aging

One theory of aging assumes that the life span of a cell or organism is genetically determined—that the genes of an animal contain a “program” that determines its life span just as eye colour is determined genetically. Although long life is recognized often as a familial characteristic, and short-lived strains of fruit flies, rats, and mice can be produced by selective breeding, other factors clearly can significantly alter the basic genetic program of aging.

Another genetic theory of aging assumes that cell death is the result of “errors” introduced in the formation of key proteins, such as enzymes. Slight differences induced in the transmission of information from the deoxyribonucleic acid (DNA) molecules of the chromosomes through ribonucleic (RNA) molecules (the “messenger” substance) to the proper assembly of the large and complex enzyme molecules could result in a molecule of the enzyme that would not “work” properly. These so-called error theories have not yet been firmly established, but studies are in progress.

As cells grow and divide, a small proportion of them undergo mutation; that is, they become “different” with a change in their chromosome structure that is then reproduced when they again divide. The “somatic mutation” theory of aging assumes that aging is due to the gradual accumulation of mutated cells that do not perform normally.