Telomere Shortening Is a Sole Mechanism of Aging in Mammals
Victor M. Mikhelson and Irina A. Gamaley
Affiliation: Institute of Cytology RAS, Russia.
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
Rights & PermissionsPrintExport