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Humans repair DNA, for example, more quickly and efficiently than mice or other animals with shorter life spans. This suggests that DNA damage and repair are in some way part of the aging puzzle. In addition, researchers have found defects in DNA repair in people with a familial susceptibility to cancer. If DNA repair processes decline with age while damage accumulates, as scientists hypothesize, it could help explain why cancer is so much more common among older people. Even within a single organism, repair rates can vary among cells, with the most efficient repair going on in sperm and egg cells. Moreover, certain genes are repaired more quickly than others, including those that regulate cell growth.’” Researchers also theorize that the body may possess certain self destructive genes that, when activated at a specific time, cause cells and tissues to waste away. It is theorized that a master gene may cause cells to overwork and then self-destruct. The master gene forces the others to produce abnormal amounts of protein, which slows down replication and other vital cellular activities. “These factors eventually cause organ degeneration and aging,” says researchers at the National Institute on Aging. The process becomes apparent in a comparison of old and young skin cells—although both types contain the same array of genes, in older cells the genes work overtime under the direction of a master gene. A single gene, which affects the production of an enzyme known as helicase, has also been identified as a possible factor in aging. Helicase plays a role in the metabolism and repair of DNA, making it an important player in the body’s ability to repair itself from ongoing damage.” Despite the identification of single genes that influence biological activity, many researchers feel that a group of genes, rather than a single aberrant gene, contribute to the aging process. However, no one knows for sure exactly how many. Out of the body’s total of 100,000 genes, those which influence the aging process may be as few as 100. |
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