Oxygen-induced mitochondrial damage and aging.
Although the views of Harman and Gerschman provide a reasonable explanation for many of the effects of aging, they fail to explain why many cell types, from amoebae to mammalian spermatogonia, do not show a time-related involution, while other cells (especially the neurons) change with age. We feel that a better understanding of senescence (from the molecular to the organ and organismic levels) can be gained by integrating the free radical theory of aging with the classic concepts of Minot and Pearl on the role of cell differentiation and metabolic rate in, respectively, triggering and pacing senescence. In agreement with the above, we maintain that aging is the non-programmed but unavoidable "side effect" of oxy-radical damage to the membrane and genome of the mitochondria of irreversibly differentiated cells. If oxy-radical damage to mtDNA occurs, it will block the rejuvenation of the mitochondrial population by the process of organelle division, thus leading to bioenergetic decline and cellular death.
Miquel
J
J
Laboratorio de Neurogerontologia, Facultad de Medicina, San Juan, Alicante, Spain.
de Juan
E
E
Sevila
I
I
D000375:Aging / Q000502:physiology*; D000818:Animals; D016922:Cellular Senescence / Q000502:physiology*; D005609:Free Radicals; D006801:Humans; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D013093:Spermatogonia / Q000502:physiology / Q000648:ultrastructure
D005609:Free Radicals