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At least 451 records · Page 25Linked to original sources
PubMed1990

Efficacy of various dithiol compounds in acute As2O3 poisoning in mice.

The efficacy of DL-dimercaptopropanol (British Anti-Lewisite, BAL), DL-dimercaptopropanesulfonate (DMPS), and meso-dimercaptosuccinic acid (DMSA) was compared in reducing the acute As2O3 toxicity in mice. Mice were treated with a single equimolar dose of a dithiol compound (0.7 mmol/kg i.p.) 0.5 or 30 min after the s.c. injection of various doses of As2O3. Both DMPS and DMSA were significantly (p less than or equal to 0.05) more effective in mice treated 0.5 min after the poisoning if compared to BAL on an equimolar level. The highest potency ratio (PR) (LD50 with treatment/LD50 without treatment) was found in animals injected with DMSA (PR = 8.6). The corresponding value for DMPS was 4.2, and for BAL 2.1, respectively. In animals treated 30 min after poisoning the efficacy of DMPS (PR = 2.6) was similar to the efficacy of DMSA 2.4, both being only slightly superior to BAL 2.0. DMPS and DMSA were found to be much less toxic than BAL. The LD50 of arsenic was 0.057 mmol/kg. The efficacy of BAL, DMPS, and DMSA in reducing the tissue content of arsenic following acute As2O3 poisoning was investigated in mice (n = 6/group) and guinea pigs (n = 3-4/group). The animals were injected s.c. with 0.043 mmol/kg As2O3 (containing a tracer dose of 74As(III)). Thirty minutes later the antidotes were administered i.p. (0.7 mmol/kg). From 2 to 4 h after As2O3 poisoning bile was collected from guinea pigs. Four h after As2O3 injection the content of 74As in blood, liver, kidneys, spleen, heart, lungs, brain, testes, skeletal muscle, and skin in mice and guinea pigs was measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

In vitro and in vivo effects of gold salts on chemotaxis and random migration of rat polymorphonuclear leucocytes.

The effect produced by three gold salts (sodium aurothiomalate, allochrysine, auranofin) on chemotaxis and random migration of rat polymorphonuclear leucocytes (PMN) was investigated under various experimental conditions. The drug activity was examined after incubation in vitro or after administration in vivo. PMNs were recruited after the induction of two acute inflammatory reactions (pleurisies induced by isologous serum or a suspension of calcium pyrophosphate (CaPP) crystals). The three gold salts administered in vivo and in vitro inhibited the chemotactic responses of the two cell types. This action was dose-dependent. Auranofin was the most effective substance while sodium aurothiomalate was the least. The random migration was not always significantly depressed especially for CaPP-elicited cells. Reduction in neutrophil chemotaxis might be an important additional mechanism in the action of gold salts and their activity on inflammatory PMNs recruited at inflammatory foci might be beneficial in the treatment in rheumatic diseases in which PMN migration would be implicated.

Animals↗
PubMed1985

Monocytes and granulocytes in rheumatoid arthritis (RA): phagocytic activity and superoxide anion production.

It is suggested by many tests that phagocytic cells were implied in inflammation which occurred during rheumatoid arthritis (RA). Further, three subject populations were selected for this study: Rheumatoid arthritis patients diagnosed according to American Rheumatism Association criteria (ARA mean = 6) and treated with gold compounds. Control subjects treated with the same non-steroidal anti-inflammatory drug (NSAID), diclofenac (75 mg per day). Normal subjects without disease or treatment. Blood granulocytes and monocytes were separately tested for ingestion of three different particle species (opsonized zymosan, immunoglobulin G sheep red cells, glutaraldehyde-treated sheep red cells) and stimulation of superoxide anion production by these particles. All phagocytic cells in RA patients have normal phagocytic response and superoxide anion production. Autologous serum does not inhibit the activity of these cells. In addition the NSAID (diclofenac) does not act upon phagocytosis and oxidative burst of control cells.

Adolescent↗
PubMed1989

Cholestasis and pneumonitis induced by gold therapy.

The authors describe the association of gold salt-induced cholestasis and lymphocytic alveolitis proved by liver biopsy and broncho-alveolar lavage. To our knowledge this is the third case report on the combination of liver disease and pulmonary infiltration induced by gold compounds.

Aged↗
PubMed1991

Pyruvate and lactate metabolism in livers of guinea pigs perfused with chelating agents after repeated treatment with As2O3.

The relative effectiveness of British Anti-Lewisite (BAL), dimercaptopropanesulfonic acid (DMPS), dimercaptosuccinic acid (DMSA), and a new metal binding agent 2,3-bis(acetylthio)propanesulfonamide (BAPSA) was compared by determining their effect on pyruvate metabolism in perfused livers of guinea pigs after repeated treatment with As2O3. Guinea pigs received As2O3, 2.5 mg/kg s.c. twice daily on 5 consecutive days (total dose 25 mg/kg). Sixteen hours after the last dose the livers were perfused (2.5 ml/min/g liver) with Krebs-Henseleit buffer and glucose (10 mmol/l) as substrate for 80 min. After 50 min of perfusion 0.1 or 0.7 mmol/l BAL, DMPS, DMSA, or BAPSA were added to the perfusate for 30 min. Samples of the effluent were collected every 10 min; lactate and pyruvate were determined enzymatically. As compared to controls, a significant decrease in the pyruvate and lactate efflux was observed in perfused livers of guinea pigs treated with As2O3. After influx of BAL (0.1 mmol/l), DMSA (0.7 mmol/l), and BAPSA (0.1 and 0.7 mmol/l) respectively, the pyruvate and lactate efflux and the oxygen consumption (exception BAL 0.1 mmol/l) increased and reached control values without arsenic treatment. On the other hand, the pyruvate and lactate efflux and the oxygen consumption was further significantly decreased after influx of 0.7 mmol/l BAL.

Animals↗
PubMed1987

Gold-induced aplastic anemia.

Three patients receiving gold salt treatment for rheumatoid arthritis developed severe aplastic anemia. All three patients experienced remission of their disease at the time of the occurrence of marrow aplasia. Reviewing data on these patients and recent literature indicate that fatal marrow aplasia seems to occur more frequently in sero-negative women who respond well to therapy with gold salts. Frequent blood monitoring in search for any pronounced or sustained drop in red, white or platelet count, even within normal range could serve as a warning sign for myelotoxicity. Despite intensive supportive measures and specific therapeutic attempts, all three patients eventually died of septic shock.

Adult↗
PubMed1998

Comparison of the effectiveness of 2,3-dimercaptopropanol (BAL) and meso-2,3-dimercaptosuccinic acid (DMSA) as protective agents against mercuric chloride-induced nephrotoxicity in rats.

The effectiveness of 2,3-dimercaptopropanol (BAL) and meso-2,3-dimercaptosuccinic acid (DMSA) on HgCl2-induced nephrotoxicity was studied in the rat. Seven groups of adult male rats were given a single sc toxic dose of HgCl2 (0.68 mg/kg) followed by 0.9% saline (positive control group), BAL (15, 30, and 60 mg/kg) or DMSA (50, 100, and 200 mg/kg) administered ip at 0, 24, 48, and 72 h thereafter. Although the renal function of HgCl2-exposed rats was slightly improved after BAL administration, Hg concentrations in the kidney were only reduced at 60 mg/kg. In addition, the protective effect of BAL was not dose-related. In contrast to BAL, DMSA was effective in increasing the urinary excretion of Hg and in reducing the renal Hg content. These results show that DMSA would be more effective than BAL in preventing or in protecting against inorganic Hg-induced nephrotoxicity.

Animals↗
PubMedDate not supplied

Enhancement of the kidney Cd burden by SH-containing chelating agents.

The accumulation of Cd in the kidneys is enhanced markedly if chelating agents that contain SH-groups like 2,3 dimercaptopropanol (BAL) are injected immediately after the metal. This is not a transient effect but persists for more than 3 d. It is less pronounced at higher chelate doses or when the pH of urine is increased. Our experiments indicate that chelating agents, which form unstable complexes at acid pH and are able to pass through the cell membrane, will cause metal accumulation in the kidneys.

Alkalosis↗
PubMedDate not supplied

Effects of potassium ethylxanthogenate and 2,3-dimercaptopropane sulphonate sodium on the pentobarbital pharmacokinetics and metabolism in male mice.

The effects of potassium ethylxanthogenate (PEX) and 2,3-Dimercaptopropane sulphonate sodium (Unithiol) on the pentobarbital (40 mg/kg, body weight i.v.) (PB) sleeping time, pharmacokinetics, and metabolism, were studied in comparative experiments on male albino mice. It was established that the pretreatment of animals with PEX (80 mg/kg of body weight s.c.) potentiated the PB sleeping time. Unithiol in an equimolar dose (105.2 mg/kg of body weight s.c.) had no effect. The pharmacokinetics of PB could be fitted to be a biexponential equation of the type Cp(t) = A.e-alpha t + B.e-beta t. PEX caused an almost two-fold decrease in the elimination rate constant of plasma PB, which led to a higher half-time and a lower total clearance compared with the controls. The curve for the plasma PB metabolites in the PEX-pretreated mice was significantly lower than of the controls. A higher PB level and decreased rate of elimination in PEX-pretreated animals was observed also in the: liver, lungs, kidney, and brain. A conclusion was drawn that the potentiating effect of PEX on the PB sleeping time is mainly due to inhibition of PB liver metabolism. It was suggested that the differences in the biological effects of the two thiol compounds are due to the differences in their chemical structures: PEX possesses a C = S group but Unithiol lacks this group.

Animals↗
PubMed1984

Longterm experience with oral gold in rheumatoid arthritis and psoriatic arthritis.

Oral gold (auranofin) has been used in 31 patients, 20 with active rheumatoid arthritis and 11 with active psoriatic arthritis. In rheumatoid arthritis the oral gold treatment was compared to parenteral gold treatment in a patient blind trial for two years. The psoriatic arthritis cases were incorporated in an open trial. Auranofin 6 mg once daily reduced significantly the activity in rheumatoid arthritis and in psoriatic arthritis. The beneficial effect obtained with auranofin at a dose of 6 mg/day during the first year of treatment could not be maintained by 3 mg/day in the second year. Auranofin compared to parenteral gold had a distinct advantage of better systemic tolerability, although parenteral gold was found to be more potent. There was no greater risk for toxic skin reaction to oral gold in psoriatic arthritis than in rheumatoid arthritis. The overall conclusion of this longterm study is that oral gold (auranofin) 6 mg once daily, although slightly less effective than parenteral gold, can be considered to be the first choice of gold treatment for rheumatoid arthritis and psoriatic arthritis, because the compliance, which is a reflection of a combination of tolerance and efficacy, for oral gold therapy was, in our hands, undoubtedly superior to parenteral gold.

Adult↗
PubMed2000

Biomonitoring of exposure to lewisite based on adducts to haemoglobin.

The development of a procedure for retrospective detection and quantitation of exposure to the arsenical dichloro(2-chlorovinyl)arsine (lewisite; L1) has been initiated. Upon incubation of human blood with [14C]L1 (20 nM-0.2 mM) in vitro, more than 90% of the total radioactivity was found in the erythrocytes and 25-50% of the radioactivity becomes associated with globin. Evidence was obtained for the presence of several binding sites. One type of binding was identified as L1-induced crosslinking of cysteine residues 93 and 112 of the beta-globin chain. A method was developed for extraction of bound and unbound 2-chlorovinylarsonous acid (CVAA), a major metabolite of L1, from whole blood after treatment with 2,3-dimercapto-1-propanol (BAL). Subsequent to derivatization with heptafluorobutyryl imidazole, the CVAA-BAL derivative could be analysed at a 40-fmol level by means of gas chromatography-mass spectroscopy (GC-MS) under electron impact conditions. With this procedure, in vitro exposure of human blood to 1 nM L1 could be determined. The same procedure was applied to the analysis of human urine samples spiked with CVAA. In vivo exposure of guinea pigs could be established at least 240 h after subcutaneous administration of the agent (0.25 mg/kg) by the determination of bound and unbound CVAA in the blood. In the urine of these animals, CVAA could be detected for 12 h after exposure.

Animals↗