[A possible molecular mechanism for mammalian aging].
The following model of aging is proposed: 1) defective proteins with anomalous primary structures are synthesized sometimes; 2) these defective proteins are precipitated in cells and intercellular spaces; 3) the precipitated proteins block them up under the influence of radicals; 4) a decrease of cell functional ability below some level results in the destruction of the organism regulation function. A formula is concluded connecting the life span (Tlife) with DNA-repair velocity (Vrep) and time of protein exchange (Tex): Tlife = (1/3).K.(Vper/Vdum).(Tfix + Tex), where K-admitted share of fixated proteins (fixated/native), Vdam-damage velocity, Tfix-fixation time of defective proteins. This analytical dependence was probed on literature data for man, elephant, cow, rabbit, guinea pig, golden hamster, rat, mouse and shrew. Tfix is shown to equal 5 divided by 10 days. A good agreement between the theoretical dependence Tlife(Tex) and literature data was obtained with the exception of the data for man.
Kishchenko
G P
GP
D000375:Aging / Q000235:genetics*; D000818:Animals; D004260:DNA Repair; D008322:Mammals; D008433:Mathematics; D009154:Mutation; D011506:Proteins / Q000235:genetics
D011506:Proteins
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