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At least 1,549 records · Page 86Linked to original sources
PubMed1982

Antagonism of acute copper(II)-induced renal lesions by sodium 2,3-dimercaptopropanesulfonate.

Acute copper(II) sulfate poisoning in the mouse induces renal tubular degeneration and necrosis. Timely administration of sodium 2,3-dimercaptopropane-sulfonate (DMPS) effectively prevented the development of the morphological renal sequelae of copper intoxication. During the time course of this study (5 days), no copper-induced hepatic lesions were observed. DMPS and its preformed copper complex possess low inherent toxicity with no hepatorenal lesions occurring over a 5-day period. These findings suggest that DMPS may be an effective antidote in acute and chronic copper poisoning in humans.

Acute Kidney Injury↗
PubMed1982

On the cytoprotective action of sulfhydryl-containing substances.

Sulfhydryl substances (cysteine, glutathione, cysteamine and BAL) provide protection against experimental gastric ulcer induced by indomethacin while being ulcerogenous in stress-ulcer. Experimental data indicate the necessity to distinguish between "real" and "occasional" cytoprotective drugs.

Animals↗
PubMed1980

Toxicological studies on sodium 2,3-dimercaptopropane-1-sulfonate in the rat.

The toxicity of Na-2,3-dimercaptopropane-1-sulfonate (DMPS) was investigated in rats. The lethality after large i.p. doses is diminished by a factor of approx. 6 if a single dose is divided into several doses on consecutive days. Chronic treatment with 600 mumol DMPS/kg and day p.o. did bring about adverse effects except a reduction in Cu-concentration in some organs, especially in the kidneys, immediately after DMPS-treatment, which was normalized within 1 week. The offspring of DMPS treated female rats showed no abnormalities.

Animals↗
PubMed1980

99mTc-unithiol complex, a new radiopharmaceutical for kidney scintigraphy. IV. Autoradiographic localisation of its cellular distribution in the kidney.

The distribution of 99mTc-Unithiol complex was studied by macro-autoradiography in rats and in rabbit kidneys, and the presence of activity in the renal cortex was easily demonstrated. Using micro-autoradiography, the accumulation of activity in various parts of the nephron was observed to concentrate in the cells of the proximal and distal tubuli to a larger extent than in the glomeruli.

Animals↗
PubMed1980

[Control of trace elements in the rat using the heavy metal antidote "Unithiol" (sodium-2,3- dimercaptopropane sulfonate)].

The trace element balance in laboratory rats was found to be affected by somewhat lasting application of "Unitiol". Unambiguous decline of manganese, copper, and zinc concentrations was recorded from blood and liver. Complex fixation of copper was stronger than that of the other elements tested. No dose-dependent changes were observed with the experimental arrangement described. The chromium levels in all examined organs were affected but slightly or not at all. The proposal is made that long-term therapeutic use of chelate formers should be accompanied by properly balanced application of essential trace elements.

Animals↗
PubMed1979

Clinical spectrum of Wilson's disease (hepatolenticular degeneration).

Fifty-eight patients with Wilson's disease are reviewed, of whom 25 symptomatic patients experienced liver disease first and 28, brain disease. Ten of these patients presented with liver disease alone, 19 with brain disease alone, and 24 with evidence of both liver and brain disease. The remaining five were discovered as asymptomatic siblings of known patients. Three of the patients with hepatic presentation and one with neurologic presentation later experienced the other type of symptomatology, bringing the total number of patients with mixed disease to 28. Of the 44 patients with brain disease, 12 presented primarily with extrapyramidal findings, 6 with cerebellar findings, and 17 with both; pseudobulbar findings were noted in 9 patients, all of whom had other symptoms of severe nervous system disease. In addition to these presentations, in an appreciable number of patients the first symptoms were of a mental or emotional disorder. Disease of other organ systems, such as the joints and kidneys, also occurred but infrequently. Where adequate family information was available, 13 of 65 siblings (20%) were known to have had or were suspected of having had Wilson's disease. This is consistent with the autosomal-recessive pattern of inheritance.

Adolescent↗
PubMed1993

Complex effects of phenylarsine oxide in T cells. Induction of tyrosine phosphorylation and calcium mobilization independent of CD45 expression.

The effects of phenylarsine oxide, a phosphotyrosine phosphatase inhibitor, on early signal transduction events in human T cells were studied. Simultaneous stimulation of T cells with anti-CD3 monoclonal antibody and phenylarsine oxide prevented increased tyrosine phosphorylation of phospholipase C gamma 1. In contrast, treatment of resting T cells with phenylarsine oxide alone resulted in increased tyrosine phosphorylation of a number of other intracellular substrates. Further, phenylarsine oxide was able to cause an immediate disruption of signal transduction in T cells after anti-CD3 stimulation, as measured by a return of intracellular calcium concentration and inositol 1,4,5-trisphosphate production to base-line levels. Surprisingly, in view of the inhibitory effects of phenylarsine oxide on T cell receptor signal transduction, treatment of T cells with phenylarsine oxide alone caused a dose-dependent increase in intracellular-free calcium concentration that was not accompanied with detectable increases in inositol 1,4,5-trisphosphate production. The phenylarsine oxide-induced increase in free calcium had distinct kinetics from antigen receptor-activated calcium mobilization and was derived from both intracellular sources and increased plasma membrane calcium permeability. This effect was independent of the CD45 transmembrane tyrosine phosphatase. Phenylarsine oxide thus has complex effects on signal transduction in T cells that suggests multiple intracellular targets, and these should be considered in the interpretation of experiments using this agent to study cellular kinase and phosphatase interactions. Finally, the effects of phenylarsine oxide on cellular calcium homeostasis may provide a mechanism of action for the therapeutic and/or toxic effects of arsenicals used for various forms of chemotherapy.

Arsenicals↗
PubMed1995

Evidence for participation of vicinal dithiols in the activation sequence of the respiratory burst of human neutrophils.

Phenylarsine oxide (PAO) specifically forms a stable ring complex with vicinal dithiols that can be reversed with 2,3-dimercaptopropanol (DMP). Pretreatment of human neutrophils with micromolar concentrations of PAO inhibited release of superoxide anion (O2-) stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or phorbol 12-myristate 13-acetate (PMA); the inhibition was reversed with DMP, but not with 2-mercaptoethanol. PAO did not affect O2- release in previously stimulated cells. PAO did not affect the FMLP-induced Ca2+ response, suggesting that PAO affects a postreceptor event that does not modulate the Ca2+ transient. Treatment of isolated membrane or cytosolic fractions with PAO did not change the rates of arachidonate-stimulated O2- production in a cell-free system. Pretreatment of unstimulated neutrophils with PAO inactivated cytosolic protein kinase C (PKC); the inactivation was reversed with DMP. However, PAO did not affect PMA-induced translocation of beta-PKC protein or reduce the PKC activity translocated to the membrane. PAO had no effect on tyrosine kinase activity but inactivated phosphotyrosine phosphatase; stimulus-induced tyrosine phosphorylation of several proteins was markedly enhanced. These results suggest that vicinal dithiols play an essential role in activation of the respiratory burst oxidase. Possible sites for the activity of these essential vicinal dithiols include PKC and the regulatory balance of tyrosine phosphatase activity and tyrosine phosphorylation.

Arachidonic Acid↗