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At least 739 records · Page 41Linked to original sources
PubMed1990

Graft-versus-host reactions in the rat mimic toxin-induced autoimmunity.

Gold salts, D-penicillamine or mercurials induce autoimmunity in Brown Norway (BN) rats and provoke an immunosuppression in Lewis (LEW) rats. It has been suggested that immunologically mediated manifestations induced by drugs could result from graft-versus-host (GVH) like reactions. We show that BN spleen cells transferred into (LEW x BN)F1 hybrids induce a chronic GVH reaction (GVHR). This reaction led to an autoimmune disease quite similar to that induced by drugs in BN rats. In both situations, a common part of the B cell repertoire is triggered. In contrast, LEW spleen cells transferred into (LEW x BN)F1 hybrids provoke a lethal GVHR. This is to be compared with the CD8-mediated immunosuppression observed in LEW rats injected with HgCl2. These findings are in agreement with the prediction that immune dysregulation induced by drugs leads to GVH-like reactions either stimulatory or suppressive depending upon the strain tested.

Animals↗
PubMed1987

The site of inhibition of the chloroplast electron-transport system by 2,3-dithiopropan-1-ol (BAL).

BAL (2,3-dithiopropan-1-ol) treatment of chloroplasts has previously been reported to induce a block in electron transport from water to NADP+ at a site preceding plastocyanin [Belkin et al. (1980) Biochim. Biophys. Acta 766, 563-569]. In the present work the block was further characterized. The following properties of BAL treatment are described. Inhibition of electron transport from water to lipophilic acceptors but not to silicomolybdate. Inhibition of the slow, sigmoidal phase of chlorophyll a fluorescence induction. Inability of N,N,N',N',-tetramethyl-p-phenylenediamine to bypass the inhibition of NADP+ photoreduction with water as the electron donor. Inhibition of electron transport from externally added quinols to NADP+. Inhibition of cytochrome f reduction by photosystem II, but not its oxidation by photosystem I. Inhibition of cytochrome b6 turnover and cytochrome f rereduction after single-turnover flash illumination under cyclic electron-flow conditions. The BAL-induced block is therefore located between the secondary quinone acceptor (QB) and the cytochrome b6f complex. It was further found that (a) the isolated cytochrome complex is not inhibited after BAL treatment; (b) BAL-reacted plastoquinone-1 inhibits electron transport in chloroplasts; (c) BAL does not inhibit electron transport in chromatophores of Rhodospirilum rubrum or Rhodopseudomonas capsulata. It is suggested that the inhibition of electron transport in chloroplasts results from specific reaction of BAL with the endogenous plastoquinone.

Bacterial Chromatophores↗
PubMed1978

The neurological manifestations of chronic inhalation of leaded gasoline.

Abnormal neurological signs were found in 46 of 50 children and adolescents chronically sniffing leaded gasoline. These abnormalities resolved within eight weeks in all but one case. Exaggerated deep reflexes, postural tremor and evidence of cerebellar dysfunction occurred in a highly significnat number of patients. Forty-nine had blood lead levels greater than or equal to 40ug/dl. The mean blood lead levels were significantly higher in those with (a) abnormally brisk deep reflexes and (b) with evidence of cerebellar dysfunction, than in those without these findings. Five optional treatment regimes were employed and a classification was used, based on clinical findings, initial blood lead levels and the response to the calcium disodium edatate mobilization test. 39 patients received chelation therapy. These data suggest that neurological manifestations occur frequently in those abusing leaded gasoline and that chelation therapy has an important place in their management.

Adolescent↗
PubMed1988

Rabbit articular chondrocytes: an in vitro model for studying the effect of sodium aurothiopropanol sulfonate on proliferation kinetics, type II collagen phenotype and mitochondrial activity.

Despite the benefits of chrysotherapy the responsible mechanism of action of gold compounds remains unclear. At a concentration of 5 x 10(-4) M, sodium aurothiopropanol sulfonate (SAS) modified the in vitro proliferation kinetics of articular chondrocytes by reducing growth, viability and plating efficiency. Flow cytometry analysis, using propidium iodide DNA staining, revealed slight but significant cell arrest in G2+M which, in fact, represents an increase in the proportion of binucleate cells. SAS did not induce any variations in chondrocyte phenotype stability as far as the biosynthesis of type II collagen was concerned, and no appreciable changes in overall mitochondrial activity reflected by rhodamine 123 incorporation.

Animals↗
PubMed1969

Combined effect of sodium maleate and some thiol compounds on mercury excretion and redistribution in rats.

1. (+)-Penicillamine in a dose of 193 mumoles/kg given subcutaneously twice a day on the sixth and seventh days after the administration of 100 mug mercury increased the urinary excretion of rats more than the equimolar dose of N-acetyl-(+)-penicillamine but less than 2,3-dimercaptopropanol 48.3 mumoles/kg.2. Sodium maleate in a dose of 156 mumoles/kg given on the sixth and seventh days after the mercury did not influence mercury excretion or redistribution. Sodium maleate in the same dose increased considerably the effect of (+)-penicillamine on the urinary excretion and redistribution of mercury. It increased the effect of N-acetyl-(+)-penicillamine only slightly. There was a tendency to decrease the effect of 2,3-dimercaptopropanol.3. All the complexing agents decreased the kidney content of mercury and increased the liver and blood concentration of mercury. These changes were highest with 2,3-dimercaptopropanol. The combination of sodium maleate with (+)-pencillamine caused higher mercury excretion and lower kidney content but a smaller increase in the liver and blood mercury contents than 2,3-dimercaptopropanol.

Animals↗
PubMed1972

The inactivation of bradykinin in the pulmonary circulation of isolated lungs.

1. The isolated lungs of guinea-pigs, rats and dogs, perfused with Krebs bicarbonate solution via the pulmonary artery, inactivated 95, 98 and 99% respectively of the bradykinin infused through them.2. This inactivation process was not inhibited by 2-mercaptoethanol (1 mM) or EDTA (500 muM).3. The inactivation was inhibited by 2:3-dimercaptopropanol (100 muM), N-ethylmaleimide (100 muM), and several of the bradykinin potentiating peptides from Bothrops jararaca, in both natural and synthetic forms.4. The effect of these compounds, 2-mercaptoethanol, EDTA, 2:3-dimercaptopropanol, N-ethylmaleimide and Bothrops peptides on the pulmonary bradykininase activity is the same as their effect on pulmonary angiotensin I converting enzyme.

Animals↗
PubMed1980

Removal of internally deposited gold by 2,3-dimercaptopropane sodium sulphonate (Dimaval).

1 Orally administered 2,3-dimercaptopropane sodium sulphonate (DMPS, Dimaval) reduced the concentration of gold in rats treated with Auro-Detoxin and increased the urinary excretion of the metal. 2 In a long-term experiment, DMPS decreased significantly the concentration of gold in the kidneys and in the skin and increased it in plasma. 3 DMPS appears to be of interest as a possible antidote to gold, which could replace the more toxic 2,3-dimercaptopropanol (BAL).

Animals↗
PubMed1980

The effect of immediate and delayed treatment with 2,3-dimercaptopropane-1-sulphonate on the distribution and toxicity of inorganic mercury in mice and in foetal and adult rats.

The distribution and excretion of mercury were studied in mice and rats given a single injection of HgCl2 combined with chelation treatment. BAL-sulph (2,3-dimercaptopropane-1-sulphonate) given intravenously (500 mumol SH/kg) to mice 24 hrs after the mercury injection (2.0 mumol Hg/kg) reduced the kidney Hg-level significantly, while NAPA (N-acetyl-DL-penicillamine) and BAL (2,3-dimercaptopropanol) did not. Severe kidney damage with oliguria was observed in pregnant as well as in non-pregnant rats after injection of 5 mumol/kg of HgCl2. The gross pathological changes could be avoided with immediate treatment with BAL-sulph (500 mumol SH/kg), and such treatment protect against the oliguric reaction. Treatment delayed for 24 hrs reduced the renal Hg-levels significantly, but was ineffective in preventing the kidney damage. This indicates that irreversible changes might have occurred in kidneys cells at this time. The Hg-levels in the brain were either unchanged or lowered in animals given BAL-sulph treatment. BAL-sulph is supposed to act by chelation Hg++, particularly in the extracellular space. The complexes formed appears to be rapidly excreted by healthy kidneys. Mercury poisoning with severe renal damage is, however, associated with a block in urinary Hg-excretion. The poisoned animals responded on the BAL-sulph treatment with a substantial raise of faecal mercury excretion.

Animals↗