Telomere Shortening is the Sole Mechanism of Aging

Abstract

In the paper, we adduce proofs of that telomere shortening is the sole mechanism of aging. All apparent contradictions, primarily, the absence of exact inverse correlation between residual telomere length and the donor age are explained within the frames of the telomere theory. We try to explain in what way telomere shortening might be the cause of aging and life-span restriction. We also show the inability of the oxidative theory to explain a number of indisputable facts easily explained by the telomere theory, such as malignant growth of tumor cells or why a new-born child starts to age from zero level rather than the level reached by the cells of his parents at the moment of conception. We postulate that if oxidative damage was entirely absent telomeres would, nevertheless, shorten with each mitotic cycle because such is the mechanism of DNA replication, and aging would be in progress, which we invariantly observe in the presence of any antioxidants. But if telomeres do not shorten, as happens in transformed cells because telomerase works there, aging does cease and the transformed cells show no senescence. We also observe it in spite of the damaging effect of reactive oxygen species which may be even more intensive than in normal cells.