Everyone is familiar with the so-called “annual” plants which live only a few months, from the time when they sprout, until, after the production of seed, death comes to them naturally. … Natural death can be postponed if the plant be prevented from seeding.
—Elie Metchnikoff, The Prolongation of Life (1908)
Do DNA genetic clocks ticking away inside our brains turn off our vital functions so that we grow old and die? Unfortunately, this can occur. Menopause and male pattern baldness are examples. Salmon die soon after spawning as a result of damage triggered by a pituitary gland aging clock in their brains. If the pituitary gland is removed before spawning, the
salmon don’t spawn and they live for many years. The human aging clocks seem to be what limit man to a maximum life span of 110 or so years. We are just beginning to understand how these clocks work.
Some aging events are not random but may be “planned” parts of a genetic (DNA) program. Such events may be under the control of an aging clock or clocks located in the DNA. Clocks exist both at the cellular level and at higher levels (for example, under hormone control).
In 1965, Dr. Leonard Hayflick reported that cultured human WI-38 fibroblasts (fetal connective tissue cells grown atthe Wistar Institute) would divide only about 50 times and then discontinue dividing; dying soon afterwards. He postulated that there is a genetic clock in cells which limits. their number of divisions, thus supporting the theory of a cellular aging clock. Fibroblasts from young humans would divide more times than those from older ones; however, they still divided only about 50 times before discontinuing division. For several years, it was thought that this was an ultimate limit for cell division and that life span was correlated with cell-doubling capacity.
However, recently it has been found at MIT that the keratinocytes (a type of skin cell) can divide 150 times and more if they are supplied with a natural polypeptide hormone called epidermal growth factor (EGF). This hormone is‘very similar to nerve growth factor, NGF. It was also found that the original WI-38 fibroblasts used by Hayflick and others in cell division experiments inadvertently came from a family with a high incidence: of diabetes; it is now known that cells derived from diabetics seem to have a more limited life span than cells from normal individuals. Only the diabet ic-derived cells seem to divide just 50 times. Moreover, mouse tongue epithelium divided 565 times in one study, even though mice have a far shorter life span than humans. Drs. Halliday and Tarrant are investigating the possibility that there is a small population of cells which can divide indefinitely, but that in cell culture techniques these “immortals”
are diluted to a very low level approaching zero by the serial dilution culture techniques usually used. Such indefinitely dividing cells would be used as a store of cells for later differentiation for specific functions and would not be needed in large numbers.
Some familiar higher-level aging clocks are menopause and balding. Note that in women approaching menopause, the incidence of genetic defects in offspring increases rapidly. Such reproductive errors are caused by altered DNA in egg cells in the ovaries, degenerative changes that we believe are
monitored by a clock or clocks that eventually, at a certain level of damage, turn off reproduction. There is some evidence that repair mechanisms which sustain life may also be turned off by this aging clock mechanism to inhibit reproduction. In rats, it has been found that lipofuscin builds up in the Leydig cells of the testis, where testosterone is produced and released to stimulate mating behavior. On the other hand, no lipofuscin is found in the spermatagonia cells of the rat testis,
Where the DNA-containing sperm is produced. This may indicate that the sperm-making tract has considerable protection against oxidative processes which would otherwise cause lipofuscin buildup, but that the testosterone-producing cells do not have such good protection. Such a process would as-
sure that the clock monitoring mutations will turn off the testosterone (and, as a result, mating behavior) before a high level of damage is found in the sperm genetic (DNA) material.
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