Error Catastrophe Theory
This theory proposes that over time an accumulation of errors in protein synthesis results in impaired cellular function. No biologic process is 100% accurate, and errors in transcription and translation could lead to protein abnormalities. However, most research indicates that transcription and translation continue to function well with advancing age; if this theory were correct, aging would occur at an unchanged pace from birth. Other findings that do not support this theory include evidence that there is (1) no change in amino acid sequence in proteins from young and old animals, (2) no increase in defective tRNAs with age, and (3) no age-related differences in the accuracy of poly(U)-directed protein synthesis. In fact, most alterations of protein found with aging are posttranslational.
Cross-Linking Theory
This theory proposes that the cross-linking of proteins and other cellular macromolecules leads to age-dependent diseases and disorders. Although this theory cannot explain all the changes associated with aging, it may account for some. Extracellular collagen becomes increasingly cross-linked in humans and animals. Although this cross-linking decreases mobility of certain tissues, it does not appear to have a major clinical impact. However, the cross-linking of glycosylated proteins may play an important role in age-dependent opacification in crystalline lens protein and eventual cataract development. Cross-linking between glycosylated immunoglobulins and glomerular basement membrane proteins and between glycosylated lipoproteins and arterial wall proteins has also been proposed as important in the development of age-dependent glomerular and arterial diseases in humans and in animals.
Wear and Tear Theory
This theory proposes that the cumulative damage to vital irreplaceable body parts leads to the death of cells, tissues, organs, and finally the organism. For example, DNA is constantly damaged throughout life, and recent studies indicate the loss of DNA at the ends of chromosomes (telomeres) in certain organisms with aging. If DNA repair is incomplete or age-related impairments in repair mechanisms occur, cellular function might progressively decline. In fact, DNA repair capacity positively correlates with species life span, suggesting a role of efficient DNA repair in the evolution of longevity. However, studies of DNA repair during the aging of experimental animals do not show a consistent decline with aging. (Some studies show a decline; others show no change.) Such studies are complicated by multiple DNA repair mechanisms and uncertainty about which mechanisms are most critical to aging. Further refinement of the techniques for detecting DNA damage may help clarify whether it does accumulate with aging.
Free Radical Theory
Free radicals are highly reactive molecules that can damage membrane proteins, enzymes, and DNA. The most important source of free radicals is oxygen metabolism, which yields the superoxide radical O2¯. Proponents of this theory believe that low-level free-radical damage accumulates over time, resulting in the findings associated with aging. Studies in which various antioxidants were fed to animals found an increase in life expectancy, but in many of these studies antioxidant administration was accompanied by weight loss–a potential confounder because it independently produces a significant increase in life expectancy. However, levels of the naturally occurring cellular antioxidant superoxide dismutase correlate well with life span in primates, supporting this theory. Finally, in some lower forms of life, mutations leading to defects in the production of free-radical-quenching enzymes are also associated with shorter life span.
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