Free Radical Theory Of Aging

1.2 THEORIES OF AGING

The major theories of aging are all specific of a particular cause of aging, providing useful and important insights for the understanding of physiological changes occurring with aging. The search for a single cause of aging has recently been replaced by the view of aging as an extremely complex, multifactorial process. In fact, it is very likely that several processes simultaneously interact and operate at different levels of functional organization. It is difficult to decipher a single cause of aging per se. Rather, it is caused due to an amalgamation of different individual processes ultimately leading to death ; current theories either expound on the damage concept, wherein the accumulation of damage (viz., DNA breaks

It was formulated in 1950s by Harman who hypothesized a single common process, modifiable by genetic and environmental factors, in which the accumulation of endogenous oxygen radicals generated in cells could be responsible for the aging and death of all living beings (Harman 1957, Finkel and Holbrook 1971). It was revised in 1972 after the knjnnjnjnjNFormation of free-radicals formulation of the mitochondrial theory of aging gfytfytfytfyufyugyugyugughiuhiuhiuhiuhiuhiuhi since mitochondria is responsible for the production of most of these free radicals which are required in regulated

For example, it has been hypothesized that mutations in mitochondrial DNA accelerate free radical damage by introducing altered enzyme components into the electron transport chain. Faulty electron transport consequently results in elevated free radical leakage and ultimately more mitochondrial DNA mutation and exacerbated oxidant production. This vicious cycle of mutation and oxidant production may then eventually lead to cellular/organ failure, and senescence (Mandavilli et al 2002). Another hypothesis argues that free radicals cause aging because of the accumulation of oxidized proteins in cells. The age-dependent reduction in the capacity of degradation of oxidized proteins may be responsible for the build-up of damaged, dysfunctional molecules in the cell (Shringarpure and Davies 2002). It has been suggested that oxidative damage may be an important source of somatic mutations at the basis of the so-called “somatic mutation theory of aging”. This theory hypothesizes that the accumulation of genetic mutations in somatic cells represents the specific cause of senescence (Beckman and Ames