Abstract
Aging is controlled by a complex interplay of both genetic and environmental factors. Because of this, many theories have been advanced that seek to explain the etiology of both cellular and organismal aging (Jazwinski 1996; Holliday 1997). In some cases, these theories are not mutually exclusive. One particularly popular theory posits that free radicals, especially those of molecular oxygen, can accelerate aging (Harman 1986). Martin et al. (1996) have eloquently articulated seven different classes of genetic loci that could modulate aging through oxidative damage. These include, for example, genes that would affect the generation of free radicals and others that modulate the scavenging of free radicals. A third class is those genes that specify repair enzymes. In addition, Cutler (1985) summarized a variety of data that support the notion that oxidative damage impacts aging. These include correlations between either free radical production or defenses against free radicals as compared with aging or life span. For example, the product of the standard metabolic rate and the maximum life span is roughly constant for various animals, indicating that animals with lower standard metabolic rates can live for longer periods than animals with higher rates. This concept, called the LEP (life-span energy potential), strongly suggests that oxygen radicals may exacerbate aging. More directly, the concentration of antioxidants in various mammalian tissues is inversely related to their maximum life-span potential (MLSP).
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