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S K Tandon

Publications and source records attributed to S K Tandon.

At least 19 recordsLinked to original sources
PubMed2003

Reversal of cadmium induced oxidative stress by chelating agent, antioxidant or their combination in rat.

The influence of an antioxidant agent such as N-acetyl cysteine (NAC) or mannitol on the cadmium chelating ability of monoisoamyl 2,3-dimercaptosuccinate (MiADMS) was investigated in cadmium pre-exposed rats. This ester of 2,3-dimercaptosuccinic acid (DMSA), an accepted drug for lead poisoning, being lipophilic in nature was expected to be an efficient cadmium chelator. The treatment of cadmium intoxicated animals with MiADMS reversed cadmium induced increase in blood catalase, superoxide dismutase (SOD) and malondialdehyde (MDA), liver MDA and brain SOD and MDA levels but not the decrease in blood, liver brain reduced glutathione (GSH) and increase in oxidized glutathione (GSSG) levels, consistent with the lowering of tissue cadmium burden. The administration of NAC or mannitol reversed the cadmium induced alterations in blood and liver GSH, GSSG, blood catalase, SOD, MDA, liver SOD, MDA and brain MDA levels without lowering blood and tissue cadmium contents. However, treatments with the combination of MiADMS and NAC or MiADMS and mannitol reversed these alterations as well as reduced blood and tissue cadmium concentrations. The combined treatment with MiADMS and mannitol was better than that with MiADMS and NAC, and was significantly more effective in normalizing blood, liver GSH, GSSG, brain GSSG, and their GSH/GSSG ratios than that by either of them alone. The combined treatments also improved liver and brain endogenous zinc levels, which were decreased due to cadmium toxicity. The results suggest that the administration of an antioxidant during chelation of cadmium may provide beneficial effects by reducing oxidative stress without its cadmium removing ability.

Acetylcysteine↗
PubMed2002

Reversal of lead-induced oxidative stress by chelating agent, antioxidant, or their combination in the rat.

The influence of N-acetyl cysteine (NAC), an antioxidant, on the therapeutic efficacy of meso-2,3-dimercaptosuccinic acid (DMSA), a hydrophilic, and its ester, monoisoamyl 2,3-dimercaptosuccinate (MiADMS), a lipophilic, both soft tissue lead mobilizers, was investigated in lead-preexposed rats. The subsequent treatment of lead-exposed animals with DMSA, MiADMS, or NAC reversed the lead-induced alterations in blood delta-aminolevulinic acid dehydratase, catalase, malondialdehyde (MDA), reduced glutathione, oxidized glutathione, and brain MDA levels. The combined treatment with DMSA and NAC was more effective than that with MiADMS and NAC in enhancing the restoration of all these parameters indicative of lead-induced oxidative stress. These reversals were consistent with the lead-removing ability of DMSA and MiADMS but not that of NAC. As the reversal of these parameters by NAC was independent of its lead-mobilizing capability, this ought to be mainly due to its strong antioxidant property. The increase in blood and brain zinc levels upon lead exposure appears to be the result of the redistribution of endogenous zinc due to lead. Subsequent treatment with DMSA, MiADMS, NAC, or their combination decreased the brain zinc as its excretable complexes with a transient increase in blood zinc level. The ideal treatment of lead poisoning seems to be a combination of a lead chelator and an antioxidant.

Acetylcysteine↗
PubMed2001

Lead poisoning in Indian silver refiners.

The refining of silver from old silver ornaments, articles and jeweller's waste by smelting these with lead scraps for the fabrication of new jewellery is an important small scale industry in India. The present survey and clinical investigations have shown that 31 out of 50 silver refiners with a mean blood lead level of 32.84+/-1.78 microg/dl (range 20.3-64.9), decrease in blood delta-aminolevulinic acid dehydratase (ALAD) activity and thiamine (as pyruvate) level and an enhanced urinary excretion of ALA as compared to control, were suffering from lead poisoning. Most of these workers have shown anaemia, abdominal colic, blue lining of gum and muscular wasting indicative of lead toxicity. Twenty-four workers with relatively high blood lead levels were equally divided into two groups and given either vitamin B1 (75 mg, once a day) or vitamin C (250 mg. twice a day) for 1 month. The treatment with both the vitamins significantly lowered the blood lead levels and reduced blood thiamine and copper deficiency. In addition, vitamin C was also effective in reversing the inhibition of blood ALAD activity while the effect of vitamin B1 on its activity was marginal. The daily intake of vitamin B1 and vitamin C may prevent the accumulation of lead and reduce its toxic effects particularly in those regularly exposed to lead.

Adolescent↗
PubMed2001

Hepatic and renal metallothionein induction by an oral equimolar dose of zinc, cadmium or mercury in mice.

The hepatic and the renal subcellular distribution of zinc, cadmium or mercury and induction of tissue metallothionein (MT) at 24, 48 and 72 h following an oral equimolar dose (15 micro;mol metal/kg) of zinc (II) chloride, cadmium (II) chloride or mercury (II) chloride in male albino mice were investigated. There was a moderate increase in hepatic and renal zinc levels mainly in their nuclear mitochondrial fraction (NMF) 24 h post zinc chloride administration. Subsequently, the hepatic zinc increased and the renal zinc declined with time. The zinc-induced hepatic MT level was maximum at 48 h, which decreased slightly thereafter, while there was no marked increase in renal MT level at any time interval. The cadmium was equally distributed in liver and kidney more in their supernatant cytosol fraction (SCF) than in their NMF at 24 h after a dose of cadmium chloride. The cadmium levels showed a decreasing trend in hepatic fractions and an increasing trend in renal fractions with time. The cadmium-induced hepatic and renal MT were substantial at 24 h post cadmium administration, the former decreased thereafter while the latter enhanced at 48 h before declining. The accumulation of mercury in kidney was 1.5 times that in liver, which was localised more in their SCF than in their NMF at 24 h in response to a dose of mercuric chloride. The mercury levels of hepatic and renal subcellular fractions started declining after 24 h and at 72 h they were significantly lower. The induction of hepatic and renal MT was maximum at 24 h after mercuric chloride administration, which declined thereafter concomitant with the decrease in their mercury levels. However, the MT levels in both the organs remained considerably higher than in normal animals at 72 h post exposure. The results show that the accumulation of metal in liver and kidney follows the order: Hg > Cd > Zn and the induction of MT follows Hg > Cd > Zn in liver and Cd > Hg > Zn in kidney. The alterations in zinc and copper homeostasis were more marked in liver than in kidney and follows the order: Hg > Cd > Zn.

Animals↗
PubMed2000

Effect of thiamine on the cadmium-chelating capacity of thiol compounds.

The influence of thiamine on the efficacy of meso-2,3-dimercaptosuccinic acid (DMSA), diethyldimercapto succinate (DEDMS), alpha mercapto-beta-(2-furyl) acrylic acid (MFA) and alpha-mercapto-beta-(2-thienyl) acrylic acid (MTA) to mobilize cadmium and reverse cadmium-induced biochemical alterations was investigated in cadmium-exposed rats. The thiamine coadministration enhanced the efficacy of MFA and MTA in reducing hepatic and renal burden of cadmium and that of DMSA and DEDMS in mobilizing hepatic cadmium. It also improved the efficacy of DMSA, DEDMS and MFA in reversing the cadmium-induced increase in urinary alkaline phosphatase and aspartate and alanine amino transaminases. The combined treatment with thiamine and DMSA or MFA restricted the urinary loss of zinc and that with thiamine and DEDMS reduced the loss of fecal copper, a general effect of chelation. In conclusion, the administration of thiamine during chelation therapy in cadmium poisoning may be beneficial and more effective than thiol chelating agents alone, which needs to be confirmed in humans.

Acrylates↗
PubMed2000

Chelation in metal intoxication. XLIV: Efficacy of alpha-mercapto-beta-(5-substituted, 2-furyl) acrylic acids in mobilizing intracellularly bound cadmium in rat.

The efficacy of alpha-mercapto-beta-(2-furyl) acrylic acid (MFA), alpha-mercapto-beta-(5-sodiumsulfonate, 2-furyl) acrylic acid (MSFA) and alpha-mercapto-beta-(5-acetoxymethyl, 2-furyl) acrylic acid (MAFA) to mobilize intracellularly bound cadmium in liver and kidney was investigated in rats pre-exposed to cadmium. MFA was effective in reducing cadmium levels of hepatic and renal supernatant cytosolic fraction (SCF) while MSFA and MAFA were effective in lowering cadmium levels of renal SCF and hepatic SCF respectively. All the chelating agents also enhanced the excretion of cadmium more in feces than in urine. However, substitution on the furan ring lowered cadmium mobilizing efficacy of the parent compound, MFA. The treatment with MFA did not affect the status of endogenous zinc and copper while the treatment with MSFA and MAFA enhanced their excretion. MSFA increased hepatic and renal zinc and renal copper while MAFA increased their copper levels.

Acrylates↗
PubMed1998

Efficacy of amphipathic dithiocarbamates in intracellular cadmium mobilization and in modulation of hepatic and renal metallothionein in cadmium pre-exposed rat.

Forty-eight hours after an intraperitoneal injection of cadmium chloride (1.5 mg Cd/kg) to female albino rats, Cd was mainly localized in the hepatic and renal supernatant cytosolic fraction (SCF). Seventy-two hours later, the total hepatic burden remained unchanged but the total renal burden was enhanced, showing its tendency to accumulate in the kidney. A single dose (0.4 mmol/kg, i.p.) of sodium N-benzyl-D-glucamine dithiocarbamate (BG.DTC) or sodium N-(4-methoxybenzyl)-D-glucamine dithiocarbamate (MeO.BG.DTC), 24 h after Cd injection, efficiently mobilized Cd from hepatic SCF, apparently from cadmium-metallothionein (Cd-MT); MeO.BG.DTC also removed Cd from hepatic nuclear mitochondrial fraction. This treatment, however, increased the renal burden of Cd, indicating that the chelating agents, at least partly, transport Cd from the liver and possibly from other sites into the kidney. Three doses of the chelators further enhanced mobilization of Cd from hepatic as well as renal SCF, as corroborated by its enhanced urinary and, to a greater extent, fecal excretion. Hepatic and renal MT were induced several-fold above normal after a single dose of Cd as well as single or repeated doses of BG.DTC or MeO.BG.DTC. Seventy-two hours after a Cd injection, the hepatic MT declined to half of the induced level while the renal MT remained elevated. Administration of BG.DTC or MeO.BG.DTC in Cd pre-treated rats produced an additive response in hepatic MT, but the response in renal MT was less than additive at one dose and slightly declined after three doses. Hepatic Zn and Cu and renal Zn increased on treatment with Cd but were depleted after a single or repeated injection of BG.DTC or MeO.BG.DTC in normal as well as in Cd pre-exposed animals. The results indicate that intracellular access of amphipathic dithiocarbamates effectively mobilizes MT-bound Cd, which is preferentially excreted in the feces, and helps avoid further burden on the kidney and consequent nephrotoxicity. Additionally, MeO.BG.DTC was a better inducer of hepatic MT to help increased capture of toxic metal from the initial circulation and consequent toxicity.

Animals↗
PubMed1998

Mobilization of lead by calcium versenate and dimercaptosuccinate in the rat.

1. Calcium disodium ethylenediaminetetraacetate (CaNa2 EDTA) and meso-2,3-dimercaptosuccinic acid (DMSA) individually and in permutation-combination in various doses (0.1, 0.2 and 0.4 mmol/kg bodyweight) were investigated for their efficacy to mobilize lead from vital tissues into urine and faeces and to restore the lead-sensitive biochemical parameters in lead pre-exposed rats with a view to develop the most acceptable treatment regimen for lead poisoning with a minimal loss of endogenous essential elements. 2. The combined therapy was more effective than a single chelator treatment. 3. The combination of 0.2 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA caused a lower depletion of zinc, calcium and iron but possessed almost equal capability to that of 0.4 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA to produce urinary as well as faecal excretion of lead, to reduce the tissue burden of lead, including that of the brain, and to reverse lead-induced biochemical alterations. 4. The combination of 0.2 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA has shown a definite improvement over previously reported combinations in terms of removal of lead from tissues, particularly the brain, restoration of urinary delta-aminolevulinic acid levels and a decrease in the loss of body zinc and is, therefore, recommended for the treatment of lead intoxication.

Animals↗
PubMed1997

Influence of L-lysine and zinc administration during exposure to lead or lead and ethanol in rats.

Influence of lysine and zinc administration on the lead-sensitive biochemical parameters and the accumulation of lead during exposure to lead or lead and ethanol was investigated in rats. The lead exposure inhibited blood delta-aminolevulinic acid dehydratase (ALAD) activity, increased blood zinc protoporphyrin (ZPP), urinary delta-aminolevulinic acid (ALA), serum glutamic oxalacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), blood and tissue lead levels, and decreased blood and hepatic glutathione (GSH) contents. Some of these effects were enhanced on coexposure to ethanol. The simultaneous administration of lysine and zinc reduced tissue accumulation of lead and most of the lead-induced biochemical alterations irrespective of exposure to lead alone or lead and ethanol. The depletion of endogenous calcium and magnesium owing to lead or ethanol exposure was also prevented by co-administration of lysine and zinc.

Alanine Transaminase↗
PubMed1997

Chelation in metal intoxication LI: efficacy of amphipathic dithiocarbamates in mobilization of lead in the rat.

N-benzyl-D-glucamine dithiocarbamate (BG.DTC) and its analog, N-(4-methoxybenzyl)-D-glucamine dithiocarbamate (MeO-BG.DTC) which are effective chelators of cadmium were investigated for their efficacy to induce excretion of lead, to reduce tissue burden of lead and to reverse certain lead sensitive biochemical alterations in lead pre-exposed rats. These were quite effective in reducing hepatic and renal but not brain lead levels as reflected by the enhanced urinary and fecal excretion of lead and in partially restoring lead inhibited blood delta-aminolevulinic acid dehydratase activity. The introduction of a methoxy group at para-position of benzyl ring, unlike in case of cadmium, did not improve the lead chelating ability of the compound. The treatment with BG.DTC and MeO-BG.DTC caused depletion of endogenous essential elements such as zinc, copper and calcium as evidenced by their enhanced excretion and decreased tissue contents which were more marked in animals treated with the latter.

Animals↗
PubMed1996

Chelation in metal intoxication. XXXVIII: Effect of structurally different chelating agents in treatment of nickel intoxication in rat.

Some structurally different chelating agents viz. alpha-mercapto-beta-(2-furyl) acrylic acid (MFA), alpha-mercapto-beta-(2-thienyl) acrylic acid (MTA), meso 2,3-dimercaptosuccinic acid (DMSA), 2,3-dimercaptopropane-1-sulfonate (DMPS), diethyl dithiocarbamate (DE-DTC), and N-benzyl-D-glucamine dithiocarbamate (NBG-DTC) were evaluated for their efficacy to mobilized nickel and reverse some nickel-induced biochemical alterations in experimental nickel intoxication. MFA, DMSA, and NBG-DTC appear more effective than their corresponding homologs, MTA, DMPS and DE-DTC, respectively, in enhancing urinary and fecal excretion of nickel and lowering tissue burden of nickel in nickel preexposed rats. These, particularly NBG-DTC, appear promising in the treatment of nickel (II) poisoning. However, there seems no definite relationship between the structure of the chelating agents examined and their ability to counteract the effects of nickel.

Acrylates↗
PubMed1995

Influence of vitamin E on preventive or therapeutic effect of MFA and DTPA in cadmium toxicity.

The influence of vitamin E supplementation on the ability of alpha-mercapto-beta(2-furyl) acrylic acid (MFA) or calcium trisodium diethylenetriamine pentaacetate (DTPA) to reduce body burden of cadmium and reverse Cd-induced biochemical alterations was investigated in Cd-exposed rats. The treatment with MFA-vitamin E or CaNa3 DTPA-vitamin E was more effective than either vitamin E or chelating agent alone, in depleting blood and tissue Cd. However, the combined treatment showed only limited advantage over the individuals in restoring Cd-induced biochemical changes. Further, the treatment with chelator-vitamin E concomitantly with the exposure to Cd was more effective than post-Cd exposure treatment.

Acrylates↗
PubMed1994

Influence of dietary iron deficiency on nickel, lead and cadmium intoxication.

The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal, and intestinal metallothionein (MT), disposition of the metals and alterations in hematological parameters, was investigated in young rats to ascertain whether the toxic effects of these metals modify under anemic conditions. The administration of Cd induced hepatic, renal and intestinal MT while that of Ni or Pb induced hepatic MT only. While dietary Fe deficiency did not affect MT induction by Cd, it enhanced the synthesis of renal and intestinal MT by Ni and Pb. The accumulation of Pb in liver and kidney and that of Cd in liver only, were enhanced by Fe deficiency; the tissue deposition of Ni remained unaffected by Fe deficiency. The induction of hepatic MT by Ni, Pb or Cd appears to be related to the concomitant rise in the hepatic Zn, Ca and Fe levels in normal rats. However, dietary Fe deficiency increased the hepatic Zn in response to Ni or Cd and the hepatic Ca in response to Pb administration.

Animals↗
PubMed1994

Distribution and relative prevalence of anophelines in district south 24-Parganas, West Bengal, India.

The anopheline survey of district South 24-Parganas revealed presence of sixteen species including Anopheles annularis, An. subpictus, An. fluviatilis, An. varuna, An. culicifacies and An. sundaicus known to be associated with malaria transmission in the country. A total of 14, 12 and 8 species were encountered in cattlesheds (CS) in contrast to 7, 5 and 4 species in human dwellings (HD) during monsoon, winter and summer respectively. The population density of anophelines in CS was significantly higher than in HD in all the three seasons.

Animals↗
PubMed1994

Influence of methionine and zinc supplementation during chelation of lead in rats.

The influence of methionine and Zn supplementation on the therapeutic efficacy of calcium disodium ethylenediamine tetraacetic acid (CaNa2 EDTA) and 2,3-dimercaptopropane 1-sulphonate (DMPS) in lead intoxication was investigated in rats. The combined treatment with CaNa2 EDTA and methionine +Zn or DMPS and methionine +Zn was more effective than the respective chelator alone in decreasing the blood and tissue burden of Pb and increasing urinary excretion of Pb, with the former combination being more effective than the later. However, simultaneous supplementation of the amino acid and essential trace element did not improve upon the efficacy of the chelator in reversing lead-induced biochemical alterations.

Aminolevulinic Acid↗
PubMed1993

Influence of dietary iron deficiency on acute metal intoxication.

The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal and intestinal metallothionein (MT), disposition of the metals, and alterations in hematological parameters was investigated in rats. The administration of cadmium induced the hepatic, renal and intestinal MT while that of nickel or lead induced hepatic MT only. However, dietary iron deficiency did not influence the cadmium induced tissue MT but enhanced the ability of nickel or lead to restore the normal synthesis of renal and intestinal MT lowered under the influence of reduced body iron status. The accumulation of lead in liver and kidney and that of cadmium enhanced in liver only, while tissue deposition of nickel remained unaffected by iron deficiency. The induction of hepatic MT by three metals appears related to the concomitant rise in the hepatic zinc, calcium and iron levels in normal rats. However, dietary iron deficiency increased the hepatic zinc in response to nickel or cadmium and that of heptic calcium in response to lead.

Animals↗
PubMed1992

Influence of selenium supplementation during chelation of lead in rats.

The influence of selenium supplementation during chelation therapy to reduce body burden and toxicity of lead was investigated in rats. Selenium had marginal effects on liver, kidney and blood lead decorporation by calcium disodium ethylenediamine tetra acetic acid (CaNa2EDTA) and activation of inhibited delta- aminolevulinic acid dehydratase (ALAD) activity by calcium trisodium diethylenetriamine penta acetic acid (CaNa3DTPA). Selenium supplementation however, had no influence on lead induced inhibition of renal and hepatic transaminases and alkaline phosphatase. The results suggest that selenium supplementation slightly augments lead mobilization by chelating drugs.

Administration, Oral↗