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Abstract
The free radical theory proposes that ageing is the cumulative result of oxidative
damage to the cells and tissues of the body that arises primarily as a result of aerobic
metabolism. Several lines of evidence have been used to support this hypothesis including
the claims that: (1) variation in species life span is correlated with metabolic rate
and protective antioxidant activity; (2) enhanced expression of antioxidative enzymes
in experimental animals can produce a significant increase in longevity; (3) cellular
levels of free radical damage increases with age; and (4) reduced calorie intake leads
to a decline in the production of reactive oxygen species and an increase in life
span. The free radical theory may also be used to explain many of the structural features
that develop with ageing including the lipid peroxidation of membranes, formation
of age pigments, cross-linkage of proteins, DNA damage and decline of mitochondrial
function. Despite this, many uncertainties concerning the role of oxidative damage
in ageing remain and alternative explanations cannot be ruled out. Free radicals only
occur in trace quantities in biological tissues, their cellular levels and actions
cannot be measured in vivo, and definitive proof that oxidised molecules are the primary
cause of ageing is lacking. Moreover, ageing is also likely to be a multifactorial
process and not reducible to any one single cause. Thus, despite its positive features,
the evidence for the free radical theory is either correlative or inconclusive.