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Biomedical subjects

S K Tandon

Publications and source records attributed to S K Tandon.

At least 73 records · Page 4Linked to original sources
PubMed1986

The stimulation and inhibition of the exhalation of volatile selenium.

Administration of methylmercury (1.5-24 mumol kg-1; s.c.) to female rats simultaneously with Na2 75SO3 (0.25 or 24 mumol kg-1; s.c.) causes a dose-dependent increase in the exhalation of dimethylselenide. At the low selenite dose level, exhalation of 75Se over a 24 hr period is about fourfold greater after treatment with 24 mumol kg-1 methylmercury than that (approximately 0.75% of the dose) in the controls, but excretion by other routes (urine, faeces) and the liver and kidney contents of 75Se are not affected significantly. At the higher selenite dose level (24 mumol kg-1) exhalation of 75Se is correlated with the log dose of methylmercury. The faecal and urinary excretion remains essentially unaffected, and in rats treated with 24 mumol kg-1 methylmercury the 75Se contents of the liver, kidneys and blood are reduced by 78%, 86% and 18% respectively. The effects of the alkylmercurial are not specific since, at this selenite dose level, ethylmercury increases the exhalation and decreases the liver and kidney contents of 75Se approximately to the same extent as an equimolar dose of methylmercury. In methylmercury-treated and control animals dosed with 24 mumol kg-1 Na 75SeO3 the exhalation of 75Se is inhibited to the same extent by periodate-oxidized adenosine (PAD; 15 mumol kg-1, i.p.) in the first 6 hr. Later inhibition is less pronounced in methylmercury-treated rats. Under these conditions PAD has little effect on the renal content, but increases the hepatic content of 75Se. It seems, therefore, that the methylation of selenite occurs mainly in the liver and in both control and methylmercury-treated animals, S-adenosylmethionine is the major methyl donor. It is possible that methylmercury does not affect directly the methylation enzyme system but, by competition for protein sulphydryl groups, increases the availability of the intermediary selenide anion.

Animals↗
PubMed1986

Chelation in metal intoxication XVIII: Combined effects of thiamine and calcium disodium versenate on lead toxicity.

Calcium disodium ethylenediaminetetraacetate (Ca-Na2EDTA; Versenate) was more effective than thiamine (vitamin B1) in enhancing the urinary excretion of lead, reducing tissue lead and restoring lead induced biochemical alterations in rats. However, the combination of CaNa2EDTA and vitamin B1 enhanced the beneficial effect of CaNa2EDTA in lead intoxication and was particularly effective in reducing the brain concentration of lead.

Animals↗
PubMed1986

Chelation in metal intoxication. XIX. alpha-Mercapto-beta-aryl acrylic acid as antidotes to nickel and lead toxicity.

In view of the reported effectiveness of alpha-mercapto-beta-(2-furyl) acrylic acid (MFA) as an effective antidote to inorganic mercury toxicity, some alpha-mercapto-beta-aryl acrylic acids were synthesized and examined for their efficacy in counteracting nickel and lead intoxication in rats. alpha-mercapto-beta-(3,4-dimethoxyphenyl)acrylic acid (MDA) was most effective and other compounds were less but about equally effective in enhancing urinary excretion and in reducing tissue concentration of Ni. MDA was the only compound to remove Ni from the brain. MFA was also more effective than other structurally related compounds in enhancing urinary and faecal excretion and in lowering body burden of Pb. All the compounds significantly reduced the inhibition of the activity of blood delta-aminolevulinic acid dehydratase (delta-ALA-D) and increase in the urinary excretion of delta-aminolevulinic acid (delta-ALA) caused by Pb. The results do not show any relationship between the nature of the substitution at the beta-position of alpha-mercapto acrylic acids and their ability to reduce the concentration and the toxic effects of the two metals. However, these thiol chelating agents appear promising as antidotes to Ni and Pb poisoning.

Acrylates↗
PubMed1986

Influence of copper and iron on subacute cadmium intoxication in protein-malnourished rats.

Male albino rats maintained on low-protein (9%) diets were dosed intraperitoneally with 0.75 mg Cd/kg, as cadmium chloride, for 20 days. Groups of these animals were provided with diets supplemented with 40 ppm Cu, 400 ppm Fe or a combination of both during the exposure period. Hepatic and renal distribution of Cd, Zn, Cu, and Fe along with activity of acid and alkaline phosphatases and ribonuclease and glutathione content were studied. Uptake of Cd both in liver and in kidney was significant and was accompanied by increased Zn and depletion of Fe concentration. The Cu level remained unaltered. Dietary supplementation of Cu or Fe interacted effectively and influenced the metal distribution. Acid and alkaline phosphatases in both liver and kidney were inhibited by Cd exposure. However, Cu and/or Fe supplements could to a varying degree offset the Cd-induced inhibition. Cadmium exposure did not, however, elicit any effect on hepatic and renal ribonuclease activity of low-protein-fed animals. The glutathione concentration registered profound increase on Cd exposure, possibly to act as a defence mechanism.

Acid Phosphatase↗
PubMed1986

Preventive and therapeutic effects of thiamine, ascorbic acid and their combination in lead intoxication.

Thiamine, ascorbic acid and their combination were investigated for their ability to prevent or treat the experimental lead intoxication in rats. The combination of the two vitamins was most effective in reducing the lead induced inhibition in the activity of blood delta-aminolevulinic acid dehydratase, elevation in the level of blood zinc protoporphyrin and the urinary excretion of delta-aminolevulinic acid and the uptake of lead in blood, liver and kidney. The combined treatment post lead exposure was also most effective in restoring the lead induced biochemical alterations and mobilizing lead from the tissues. The order of effectiveness was, thiamine + ascorbic acid less than ascorbic acid less than thiamine. The lead induced changes in brain biogenic amines and the brain concentration of lead remained unaffected by these vitamins.

Animals↗
PubMed1986

Chelation in metal intoxication. XX: Effect of pre-treatment with chelators on the distribution of mercury.

The effect of pre-treatment with sodium 2,3-dimercaptopropane 1-sulfonate (DMPS), sodium diethyldithiocarbamate (DDC) and calcium trisodium diethylenetriaminepentaacetate (DTPA) on the fate of injected mercuric chloride in rats was investigated. DMPS was the most effective chelator in reducing the uptake of Hg (203) in tissues and was the only chelator to enhance the urinary excretion of Hg (203). The results suggest affinity of Hg towards sulfur moiety and that the protective effects of pre-treatment are also shared by non-steroidal thiol chelators.

Animals↗
PubMed1986

Chelation in metal intoxication. XXIII: Effect of N-(2-mercaptopropionyl) glycine on lead or lead and ethanol intoxicated rats.

Efficacy of N-(2-mercaptopropionyl) glycine to reduce the body burden of lead and restore the altered biochemical parameters in lead or lead and ethanol intoxicated rats was investigated. The investigation was aimed to suggest suitable prophylaxis of lead poisoning prevalent among workers in lead industry who may also be exposed to ethanol. The rats were given lead (10 mg/kg, p.o.) or lead and ethanol (10% v/v in drinking water) daily for 8 weeks. Following exposure period a single dose of N-(2-mercaptopropionyl) glycine (0.3 mmole/kg, intraperitoneal) was given daily for 4 days. The chelator was effective in enhancing the urinary and faecal excretion of lead, reducing the concentration of lead in liver and kidney and lowering the excretion of delta-aminolevulinic acid in lead treated rats. However, the protection was more noticeable in animals treated with lead alone than with lead and ethanol.

Alcoholic Intoxication↗
PubMed1985

Induction of hepatic metallothionein in mouse liver following administration of chelating agents.

Chelating agents commonly used in therapy of heavy metal intoxication alter the levels of essential metals in liver, kidneys, and serum. Induction of metallothionein synthesis in liver occurs following exposure to a variety of chemical and environmental insults and, in some cases, has been attributed to enhanced hepatic uptake of zinc. Therefore, the effect of acute exposure to seven common metal chelators on the concentration of metallothionein in liver was investigated. Adult male Swiss Webster mice were injected intraperitoneally with the chelators and hepatic metallothionein was quantified by the cadmium radioassay. Ethylenediaminetetraacetic acid (EDTA) produced a 5- to 6-fold increase in hepatic metallothionein 24 hr after injection of 0.75 to 3.0 g/kg. No significant increase in hepatic MT was observed until 12 hr following injection of EDTA (1.5 g/kg, ip). Maximal levels were reached between 12 and 48 hr following EDTA injection. Cadmium, a known inducer of hepatic metallothionein, produced a 15-fold increase in the concentration of MT in liver 24 hr following injection. By comparison, 2,3-dimercaptopropanol and diethyldithiocarbamate produced a 9-fold and 13-fold increase in hepatic metallothionein levels, respectively, 24 hr following injection. A 4- to 6-fold increase in metallothionein was observed 24 hr following injection of 2,3-dimercaptosuccinic acid, D,L-penicillamine, diethylenetriaminepentaacetic acid, and EDTA, while nitrilotriacetic acid elevated hepatic metallothionein levels by 2-fold. Alterations in the concentration of hepatic metallothionein by chelators may have implications for their efficacy in the treatment of cadmium intoxication.

Animals↗
PubMed1985

Chelation in metal intoxication. XIV. Comparative effect of thiol and amino chelators on lead-poisoned rats with normal or damaged kidneys.

D-Penicillamine (DPA), diethyldithiocarbamate (DDC), L-cysteine, ethylenediaminetetraacetic acid (EDTA), cyclohexylenediaminetetraacetic acid (CDTA), and diethylene triamine pentaacetic acid (DTPA) were compared for their efficacy to enhance urinary excretion of Pb, to reduce Pb concentration of body organs, and to restore the enhanced urinary excretion of delta-aminolevulinic acid (delta-ALA), the inhibited activities of blood delta-ALA dehydratase, and renal enzymes in Pb-administered rats (10 mg/kg, po, 4 weeks) with normal or experimentally damaged kidneys. The acute renal damage was induced by uranyl acetate (3 mg/kg, sc, once) prior to treatment with the chelators (0.3 mmol/kg, ip, twice) and evaluated by enhanced urinary excretion of diagnostic enzymes and inhibition in their renal activities. Among thiol chelators, DPA was the most effective followed by DDC in enhancing the urinary excretion of Pb, reducing the concentration of Pb in blood, kidneys and liver, and in restoring Pb-induced biological alterations in urine, blood, and kidneys. Among amino carboxylic acids, DTPA was the most effective and EDTA and CDTA were about equally potent in countering Pb toxicity. Protection was more marked in animals with normal kidneys than in those with acutely damaged kidneys.

Alkaline Phosphatase↗
PubMed1985

Chelation in metal intoxication XVII: Antidotal efficacy of polyaminocarboxylic acids on acute chromate toxicity.

Some polyaminocarboxylic acids containing amino and carboxyl groups as metal binding sites in different structural arrangements were evaluated for their relative efficacy in protecting against acute chromate intoxication in mice. Nitrilotriacetic acid (NTA) and 1,2 cyclohexylenediamine tetraacetic acid (CDTA) were most effective in preventing mortality (50-70%) due to a lethal dose of potassium chromate at one-tenth of their respective LD50.

Amino Acids↗