Telomere Shortening Is a Sole Mechanism of Aging in Mammals

Victor      M. Mikhelson; Irina      A. Gamaley

doi:10.2174/1874609811205030006

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.

Keywords: Aging mechanism, telomere shortening, mammals, lifespan, DNA repair, oxidative theory of aging, reactive oxygen species (ROS), ageless animals, malignant growth, mitotic cycle