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Biomedical subjects

S K Tandon

Publications and source records attributed to S K Tandon.

At least 55 records · Page 3Linked to original sources
PubMed1989

Chelation of lead during co-exposure to ethanol.

Efficacy of calcium disodium EDTA, D-penicillamine (DPA), 2,3 dimercaptosuccinic acid (DMSA), and alpha-mercapto-beta-(2-furyl) acrylic acid (MFA) to reduce the body burden of lead and restore the altered biochemical variables in lead or lead + ethanol administered rats was investigated. The investigation was aimed to suggest suitable prophylaxis of lead intoxication prevalent among workers co-exposed to lead and alcohol ingestion. Administration of lead (10 mg/kg, oral, once daily for 8 weeks) produced a significant inhibition in the activity of blood delta-aminolevulinic acid dehydratase (ALAD), elevation in the blood zinc protoporphyrin (ZPP) and urinary elimination of lead and delta-aminolevulinic acid (ALA). Lead contents of blood, liver, kidney and brain were also significantly higher than the normal control. The above changes were more marked in animals co-exposed to lead + ethanol (20% in drinking water) compared to lead alone. All the chelators were effective in increasing the urinary lead elimination, reducing the above biochemical alterations and lead contents of tissues. The order of effectiveness being DMSA greater than Calcium disodium EDTA greater than DPA greater than MFA. However, the protection was more noticeable in animals treated with lead alone than with lead and ethanol.

Acrylates↗
PubMed1989

Preventive and therapeutic role of vitamin E in chronic plumbism.

The ability of vitamin E to prevent or treat experimental lead intoxication was investigated in rats. Lead ingestion (10 mg/kg, lead as lead acetate, orally for 6 weeks) significantly inhibited the activity of blood delta-aminolevulinic acid dehydratase (ALAD), reduced the brain dopamine (DA) contents, enhanced the blood zinc protoporphyrin, and enhanced the urinary excretion of delta-aminolevulinic acid (ALA). Lead exposure also elevated brain norepinephrine, homovanillic acid, and 5-hydroxyindole acetic acid (5-HIAA) levels and concentration of lead in blood and tissue. Simultaneous supplementation of vitamin E along with lead significantly reduced the inhibition of blood ALAD activity, brain DA and 5-HIAA levels, and elevation of urinary ALA excretion. Blood and liver lead concentrations were also significantly reduced by simultaneous supplementation with vitamin E. Postlead exposure treatment with vitamin E was ineffective in reducing the lead-induced effects, except that the inhibition of blood ALAD activity was slightly reduced. The present results suggest that vitamin E given simultaneously with lead is effective in reducing the severity of lead intoxication.

Aminolevulinic Acid↗
PubMed1989

Effect of trisodium pentetat on the distribution of cadmium in some body organs & on hepatic metallothionein in rats.

The pre- and post-treatment with calcium trisodium diethylene-triaminepentaacetic acid (CaNa3DTPA) was investigated for their efficacy to mobilize cadmium (Cd) from various tissues and hepatic metallothionein (MT) in Cd-exposed rats. Pretreatment with CaNa3 DTPA significantly reduced the hepatic and renal Cd absorption while, post Cd treatment with CaNa3 DTPA was effective in reducing renal and brain Cd. Pretreatment with CaNa3DTPA significantly increased the Cd induced hepatic metallothionein (MT) level, MT-bound Cd, Zn and Cu contents while, post treatment with CaNa3DTPA reduced the hepatic MT, MT-bound Cd compared to Cd alone treated rats.

Animals↗
PubMed1989

Occupational lead poisoning among silver jewellery workers.

Seven male silver jewellery workers aged between 25 to 70 years complained of acute abdominal colic, sweet metallic taste, constipation and anorexia. Clinical, hematological examinations and urinalysis confirmed lead poisoning. Oral therapy with D-Penicillamine for seven days led to significant improvement in patients.

Adult↗
PubMed1988

Influence of thiamine and ascorbic acid supplementation on the antidotal efficacy of thiol chelators in experimental lead intoxication.

The influence of the administration of thiamine (vitamin B1), ascorbic acid (vitamin C) or their combination on the efficacy of two thiol metal chelators, viz. alpha-mercapto-beta-(2-furyl) acrylic acid (MFA) and 2,3-dimercaptosuccinic acid (DMS), in counteracting lead (Pb) toxicity was investigated in rats. Ascorbic acid or its combination with thiamine enhanced the urinary elimination of Pb, reduced the hepatic and renal burden of Pb, and reversed the Pb-induced inhibition of the activity of blood delta-aminolevulinic acid dehydratase (delta-ALA-D). All these effects were more evident in DMS- than in MFA-treated rats. The combination of MFA and DMS treatments further improved the performance of the animals in enhancing urinary Pb excretion and in reducing Pb hepatic levels.

Animals↗
PubMed1988

Distribution of cadmium in body organs and hepatic metallothionein content following chelation therapy.

1. Calcium trisodium diethylene triamine penta-acetate (CaNa3DTPA), sodium 1,2 diaminocyclohexane tetra-acetate (Na2CDTA), triethylenetetramine hydrochloride (TETA.HCl) and sodium diethyldithiocarbamate (NaDDC) were investigated for their efficacy to mobilize cadmium (Cd) from various tissues and hepatic metallothionein (MT) in Cd-exposed rats. 2. All chelating agents reduced the hepatic Cd burden but did not elicit any influence on other tissues, except that TETA.HCl lowered pancreas Cd and NaDDC increased brain Cd. 3. Cadmium-induced hepatic MT was lowered upon treatment with CaNa3DTPA while it increased further following treatment with NaDDC. 4. The chelating agents, in split doses, are capable of reducing the hepatic burden of Cd and altering the hepatic MT level. 5. While all the chelating agents decreased Cu content of hepatic MT, only CaNa3DTPA decreased its Zn content and TETA.HCl mobilized MT-bound Cd. 6. The administration of chelating agents alone in normal animals showed that NaDDC induced greater hepatic MT synthesis and increased MT-bound Zn than other chelating agents.

Animals↗
PubMed1988

Influence of glibenclamide on the efficacy of calcium trisodium pentetat as an antidote for cadmium toxicity.

Cadmium causes hyperglycemia, activation of hepatic and renal gluconeogenic enzymes such as glucose-6-phosphatase and fructose-1,6-diphosphatase, increases hepatic and renal zinc, renal copper and decreases hepatic and renal iron levels in rats. Glibenclamide, a hypoglycemic agent, significantly reversed most of the Cd effects, enhanced fecal excretion of Cd and potentiated urinary and fecal elimination of Cd by calcium trisodium diethylenetriaminepentaacetate (CaNa3DTPA), a commonly used metal chelator. However, the restoration of Cd-induced alterations in carbohydrate metabolism was not related to elimination of Cd from the tissues.

Animals↗
PubMed1988

Chelation in metal intoxication. XXVII: Chelating agents containing vicinal thioether groups as antidotes of lead toxicity.

The chelating agents containing vicinal thioether groups viz. 4,5-dicarboxy-3,6-dithiaoctanedioic acid (DMSA), disodium-3,6-dithia - 1,8-octanediol-4,5 dicarboxylate (DMES) and 2,9 diamino- 5,6 dicarboxy-4,7 dithiadecanedioic acid (DCSA) were about equally effective but far more effective than pounds-mercapto- beta -(2-thienyl) acrylic acid (MTA) in enhancing excretion of lead, reversing certain Pb induced biochemical alterations and mobilizing tissue Pb in poisoned rats. The results indicate that vicinal thioether groups participate in chelation of Pb. However, none of them could decrease brain Pb. Owing to their water solubility, low toxicity and ability to chelate toxic metals, the chelators with vicinal thioether groups appear as promising antidotes of Pb intoxication.

Animals↗
PubMed1988

Chelation in metal intoxication. XXVIII: Effect of thiochelators on mercury (II) toxicity: pre- and post treatment.

The effect of treatment with alpha-mercapto-beta-(2-furyl)acrylic acid (MFA), N-(N-mercaptopropionyl) glycine (MPG) and N-acetylcysteine (NAC) compared to spironolactone (SPL), a steroid, before and after 203 mercury (II) exposure, on the disposition of Hg and induction of tissue metallothionein (MT), was investigated in rats. The pretreatment with SPL, MFA and MPG enhanced faecal elimination of Hg and reduced its accumulation in liver particularly, the "heat stable fraction" resulting in lowered hepatic MT induction. Neither the renal uptake of Hg nor induction of tissue MT was affected by pre-treatment with the chelating agents; SPL and MFA causing re-distribution of Hg among the renal sub-cellular fractions. The post-Hg exposure treatment with MFA enhanced the faecal and MPG the urinary excretion of Hg. However, both the chelating agents increased the hepatic burden of Hg as reflected in the subcellular fractions and increased MT contents indicating mobilization of Hg from other tissue binding sites. The post-treatment with MPG however, depleted renal Hg as reflected by the sub-cellular distribution, without affecting renal MT levels. The results show that MFA and MPG are more promising preventive than therapeutic agents in Hg intoxication acting as metal chelators.

Acetylcysteine↗
PubMed1987

Effect of combined exposure to lead and ethanol on some biochemical indices in the rat.

We investigated the effect of daily oral administration to young rats of lead (10 mg/kg) and ethanol (10%, v/v, in drinking water), either alone or in combination, for 8 weeks on the uptake of lead in tissues, brain biogenic amines, hepatic alcohol dehydrogenase and cytosolic and mitochondrial aldehyde dehydrogenase and some selected lead-sensitive variables. Lead given in combination with ethanol produced more pronounced inhibition in the activities of hepatic glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) as compared to lead alone treatment. Simultaneous exposure to lead and ethanol produced a greater depression of dopamine (DA) and 5-hydroxytryptamine (5-HT) levels in the whole brain of rats, compared to rats treated with lead alone. The concentrations of lead in blood, liver and brain were significantly higher in rats exposed simultaneously to lead and ethanol. Though ethanol treatment alone inhibited the activities of hepatic alcohol dehydrogenase and cytosolic and mitochondrial aldehyde dehydrogenase, no effect of lead treatment alone on these variables was observed. The results suggested that animals exposed to ethanol and lead are more vulnerable to the neurologic and hepatotoxic effects and the systemic toxicity of lead.

Administration, Oral↗
PubMed1987

Influence of metal chelators on metalloenzymes.

The influence of chelating agents (1 mmol/kg/day X 6,i.p.) on trace metal mobilization and activities of certain metalloenzymes was investigated in rats. Calcium disodium ethylenediamine tetraacetate (CaNa2EDTA) and calcium trisodium diethylenetriamine pentaacetate (CaNa3DTPA) enhanced urinary excretion of Zn, while sodium 2,3-dimercaptopropane-1-sulfonate (NaDMPS) and sodium diethyldithiocarbamate (NaDDC) increased that of Cu. The activity of Zn-metalloenzymes-blood delta-aminolevulinic acid dehydratase (delta-ALA-D), plasma alkaline phosphatase (ALP) and that of Cu-metalloenzyme-plasma amine oxidase was decreased as a consequence of chelation therapy. However, hepatic levels of delta-ALA-D, ALP and alcohol dehydrogenase remained unaffected by chelation. The activity of hepatic Fe-metalloenzyme-catalase was increased by polyaminocarboxylic acids and lowered by thiol chelators. The metal chelators decreased the hepatic glutathione levels.

Alcohol Dehydrogenase↗
PubMed1987

The effects of treatment with selenite before and after the administration of [75Se]selenite on the exhalation of [75Se]dimethylselenide.

The exhalation of dimethylselenium, as indicated by the respiratory loss of 75Se from injected Na75SeO3, depends not only on the dose, but also on previous exposure. Three days pretreatment with 1.2 mumol/100 g unlabelled selenite increased exhalation of 75Se from 0.1 or 1.2 mumol/100 g Na2 75SeO3 and decreased the retention of 75Se in blood and liver from the higher dose. Similarly the injection of 1.2 mumol/100 g unlabelled selenite 24 h after the last of 3 daily doses of 1.2 mumol/100 g labelled selenite increased the exhalation of 75Se in the following 24 h period. Thus, pre-exposure to selenium increased the exhalation of 75Se by making a higher proportion of the newly injected dose accessible for methylation. The exhaled dimethylselenide, however, is not derived solely from the injected dose, since in pretreated animals, it is possible to demonstrate exchange between injected and deposited selenium.

Animals↗
PubMed1987

Chelation in metal intoxication. XXIV: Influence of various components of vitamin B complex on the therapeutic efficacy of disodium calcium versenate in lead intoxication.

The supplementation of vitamin-B complex reduces lead intoxication. With a view to identify the components of vitamin-B complex responsible for such protection, riboflavin, calcium pentothenate, pyridoxine, nicotinamide, folic acid and cyanocobalamine were investigated for their ability, and their influence on the efficacy of disodium calcium versenate (Na2CaEDTA), to enhance the urinary excretion of lead, mobilize tissue lead and restore lead induced biological alterations in lead intoxicated rats. Folic acid and pyridoxine besides thiamine may be the responsible factors in prophylaxis of lead poisoning by vitamin B complex or in enhancing the antidotal properties of Na2CaEDTA.

Aminolevulinic Acid↗
PubMed1987

Chelation in metal intoxication. XXV: Mercaptoacrylic acids as antidotes of lead and nickel toxicity.

beta-1,2-Phenylene di-alpha-mercaptoacrylic acid (1,2-PDMA), beta-1,4-phenylene di-alpha-mercaptoacrylic acid (1,4-PDMA) and alpha-mercapto-beta-(2-hydroxyphenyl) acrylic acid (MHA) were synthesized and compared with 2,3-dimercapto-propane-1-sulfonate (DMPS) for their ability to counteract toxic effects of lead and nickel in rats. 1,2-PDMA and DMPS were most effective in enhancing the excretion of metals, restoring most of the metal induced biochemical alterations and reducing the body burden of the metals; These observations confirm that the chelating agents with two adjacent sulfhydryl groups are better than those with non-adjacent SH groups as metal antidotes. The success of MHA in mobilizing the tissue metals and increasing their urinary excretion indicates participation of the hydroxy group on the benzene nucleus besides the SH group of the MHA molecule, in chelation of the metals.

Acrylates↗
PubMed1987

Effect of combined exposure to cadmium and ethanol on regional brain biogenic amine levels in the rat.

The effect of ethanol ingestion on regional brain biogenic amine levels in cadmium exposed animals was examined. The rats were given either ethanol (1 g/kg, first week, 5 g/kg, second week and 10 g/kg for rest of the weeks) or cadmium (40 ppm in drinking water) or a combination of both for 8 weeks. Simultaneous exposure to cadmium and ethanol produced a greater elevation of norepinephrine in hypothalamus and mid brain when compared with rats receiving only cadmium. A significant elevation of 5-hydroxy-tryptamine in medulla oblongata was also noticed in cadmium and ethanol treated rats compared to cadmium alone treatment animals. The present results suggest industrial workers consuming alcohol may be more susceptible to cadmium neurotoxicity.

Animals↗