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Biomedical subjects

S K Tandon

Publications and source records attributed to S K Tandon.

At least 37 records · Page 2Linked to original sources
PubMed1992

Preventive effect of vitamin E in cadmium intoxication.

The influence of vitamin E on cadmium intoxication was investigated in rats. The exposure to cadmium (1 mg/kg, Cd as CdCl2.2H2O, intraperitoneally for 7 days) decreased the activity of hepatic and renal glutamic oxalacetic and glutamic pyruvic transaminases (GOT, GPT) and alkaline phosphatase (ALP) accompanied by increase in the levels of serum GOT and GPT and urinary protein. Simultaneous administration of vitamin E (5 mg/kg, intramuscularly for 7 days) reduced these Cd induced biochemical alterations. The accumulation of Cd in blood, liver and kidney also decreased significantly upon co-exposure to vitamin E. The antioxidant property of vitamin E seems to be responsible for the observed protection of Cd intoxication.

Alanine Transaminase↗
PubMed1991

Biochemical response to cadmium. Dose-time effect.

Dose- and time-related effects of Cd (II) (0.5 or 1.0 mg/kg, Cd as CdCl2.H2O, subcutaneously, daily for 48 h, 1, 3, or 6 wk) were investigated in rats. A dose-related increase in the activity of plasma alkaline phosphatase (ALP), lactate dehydrogenase (LDH), aspartate aminotransferase (GOT), and alanine aminotransferase (GPT) was evident only at 6 wk, whereas an early rise in ALP and LDH was seen at 3 wk in 1.0 mg Cd group only. The hepatic and renal metallothionein (MT) induction displayed a dose- as well as time-related increase with Cd accumulation. A significant increase in hepatic Zn and renal Cu, no change in hepatic Cu, and a slight increase in renal Zn was observed. Urinary ALP and leucine aminopeptidase (LAP) showed an initial increase at 48 h, thereafter returned to near normal. A second phase of enzymuria (ALP, LAP, GOT, GPT, gamma-glutamyl transpeptidase), proteinuria, and aminoaciduria occurred at 6 wk in a dose-related manner. The urinary excretion of specific renal enzymes appeared closely related to the MT induction and organ Cd levels.

Alanine Transaminase↗
PubMed1991

Chelation in metal intoxication. XXXIV. Mixed ligand chelation in lead poisoning.

The effectiveness of alpha-mercapto-beta-(2-furyl)acrylic acid (MFA) and N-benzyl-N-dithiocarboxy-D-glucamine (NaB), used in combination, in the mobilization and excretion of lead was investigated in rats. Male Wistar rats received 10 mg Pb/kg as lead acetate intragastrically daily for 6 weeks. The lead-exposed rats were treated with either MFA or NaB or both 200 mumol/kg i.p., each, daily for 3 days. Both chelating agents provoked significant urinary and faecal excretion and lowered the soft-organ lead burden. However, combined therapy did not elicit any additive or synergistic response.

Acrylates↗
PubMed1991

Effects of combined exposure to aluminium and ethanol on aluminium body burden and some neuronal, hepatic and haematopoietic biochemical variables in the rat.

The effects of the daily administration of aluminium (25 mg kg-1, orally), ethanol (10% v/v, in drinking water) or both to adult rats, for 6 weeks, on the amount of aluminium present in the tissues and the functioning of brain biogenic amines, hepatic and serum transaminases and some haematopoietic variables were investigated. Ethanol alone was seen to inhibit the activity of delta-aminolevulinic acid dehydratase (ALAD), while aluminium alone elevated the activity of blood ALAD. However, aluminium and ethanol combined produced a more pronounced inhibition of blood ALAD and hepatic glutamic pyruvic transaminase (GPT) than either aluminium or ethanol alone. Simultaneous exposure to aluminium and ethanol also produced a significant elevation in urinary delta-aminolevulinic acid (ALA) blood zinc protoporphyrin (ZPP), serum glutamic oxaloacetic transaminase (GOT) and brain homovanillic acid (HVA), and a depletion in brain dopamine (DA) and 5-hydroxytryptamine (5-HT) levels, when compared to rats given aluminium alone. The concentration of aluminium in the blood and liver was significantly higher in rats exposed to both aluminium and ethanol than in those exposed to aluminium alone. Thus the consumption of alcohol may increase the rat's susceptibility to certain effects of aluminium.

Administration, Oral↗
PubMed1991

Time related influence of alpha-mercapto-beta-(2-furyl)acrylic acid (MFA) in cadmium toxicity.

The effect of alpha-mercapto-beta-(2-furyl) acrylic acid (MFA, 200 mg/kg, oral) administered 30 min or 24 h post cadmium (1 mg/kg, i.p.) exposure on cadmium toxicity, was investigated in rats. The Cd induced hepatic metallothionein was reduced by MFA treatment parallel to the depletion of hepatic Cd. However, in renal tissue, MFA caused only redistribution of metal from the particulate to the soluble fraction. Hepatic and renal Zn and renal Cu were significantly increased on Cd exposure. MFA therapy, however, lowered the hepatic Zn and increased the renal Cu levels. The action of MFA appears to be via metal chelation rather than by MT induction.

Acrylates↗
PubMed1991

Chelation in metal intoxication. XXXVI: Effect of substituted piperazine dithiocarbamates in lead-exposed rats.

Chelation is most acceptable means of managing heavy metal poisoning. Piperazine hexahydrate dithiocarbamate (PHD), N-methyl piperazine dithiocarbamate (MPD), N-3-chloro-phenyl piperazine dithiocarbamate (CPD), and N-benzyl piperazine dithiocarbamate (BPD) were investigated for their efficacies to mobilize lead and restore Pb-induced hematopoietic alterations in experimentally intoxicated rats. MPD and CPD were effective in enhancing the urinary excretion of Pb. While PHD and MPD were successful in lowering hepatic Pb, CPD, and BPD were effective in doing so from renal tissue. All the chelating agents decreased the blood level of Pb. The lowering of Pb body burden had no influence on the restoration of biochemical changes which indicates that the latter may not be directly related to the metal mobilizing potential of the chelating agents. None of the compounds caused excessive depletion of body Cu or Zn. No relationship between efficacies of the chelating agents and their structures was seen. However, MPD and CPD appeared to be promising antidotes of Pb poisoning.

Animals↗
PubMed1990

Nickel-selenium interaction-time dependent biochemical alterations and metal decorporation in rats.

The influence of selenium on the disposition of nickel and on Ni induced metallothionein levels was studied in female rats. Concomitant administration of Se (6.3 mumol/kg, intraperitoneally) and 63Ni (0.12 mmol/kg subcutaneously) lowered the Ni burden of all the soft organs and the plasma ceruloplasmin levels. Selenium caused no potentiating effect on the Ni induced hepatic MT. However, 3 days later, the lowered MT levels appeared related to the corresponding decrease in hepatic Ni content at day 6. The Ni selenide excretable complex and Ni-selenide protein complex appear to be probable mechanisms of the Ni-Se interaction in the present study.

Animals↗
PubMed1990

Beneficial effects of zinc supplementation during chelation treatment of lead intoxication in rats.

The ability of zinc to enhance the efficacy of commonly used chelating drugs in lead intoxication and to reduce the resulting zinc imbalance, was investigated in rats. The simultaneous zinc supplementation increased urinary lead elimination by calcium disodium ethylenediaminetetraacetate (Ca disodium EDTA) and 2,3 dimercaptosuccinic acid (DMSA). Combination therapy was also effective in potentiating the depletion of blood, hepatic and renal lead by calcium disodium EDTA and D-penicillamine (DPA), renal lead by DMSA and reversal of inhibited blood delta-aminolevulinic acid dehydratase (ALAD) activity by calcium disodium EDTA and DPA. The body zinc status was also maintained as reflected by urinary, blood and tissue levels of zinc.

Acetates↗
PubMed1990

The lead-chelating effects of substituted dithiocarbamates.

The effectiveness of certain substituted dithiocarbamates in mobilizing lead from preexposed rats was investigated. The animals received 10 mg Pb/kg/day, intragastrically, for 8 weeks and were treated thereafter with 400 mumol/kg, intraperitoneally, of morpholine dithiocarbamate, tetraammonium ethylenediamine diacetic acid dithiocarbamate (EDDTC), ammonium diethanolamine dithiocarbamate (ADDTC), sodium diethyldithiocarbamate, N-benzyl-D-glucamine dithiocarbamate (NBGDTC), or dimercaptosuccinic acid, daily for 5 days. All the chelating agents were effective in lowering the hepatic and renal burden of Pb. ADDTC, EDDTC, and NBGDTC were also able to lower the long bone Pb content. The lowering of Pb burden had no relationship to restoration of Pb-induced hematopoietic alterations. The relatively lower lipophilicity of substituted dithiocarbamates, owing to the presence of hydrophilic groups, seems to be advantageous in preventing passage of metal chelate into the brain. None of the substituted dithiocarbamates caused excessive excretion of urinary Cu and Zn. ADDTC and EDDTC appear to be promising in the management of Pb poisoning.

Animals↗
PubMed1989

Dose and time effects of combined exposure to lead and ethanol on lead body burden and some neuronal, hepatic and haematopoietic biochemical indices in the rat.

Ethanol (1, 2 or 5 g kg-1) and lead (0.55 g l-1 in drinking water) were given either alone or in combination for 4 months to rats. The uptake of lead in tissues, some lead-sensitive variables, the levels of biogenic amines in different brain regions, hepatic lipid peroxidation, glycogen and blood glucose concentrations were measured. Ethanol or lead when given alone inhibited the activity of blood delta-aminolevulinic acid dehydratase (ALAD). The co-administration of 5 g kg-1 but not 1 or 2 g kg-1 ethanol significantly enhanced the lead-induced inhibition of blood delta-ALAD activity and the elevation of delta-aminolevulinic acid (ALA) excretion. Co-exposure to lead and ethanol (5 g kg-1) produced a more pronounced increase in hepatic lipid peroxidation and blood glucose level than either ethanol or lead alone. This combination also caused a significant increase in the dopamine (DA) contents of striatum, midbrain and pons medulla, norepinephrine (NE) contents in midbrain and 5-hydroxytryptamine (5-HT) contents of hypothalamus, striatum, midbrain and pons medulla over levels produced by lead alone. However, the level of NE in hypothalamus decreased upon co-administration. The uptake and retention of lead was significantly higher in blood, liver, kidney and brain in animals co-exposed to lead and 5 g kg-1 ethanol. Blood and kidney lead was also increased by 2 g kg-1 ethanol. The results suggest that prolonged and heavy consumption of alcohol may increase the toxicity of lead.

Animals↗
PubMed1989

Interrelationship between iron deficiency and lead intoxication (Part 1).

The influence of lead exposure, iron deficiency, or their combination on certain biochemical parameters in blood, plasma, and urine of rats was investigated in an attempt to identify the specific diagnostic tests of the two conditions and to draw a possible interrelationship between the two factors. The decrease in blood-glutathione peroxidase activity, -packed cell volume, plasma-ceruloplasmin, and-Fe levels and increase in urinary excretion of delta-aminolevulinic acid, plasma-cholesterol, and-total Fe binding capacity occur under Fe deficiency as well as Pb intoxication. However, increase in the activity of blood delta-aminolevulinic acid dehydratase (ALAD) without any change in blood zinc protoporphyrin (ZPP) level appears to be a specific effect of Fe deficiency that could be distinguished from Pb intoxication, a condition characterized by the inhibition in blood ALAD activity accompanied by an increase in blood ZPP level. The linear regression analysis of the data showed that the blood Pb and plasma free cholesterol levels increase with the decrease in plasma Fe level.

Animals↗
PubMed1989

Interrelationship between iron deficiency and lead intoxication (Part 2).

The influence of dietary iron deficiency, lead exposure or their combination on certain enzymes, and the accumulation of Pb and essential metal levels in vital organs of rats was investigated. Iron deficiency caused alterations in the activity of muscle, hepatic and renal succinate dehydrogenase, and hepatic mitochondrial succinate cytochrome c reductase, whereas Pb exposure had no influence on these enzymes. There was no synergistic effect of the two factors on the activity of the enzymes. However, feeding of a Fe-deficient diet during Pb exposure enhanced the accumulation of Pb in soft tissues and flat bones. The hepatic copper and zinc levels were lowered upon either feeding a Fe-deficient diet or Pb exposure. However, the synergistic effect of the two factors was evident in hepatic Cu, but not in hepatic Zn. The feeding of a Fe-deficient diet decreased liver, kidney, and spleen levels of Fe, whereas Pb exposure decreased kidney and spleen Fe. The synergistic influence of the two factors could be observed only in liver and kidney.

Animals↗
PubMed1989

Influence of dietary protein deficiency on lead-copper interaction in rats.

The influence of dietary protein deficiency on the effects of exposure to lead or its combination with copper was investigated in rats. The administration of lead (100 ppm in drinking water) inhibited the activity of blood delta-aminolevulinic acid dehydratase; decreased hemoglobin, brain dopamine, and 5-hydroxytryptamine; and increased urinary excretion of delta-aminolevulinic acid, blood zinc protoporphyrin, and tissue accumulation of lead more markedly in animals fed a protein-deficient diet (10% casein) than in those fed a normal diet (21% casein). The simultaneous supplementation of copper (100 ppm in diet) reduced some of the lead-induced alterations and body uptake of lead more efficiently in animals fed a normal diet than in those fed a protein-deficient diet, which shows that the beneficial effects of copper in lead toxicity are adversely affected by low dietary protein.

Aminolevulinic Acid↗
PubMed1989

Chelation in metal intoxication. XXIX: Alpha-mercapto-beta-aryl acrylic acids as antidotes to mercury (II) toxicity.

alpha-Mercapto-beta-(2-furyl) acrylic acid (MFA), alpha-mercapto-beta-(phenyl) acrylic acid (MPA), alpha-mercapto-beta-(2-hydroxyphenyl) acrylic acid (MHA), alpha-mercapto-beta-(4-methoxyphenyl) acrylic acid (MMA), beta-1,2-phenylene di-alpha-mercapto acrylic acid (1, 2-PDMA) and beta-1, 4-phenylene di-alpha-mercapto acrylic acid (1, 4-PDMA) enhanced faecal excretion and reduced liver, spleen and blood burden of inorganic mercury when administered (0.5 m mol/kg, in two split doses) 24 hr after Hg (II) (1 mg/kg) in rats. MFA, MPA, MHA, and MMA were also effective in lowering renal Hg mainly from the cytosol, without any significant increase in urinary excretion of Hg. The results indicate that all the mono-mercapto acrylic acids including MFA were more effective than di-mercapto acrylic acids and act through the mechanism characteristic of thiol chelators, that is, mobilization of Hg as their complexes, contrary to the reported observation that MFA acts through the induction of metallothionein.

Acrylates↗
PubMed1989

Chelation in metal intoxication XXX: Alpha-mercapto-beta-aryl acrylic acids as antidotes to cadmium toxicity.

alpha-Mercapto-beta-(2-furyl) acrylic acid (MFA), alpha-mercapto-beta-(2-hydroxyphenyl) acrylic acid (MHA), beta-1,2-phenylene di-alpha-mercaptoacrylic acid (1,2-PDMA) and beta-1,4-phenylene di-alpha-mercapto acrylic acid (1,4-PDMA) were compared to sodium N-benzyl-D-glucamine dithiocarbamate (NBG-DTC) an effective cadmium chelator, for their ability to mobilize Cd and influence the Cd induced tissue metallothionein (MT) in rats administered 109CdCl2, 72 hr earlier. MFA was almost as effective as NBG-DTC but more effective than MHA in enhancing urinary and faecal excretion of Cd, reducing tissue and blood levels of Cd and in lowering Cd induced increase in hepatic and renal MT contents. 1,2-PDMA and 1,4-PDMA were effective only in reducing the hepatic burden of Cd. The resuls do not indicate any direct relationship between the efficacy of alpha-mercapto-beta-aryl acrylic acids to decorporate body Cd and their lipophilic-hydrophilic character or number-arrangement of their sulfhydryl groups.

Acrylates↗
PubMed1989

Influence of diethyldithiocarbamate on nickel-induced hepatic metallothionein in rats.

The influence of sodium diethyldithiocarbamate (DDC) on 63nickel chloride-induced metallothionein (MT) and alterations in essential metal levels in the liver of rats was investigated. The induction of MT, Zn and Cu levels of the hepatic cytosolic "heat stable fraction" (HSF) by DDC increased with time up to 24 hr. Although MT, Zn and Cu were significantly greater at 17 hr than those at 6.5 hr after 63Ni administration, the Ni level decreased. The treatment with DDC at 6 hr, but not at 10 min, prior to 63Ni administration increased significantly the MT, Zn and Cu contents 17 hr after 63Ni administration over that caused by 63Ni alone at 17 hr., showing a synergistic effect. The induction of hepatic MT by 63Ni or DDC alone was prevented by cycloheximide but not by actinomycin D and seemed to be regulated at the protein synthesis level.

Animals↗
PubMed1989

Influence of methionine supplementation in chelation of lead in rats.

The influence of methionine supplementation on the efficacy of common antidotes to lead poisoning, calcium disodium ethylenediaminetetraacetate (CaNa2EDTA) and D-penicillamine (DPA), was investigated in rats. The animals were given lead acetate (0.1% in drinking water) for 12 weeks and thereafter treated with CaNa2EDTA. DPA (0.3 mmol/kg, intraperitoneally), DL-methionine (1.34 mmol/kg, intragastrically), or the combination of a chelating agent and methionine for 3 days. While chelating agents enhanced the urinary excretion of Pb, methionine increased the fecal excretion of Pb significantly. Treatment with the combination of a chelating agent and methionine did not potentiate the effect of each antidote. However, methionine supplementation increased the efficacy of both chelating agents in reducing the hepatic and renal Pb burden but not the blood Pb level. The Pb-induced inhibition of blood delta-aminolevulinic acid dehydratase activity and the increase in urinary excretion of delta-aminolevulinic acid were reversed to a certain extent by CaNa2EDTA, DPA, and methionine but the combination did not improve their individual performances. The beneficial effects of methionine may be attributed to its ability to increase the bioavailability of glutathione (GSH), useful in chelating Pb and counter-acting the toxic effects, as evidenced by restoration of the Pb-induced decrease in hepatic GSH level by treatment with methionine. Methionine may be useful as a supportive therapy in chelation of Pb.

Aminolevulinic Acid↗