title: Telomere shortening is a sole mechanism of aging in mammals.
abstract: We adduce proof that telomere shortening is the sole mechanism of aging. All apparent contradictions, particularly the absence of an inverse correlation between residual telomere length and donor age, are explained within the bounds of telomere theory. We explain in what way telomere shortening might be the cause of aging and lifespan restriction. We also show the inability of the oxidative theory to explain a number of indisputable (and easily explained by telomere theory) facts, such as malignant growth of tumor cells and why children begin aging not from the level reached by the cells of their parents at the moment of conception but from nothing. We postulate that if oxidative damage was entirely absent, telomeres would, nevertheless, shorten with each mitotic cycle because this is the mechanism of DNA replication. Aging would occur all the same, and it is the very thing we can observe under the effect of any antioxidants. If telomeres do not shorten, as is the case in transformed cells in which telomerase is working, aging will do stop and transformed cells will show no senescence. We also observe this in spite of the damaging effect of reactive oxygen species, which is even more intensive in transformed cells than in normal cells.
authors: Institute of Cytology RAS, Russia. mikhels@incras.ru
authors: Victor M
authors: VM
authors: Mikhelson
authors: Irina A
authors: IA
authors: Gamaley
mesh_terms: D000367:Age Factors; D000375:Aging / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D016922:Cellular Senescence; D004249:DNA Damage; D006801:Humans; D008954:Models, Biological; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D016615:Telomere / Q000378:metabolism*; D059506:Telomere Shortening
chemical_list: D017382:Reactive Oxygen Species