The free radical theory of aging (FRTA) states that organisms age because cells accumulate free radical damage over time.[1] A free radical is any atom or molecule that has a single unpaired electron in an outer shell.[2] While a few free radicals such as melanin are not chemically reactive, most biologically-relevant free radicals are highly reactive.[3] For most biological structures, free radical damage is closely associated with oxidative damage. Antioxidants are reducing agents, and limit oxidative damage to biological structures by passivating them from free radicals.[4]
Strictly speaking, the free radical theory is only concerned with free radicals such as superoxide ( O2- ), but it has since been expanded to encompass oxidative damage from other reactive oxygen species such as hydrogen peroxide (H2O2), or peroxynitrite (OONO-).[4]
Denham Harman first proposed the free radical theory of aging in the 1950s,[5] and in the 1970s extended the idea to implicate mitochondrial production of reactive oxygen species.[6]
In some model organisms, such as yeast and Drosophila, there is evidence that reducing oxidative damage can extend lifespan.[7] In mice, interventions that enhance oxidative damage generally shorten lifespan.[8] However, in roundworms (Caenorhabditis elegans), blocking the production of the naturally occurring antioxidant superoxide dismutasehas recently been shown to increase lifespan.[9] Whether reducing oxidative damage below normal levels is sufficient to extend lifespan remains an open and controversial question.
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