Oxidants, Antioxidants, and the Degenerative Diseases of Aging

Metabolism, like other aspects of life, involves trade-offs. Oxidant by-products of normal metabolism cause extensive damage to DNA, protein, and lipid. We argue that this damage (the same as that produced by radiation) is a major contributor to aging and to degenerative diseases of aging such as cancer, cardiovascular disease, immune system decline, brain dysfunction and cataracts. Antioxidant defenses against this damage include ascorbate, tocopherol and carotenoids. Fruits and vegetables are the principal source of ascorbate and carotenoids and are one source of tocopherol. Low dietary intake of fruits and vegetables doubles the risk of most types of cancer as compared to high intake and also markedly increases the risk of heart disease and cataracts. Since only 9% of Americans eat the recommended five servings of fruits and vegetables per day the opportunity for improving health by improving diet is great.

The degenerative diseases associated with aging include cancer, cardiovascular disease, immune system decline, brain dysfunction, and cataracts. The functional degeneration of somatic cells during aging appears, in good part, to contribute to these diseases. The relationship between cancer and age in various mammalian species illustrates this point. Cancer increases with about the fifth power of age in both short-lived species, such as rats, and in long-lived species, such as humans.

Thus a marked decrease in age-specific cancer rates has accompanied the marked increase in life span that has occurred in 60 million years of mammalian evolution: i.e., cancer rates are high in a two year old rat, but low in a two year old human. One important factor in longevity appears to be basal metabolic rate, which is about seven times higher in a rat than a human and which could markedly affect the level of endogenous oxidants and other mutagens produced as by-products of metabolism. The level of oxidative DNA damage appears to be roughly related to metabolic rate in a number of mammalian species (cancer/mutation/endogenous DNA adducts/oxygen radicals)

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By Bruce N. Ames*, Mark K. Shigenaga, and Tory M. Hagen