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At least 505 records · Page 28Linked to original sources
PubMed1991

Regulation of guanylate cyclase by a guanine nucleotide binding protein, G alpha 2, in Dictyostelium discoideum.

Binding of cyclic AMP (cAMP) to the cell surface receptor induces a transient activation of guanylate cyclase in Dictyostelium discoideum. A frigid mutant (HC85) which lacks G alpha 2, a guanine nucleotide binding protein, does not respond to cAMP. We found that 2,3-dimercapto-1-propanol (BAL) induced a continuous activation both in the frigid and in its parents. Therefore, the BAL-induced continuous activation of guanylate cyclase is independent of G alpha 2. We also found that cAMP enhanced the BAL-induced continuous activation in the frigid mutant. This result suggests that an unidentified signal transduction mechanism from the cAMP-receptor besides the one involving G alpha 2 plays a role in the enhancement of activation. Lastly, we found that the BAL-induced continuous activation was terminated by cAMP in the parental strain, but not in the frigid mutant. Therefore, the cAMP-induced suppression on the BAL-induced continuous activation is mediated through G alpha 2.

Cold Temperature↗
PubMed1981

Effects of thiol agents on the accumulation of cadmium by rat liver parenchymal and Kupffer cells.

The rate of Cd accumulation by adult rat liver parenchymal cells in serum free primary culture in the presence of 100 microM CdCl2 was 10 times greater than that by non-parenchymal Kupffer cells. Addition of the monothiol chelating agents, cysteine and penicillamine, decreased Cd uptake in both cell types, the effect becoming more pronounced as the monothiol concentration was increased from 0.1 to 1.0 mM. These monothiols thus appear to reduce the availability of Cd for transport across the cell membrane. In contrast 1-10 molar excesses of the dithiol agents 2,3-dimercaptopropanol (BAL) or dithiothreitol (DTT) stimulated to variable extents the rate of Cd accumulation 2-10-fold in parenchymal cells and by over 100-fold in Kupffer cells. Supplementation of the media with 3% serum had little effect on the Cd accumulation in the presence of dithiols. Intravenous injection of Cd (0.05 mg/kg DCdCl2) with up to a 10-fold molar excess of cysteine or penicillamine had little effect on the hepatocellular Cd distribution. However Cd uptake by non-parenchymal cells was increased markedly by the simultaneous administration of BAL or DTT in 2 or 10 molar excess. Evidence is provided that these results may be partially explained by the endocytosis, particularly in Kupffer cells, of colloidal complexes of Cd which are formed with the dithiols but not the monothiols. These observations demonstrate that the physicochemical form of Cd determines its hepatocellular distribution which may be an important factor in the manifestation of Cd toxicity after thiol treatment.

Animals↗
PubMed1982

Interactions of the chelating agent 2,3-dimercaptopropane-1-sulfonate with red blood cells in vitro. I. Evidence for carrier mediated transport.

Uptake of the water soluble 1,2-dimercaptopropanol (BAL) derivative 2,3-dimercapto-1-sulfonate (DMPS) into human red blood cells was found in vitro and the mode of penetration studied in detail. The compound entered erythrocytes in a concentration dependent manner. In contrast to sealed ghosts where inside and outside concentrations reached the same value, DMPS accumulated in intact erythrocytes. Since no binding of DMPS could be detected, the reason for accumulation was assumed to be a conversion of DMPS into chelates or metabolites which penetrated the membrane in a slower rate. A facilitated transport of DMPS mediated by the anion carrier protein was concluded on the basis of the following similarities with the anion transport: inhibition of [14C]DMPS-uptake by N-ethylmaleimide (NEM), tetrathionate (90%), sulfate (50%), 5,5'-dithio bis(2-nitrobenzoic acid) (DTNB) (25%); inhibition of uptake and efflux by 4,4'-diisothiocyano-2,2'-stilbene disulfonate (DIDS) (80%), dipyridamole (55%); temperature dependency (activation energy 24 Kcal/mol); pH-dependency (pH optimum about 6.9); counter-transport; activation of uptake by preincubation with DMPS (transmembrane effect).

Cell Membrane↗
PubMed1982

Interactions of the chelating agent 2,3-dimercaptopropane-1-sulfonate with red blood cells in vitro. II. Effects on metalloproteins.

The implications of the carrier mediated uptake of 2,3-dimercaptopropane-1-sulfonate (DMPS) (D.B. Wildenauer et al., Chem.-Biol. Interact., 42 (1982) 165) on cytoplasmic components of human red blood cells have been investigated in vitro. The water-soluble chelating agent caused a mobilization of metals (zinc and copper) from metalloproteins which resulted in a permeation of the membrane. Furthermore, a cytoplasmic protein was found to be attached to the membrane after DMPS treatment of red blood cells. The protein was isolated and identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), amino acid analysis and finger-printing as carbonic anhydrase. The enzyme could be solubilized from the membrane by addition of beta-mercaptoethanol, suggesting an involvement of sulfhydryl-groups. In a reconstitution experiment, DMPS-treated human carbonic anhydrase could be attached to inside-out vesicles which were prepared from human erythrocytes. In contrast, bovine carbonic anhydrase, which is known to lack sulfhydryl-groups, failed to bind to the same vesicles. Moreover, attachment of carbonic anhydrase to the membrane did not occur when intact bovine erythrocytes were treated with DMPS. It is suggested that zinc-depletion of carbonic anhydrase causes the liberation of a sulfhydryl-group of the enzyme. This is followed by a disulfide formation with a component of the membrane which results in the observed membrane attachment.

Amino Acids↗
PubMed1983

On the toxic effects of tetraethyl lead and its derivatives on the chrysophyte Poterioochromonas malhamensis. IV. Influence of lead antidotes and related agents.

The unicellular alga Poterioochromonas malhamensis was exposed to 12.5 microM of inorganic or triethyl lead and simultaneously treated with lead antidotes and related agents at concentrations of 12.5, 31.25 and 62.5 microM. With increasing concentrations some of the antidotes alone slightly to severely inhibited algal growth (BAL, CaNa2EDTA, EDTA, Na2EDTA), whereas others (DPA, EGTA, DIZO) were non-toxic at the concentrations tested. EGTA and CaNa2EDTA, at all concentrations tested, completely suppressed the growth inhibition caused by inorganic lead; Na2EDTA and EDTA were protective at the lower or medium concentrations, but DIZO, DPA and BAL considerably enhanced lead toxicity with increasing concentrations. None of the tested agents was able to reduce the toxic effects of triethyl lead. All antidotes markedly increased inhibition of algal growth caused by triethyl lead and some were even lethal to the poisoned algae either at the highest (Na2EDTA, EDTA, DPA) or at all concentrations used (DIZO, BAL). P. malhamensis proved to be a highly sensitive and valuable tests system and the results obtained exhibited striking parallels to medical and clinical experience in therapy of human poisoning with inorganic and organic lead compounds.

Antidotes↗