interfere with PAH activation and/or binding to DNA, thereby reducing the amount of DNA damage done.
- Rate and accuracy of repair of ultraviolet (UV) light damage to DNA in seven mammalian species’ cultured fibroblasts correlates with maximum species life span. Repair of damage to DNA plays a vital role in retarding aging, although the importance of UV repair to aging is not yet known. Drs. Ronald W. Hart and R. B. Setlow demonstrated a positive correlation between life span and the ability of various species’ fibroblasts (including man’s) to repair UV damage to their
DNA. It is interesting to note that humans live about twice as long as chimpanzees and human DNA repair is about twice as good as that of chimps. Xeroderma pigmentosa is a human genetic (inherited) disease caused by faulty ultraviolet light damage repair. It is a type of progeria (premature aging), not merely a strongly increased tendency to sunburn or contract skin cancer. Figure 3 shows the DNA repair capacity of fibroblasts exposed to ultraviolet light versus life span for a number of mammals, including humans. Man’s much greater
ability to repair DNA correlates with man’s longer life span. The life span increasing effect of a greater DNA repair rate can probably be obtained by a comparable decrease in the DNA damage rate. Our self-administered experimental antioxidant mixture dramatically decreases the damage rate for both ultraviolet light and X-ray damage. In experiments on ourselves, we exhibit a three times greater resistance to both ultraviolet light and X-ray damage as measured by the amount of radiation required for skin erythema (reddening
and burning). - Superoxide dismutase levels: SOD is an important enzyme which protects the body from the serious damage that would otherwise be caused by superoxide free radicals. These oxygen radicals are constantly being produced by normal processes. Life spans of several mammalian species, including man, have been shown to be directly related to their levels of SOD protection. This tends to lend support to the free radical theory of aging (see Part Ti, Chapter 7). This also applies to the other antioxidant enzymes so far studied, such as glutathione peroxidase. SOD is the fifth most abundant protein in our
bodies, after collagen, albumin, globulin, and hemoglobin.
Surprisingly, people who live in cities with high levels of air pollution (such as Pittsburgh, Pennsylvania; Birmingham, Alabama; Newark, New Jersey; Detroit, Michigan; Los Angeles, California; and Cleveland, Ohio) do not have higher rates of cancer than people living in relatively clean cities, such as
San Francisco, California. We and other scientists think that this is so, at least in part, because the presence of the air pollutants (such as ozone, nitrogen oxides, peroxyacetylnitrile, acetaldehyde, etc.) stimulates the body to produce more of protective enzymes, particularly superoxide dismutase.
- The higher the rate of mutation in reproductive cells
(egg and sperm forming), the lower the life span for several
species. This supports the aging clock theory, in which the
clock monitors and counts mutations in reproductive cells and
turns the animal off when the damage becomes so high that
it could no longer make a net positive contribution to the existing numbers of its viable (from the standpoint of being reasonably genetically accurate) offspring.
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