Essential metal co-ordination in biochemistry.
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Biomedical subjects
Publications and source records attributed to S K Tandon.
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The influence of one, three, and six doses of ethylenediaminetetraacetic acid (EDTA), diethylenetriaminepentaacetic acid (DTPA), and triethylenetetramine (TETA) on the urinary excretion of Ca, Cu, Fe, and Zn, and on their levels in liver, kidneys, heart, and serum in rats, was investigated to ascertain their suitability in amelioration of metal intoxication. While excretion of all the essential trace metals examined was enhanced significantly, the tissue and serum levels of some of them either increased or decreased after administration of the chelators. The results suggest depletion of some of the endogenous trace metals from the body and their intertissue redistribution following treatment with these chelating agents.
Administration of zinc (Zn) simultaneously with lead (Pb) into the chick egg yolk sac reduced the accumulation of Pb and Pb-induced alterations in the activities of acid phosphatase, beta-glucuronidase and ribonuclease in the brain of the embryo. The results suggest protection against toxic effects of Pb by Zn.
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Pretreatment with nickel has earlier been shown to protect against cadmium intoxication. The effect of cadmium pretreatment on the nephro- and hepatotoxicity of nickel has been investigated. The administration of cadmium (6 mg/kg, i.m., once) to rats significantly enhanced urinary excretion of ALP, LDH, GOT, amino acids and proteins and increased the activity of serum ALP, GOT, and GPT, while the administration of nickel (6 mg/kg, i.p., 3 days) altered these parameters less significantly. These changes in urine and serum were used as a measure of renal and hepatic damage. The administration of nickel for three days, one week after cadmium treatment, caused significantly more marked enzymuria, aminoaciduria, proteinuria and an increase in the activity of serum enzymes than induced by either of them individually. However, cadmium pretreatment had no influence on urinary excretion or hepatic uptake of nickel, but increased renal uptake of nickel on the fourth day. The results suggest that cadmium enhances the nephro- and hepatotoxicity of nickel.
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The administration of selenium concomitantly with lead in rats restrained the lead induced enzymuria, proteinuria, enhanced urinary excretion of delta-aminolevulinic acid, inhibition of the activities of certain renal enzymes, blood delta-aminolevulinic acid dehydratase and blood, liver and kidney uptake of lead. The protective effect of selenium against lead toxicity may be attributed to a competition between selenium and lead for binding with the functional bioligands or to the in vivo formation of lead selenide.
Influence of 2,3 dimercaptosuccinic acid, diethyldithiocarbamate and DL-penicillamine on the levels of essential metals in liver, kidney and serum was investigated. The hepatic zinc increased while renal copper decreased significantly upon treatment with these commonly used thiol metal chelators. On the other hand, hepatic copper decreased on treatment with DL-penicillamine. The renal zinc and serum copper and zinc remained practically unaffected on treatment with these metal chelators.
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