The cadmium toxicity hypothesis of aging: a possible explanation for the zinc deficiency hypothesis of aging.
Although cadmium and zinc have similar chemical properties, they affect living organisms diversely: while zinc is an essential element for growth, development and functioning of all living cells, cadmium is a highly toxic material. Cadmium has an extremely long biological half-life and may be considered a cumulative toxin. It has been shown to have sterilizing, teratogenic and carcinogenic effects and most of these effects could be reduced or even prevented by zinc administration. An increase in cadmium concentration with age has been proven in various species and in different tissues and these facts led some investigators to the assumption that cadmium accumulation might play an important role in senescence. Zinc essentiality and the lack of a reliable index of intracellular zinc status, formed the rationale for the zinc deficiency hypothesis of aging. This hypothesis suggests a gradual time related zinc deficiency occurring in each living cell, making zinc less available for its metalloenzymes. The sum of all deleterious effects resulting from the distorted function of different zinc enzymes, is later manifested as aging processes. When cadmium concentration increases, zinc concentration in various tissues decreases. Cadmium may inhibit zinc activities at many stages, interfering with zinc absorption, distribution to different tissues and transport into cells or into several intracellular structures. Therefore, it is reasonable to assume that a slowly developing cadmium toxicity may result in a gradual time related zinc deficiency.
Bin
Q H
QH
Human Province, Ma-Wang-Dui Sanatorium, Chang Sha, PR China.
Garfinkel
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D
D000375:Aging / Q000378:metabolism*; D000818:Animals; D002104:Cadmium / Q000009:adverse effects* / Q000493:pharmacokinetics / Q000633:toxicity; D002318:Cardiovascular Diseases / Q000139:chemically induced; D002986:Clinical Trials as Topic; D004311:Double-Blind Method; D006207:Half-Life; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects; D008268:Macular Degeneration / Q000517:prevention & control; D009154:Mutation / Q000187:drug effects; D009374:Neoplasms, Experimental / Q000139:chemically induced; D015032:Zinc / Q000172:deficiency / Q000502:physiology* / Q000627:therapeutic use
D002104:Cadmium; D015032:Zinc