organisms. In turn, micro-organisms genetically engineered to lack superoxide dismutase (SOD), lose virulence. 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.
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. Other proteins, which can be both oxidized and reduced by superoxide, have weak SOD-like activity (e.g. hemoglobin). Genetic inactivation ("knockout") of SOD produces deleterious phenotypes in organisms ranging from bacteria to mice and have provided important clues as to the mechanisms of toxicity of superoxide in vivo.
Yeast lacking both mitochondrial and cytosolic SOD grow very poorly in air, but quite well under anaerobic conditions. Absence of cytosolic SOD causes a dramatic increase in mutagenesis and genomic instability. Mice lacking mitochondrial SOD (MnSOD) die around 21 days after birth due to neurodegeneration, cardiomyopathy and lactic acidosis. Mice lacking cytosolic SOD (CuZnSOD) are viable but suffer from multiple pathologies, including reduced lifespan, liver cancer, muscle atrophy, cataracts, thymic involution, haemolytic anemia and a very rapid age-dependent decline in female fertility.
Superoxide may contribute to the pathogenesis of many diseases (the evidence is particularly strong for radiation poisoning and hyperoxic injury), and perhaps also to aging via the oxidative damage that it inflicts on cells. While the action of superoxide in the pathogenesis of some conditions is strong, for instance, mice and rats overexpressing CuZnSOD or MnSOD are more resistant to strokes and heart attacks, the role of superoxide in aging must be regarded as unproven for now. In model organisms (yeast, the fruit fly Drosophila and mice), genetically knocking out CuZnSOD shortens lifespan and accelerates certain features of aging (cataracts, muscle atrophy, macular degeneration, thymic involution), but the converse, increasing the levels of CuZnSOD, does not seem (except perhaps in Drosophila), to consistently increase lifespan. The most widely accepted view is that oxidative damage (derived amongst other factors, from superoxide) is but one of several factors limiting lifespan.
- Ozonide, O3−
- Peroxide, O22−
- Oxide, O2−
- Dioxygenyl, O2+
- Antimycin A - used in fishery management, this compound produces large quantities of this free radical.
- Paraquat - used as an herbicide, this compound produces large quantities of this free radical.
- ^ IUPAC: Red Book. p. 73 and 320.
- ^ Sawyer, D. T. Superoxide Chemistry, McGraw-Hill, doi:10.1036/1097-8542.669650
- ^ Holleman, A. F.; Wiberg, E. "Inorganic Chemistry" Academic Press: San Diego, 2001. ISBN 0-12-352651-5.
- ^ a b 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 (4): 477–503. doi:10.1016/j.freeradbiomed.2007.03.034. PMID 17640558.
- ^ a b 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
Wikimedia Foundation. 2010.