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PubMed1987

Activation of the alternative pathway of human complement by sulfhydryl compounds of analytic and therapeutic use.

Thiol-containing drugs (dimercaprol, dimercaptopropanesulfonate, captopril, penicillamine, N-acetylcysteine) and the standard reducing agent beta-mercaptoethanol, activate the alternative pathway of complement as shown by in vitro experiments. Depending on the substance tested, at concentrations of 0.5-5 mM, cleavage products of C3 and factor B were demonstrable in serum by immunoelectrophoresis. The regulatory protein factor I proved to be very sensitive to thiols; this observation offers an explanation for the alternative pathway activating effect of these substances. At concentrations of thiols that initiate the alternative pathway, the classical pathway was not or only to a minor extent activated; however, the activity of C2, C5 and one or several of the components C6-9 was directly affected. Alkylation of the thiol group of the compounds tested, abrogated their effects on the complement system.

Alkylation↗
PubMed1972

Mechanism of action of gliotoxin: elimination of activity by sulfhydryl compounds.

Gliotoxin and two other compounds, with antiviral activity against a number of ribonucleic acid (RNA) viruses and structurally related via the epidithiapiperazinedione moiety, appeared to be equally active in their oxidized and reduced forms. However, the ability of the reduced forms to inhibit viral RNA synthesis was abolished when these compounds were maintained in the reduced state by the simultaneous presence of a large molar excess of dithiothreitol or reduced glutathione. The active form therefore appeared to be that containing a disulfide bridge, and the apparent activity of the dithiol was due to cellular oxidation. Possible mechanisms by which the compounds could interact with viral proteins, e.g., viral RNA-dependent RNA polymerase, are proposed.

Alkaloids↗
PubMed1981

Enhanced bismuth digestive absorption in rats by some sulfhydryl compounds: nmr study of complexes formed.

In a preliminary paper [Thérapie 34, 397 (1979), we showed that cysteine enhances bismuth digestive absorption in rats. In this paper, we have studied in rats the effects of various thiol compounds (mercaptopropionic acid, penicillamine, cysteine, homocysteine, 2-mercaptoethylamine, mercaptoethane) and nonthiol compounds (methionine, serine, alanine) orally administered on the absorption and elimination of bismuth also given orally. Bismuth was measured in blood and urine by electrothermal atomic absorption spectrophotometry. All of the thiol substances, and particularly cysteine, homocysteine, and mercaptopropionic acid, have considerably enhanced bismuth absorption and elimination; whereas, nonthiol substances have had no effect. Moreover, the acute toxicity of bismuth was enhanced when bismuth was given as a complex with cysteine (LD50 = 156 +/- 20 mg/kg). Studies by nmr spectroscopy of interactions between bismuth and these organic compounds have shown that bismuth induces an important chemical shift of the protons of the alpha carbon of the sulfhydrile group. Mainly, studies of C and N have confirmed this fact. The selectivity of such a complexation, in our pH conditions, may be tentatively explained on the ground of hard and soft acid and base (HSAB) theory. We have suggested that an increase in the concentration of thiol compounds in the gastrointestinal tract arising from food, or more probably from microorganism synthesis, could be an explanation for human encephalopathies.

Amino Acids↗
PubMed1993

Inhibition by sulfhydryl compounds of vascular relaxation induced by nitric oxide and endothelium-derived relaxing factor.

On rings of rabbit thoracic aorta precontracted with phenylephrine, L-cysteine (Cys) and dithiothreitol (DTT) (1-100 microM), but not glutathione (GSH), produced dose-dependent augmentation of contraction in endothelium-intact, but not in endothelium-denuded rings. The augmentation appeared to be due to inhibition of basally released endothelium-derived relaxing factor (EDRF), and was abolished by pretreatment with superoxide dismutase (SOD, 15 U/ml). At a high dose (1 mM), Cys and GSH produced transient, and DTT produced sustained endothelium-independent relaxation, not influenced by SOD. Cys and DTT (10 microM), but not GSH, produced a small but significant inhibition of acetylcholine-induced endothelium-dependent relaxation, and this inhibition was prevented by SOD. In a perfusion-bioassay system in which EDRF was released by acetylcholine from endothelium of a perfused segment of rabbit aorta, Cys and DTT (20 microM), but not GSH, infused into the perfusate between the segment and an endothelium-denuded bioassay ring, partially inhibited relaxation by the EDRF, but not when SOD was present. In organ chamber experiments, the large transient relaxation of endothelium-denuded rings produced by 75 nM nitric oxide (NO) was partially inhibited in a concentration-dependent manner by Cys, DTT and GSH (0.1-100 microM). Moderate relaxation by 15 nM NO was almost completely inhibited by each compound at 10 microM. The order of potency was Cys > DTT > GSH. Cystine, glutathione disulfide and alanine did not inhibit. Inhibition of NO-induced relaxation was largely attenuated by SOD.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed2000

Effects of free radicals on cytosolic creatine kinase activities and protection by antioxidant enzymes and sulfhydryl compounds.

The main purpose of this study was to investigate the effect of free radicals and experimental diabetes on cytosolic creatine kinase activity in rat heart, muscle and brain. Hydrogen peroxide decreased creatine kinase activity in a dose dependent manner which was reversed by catalase. Xanthine/xanthine oxidase, which produces superoxide anion, lowered the creatine kinase activity in the same manner whose effect was protected by superoxide dismutase. N-acetylcysteine and dithiothreitol also significantly ameliorated the effect of Xanthine/xanthine oxidase and hydrogen peroxide. Experimental diabetes of twenty-one days (induced by alloxan), also caused a similar decrease in the activity of creatine kinase. This led us to the conclusion that the decrease in creatine kinase activity during diabetes could be due to the production of reactive oxygen species. The free radical effect could be on the sulfhydryl groups of the enzyme at the active sites, since addition of sulfhydryl groups like N-acetylcysteine and dithiothreitol showed a significant reversal effect.

Acetylcysteine↗
PubMed1991

Possibilities of the combined use of non-steroidal anti-inflammatory drugs and sulfhydryl compounds in radioprotection.

The combined preirradiation administration of indomethacin and cystamine was found to enhance synergistically the recovery of hemopoiesis in sublethally gamma-irradiated mice. This effect can be explained by a common operation of two mechanisms of radioprotection, i.e. of an increased survival of hemopoietic stem cells due to cystamine action and of stimulatory effects of indomethacin on the proliferation of surviving cells, mediated by the inhibition of prostaglandin synthesis. Attempts to prove such enhancement of protective effects on irradiated mice in terms of postirradiation lethality were unsuccessful. The reason seems to be the influence of toxic effects of the indomethacin-cystamine combination on the gastrointestinal tract. When using the less toxic combination, i.e. diclofenac and WR-2721, the additivity of protective effects is manifested even in the survival of lethally irradiated mice. The results suggest that under suitable conditions avoiding the unfavourable toxic effects, non-steroidal anti-inflammatory drugs can be successfully used with the aim to enhance the efficiency of sulfhydryl radioprotectors.

Amifostine↗
PubMed1982

The effect of sulfhydryl compounds on sister-chromatid exchanges. II. The question of cell specificity and the role of H2O2.

In contrast with earlier reports on the induction of sister-chromatid exchanges (SCEs) by SH compounds in cell lines of the Chinese hamster, cysteine, cysteamine and cystamine did not cause an increase of the SCE frequency in human lymphocyte cultures. Differences in the treatment protocols or variations of the BrdUrd concentration had no effect on the induction of SCEs by these substances. The inclusion of H2O2 and comparative investigations with V79 cells of the Chinese hamster showed that the probable reason for the SCE induction by SH compounds is the inability of the cells to degrade H2O2. Furthermore, for cystamine it became clear that additional effects must exist besides the induction of SCEs through H2O2. The present study underlines the fact that the examination of a substance within one cell system does not necessarily permit a reliable statement about the DNA-damaging property of this substance.

Animals↗
PubMedDate not supplied

In vitro proteoglycan sulfation derived from sulfhydryl compounds in sulfate transporter chondrodysplasias.

Mutations in a sulfate-chloride antiporter gene, the diastrophic dysplasia sulfate transporter (DTDST), have been associated with a family of skeletal dysplasias including recessive multiple epiphyseal dysplasia, diastrophic dysplasia (DTD), atelosteogenesis type 2, and achondrogenesis type 1B (ACG1B). DTDST function is crucial for uptake of extracellular sulfate required for proteoglycan (PG) sulfation; the tissue-specific expression of the clinical phenotype may be the consequence of the high rate of PG synthesis in chondrocytes and the ensuing high sulfate requirement. We have studied the contribution of cysteine and its derivatives to PG sulfation in fibroblast and chondrocyte cultures from sulfate transporter dysplasia patients. Incubation of ACG1B fibroblasts in medium containing different concentrations of cystine indicated partial recovery of PG sulfation as measured by HPLC disaccharide analysis of chondroitin sulfate PGs; similar results were observed after incubation with N-acetylcysteine. When both compounds were tested in primary chondrocytes from a DTD patient, partial rescue of PG sulfation was observed, suggesting that the metabolic pathways producing cytoplasmic sulfate from thiols are also active in this cell type.

Acetylcysteine↗
PubMed2006

Effect of Mouriri pusa extracts on experimentally induced gastric lesions in rodents: role of endogenous sulfhydryls compounds and nitric oxide in gastroprotection.

Several plants are used in folk medicine to treat gastrointestinal disorders. Mouriri pusa Gardn. (Melastomataceae) is a medicinal plant commonly used in the central region of Brazil against gastric ulcer. Two organic extracts methanolic (MeOH) and dichloromethane (DCM) obtained by sequential extraction from the leaves of Mouriri pusa were evaluated for their ability to protect the gastric mucosa against injuries caused by necrotizing agents (0.3M HCl/60% EtOH, absolute ethanol, non-steroidal anti-inflammatory drug, stress and pylorus ligature) in mice and rats. The best results were obtained after pretreatment with MeOH extract whereas the DCM extract did not show the same significant antiulcerogenic activity. No acute toxicity was observed in animals treated with 5 g/kg, p.o. of MeOH extract. The mechanism involving the antiulcerogenic action of MeOH extract seemed to be related to NO generation and also suggested the effective participation of endogenous sulfhydryl group in the gastroprotective action. Phytochemical investigation of the MeOH extract of Mouriri pusa yielded tannins, flavonoids and (-)-epicatechin. The presence of these phenolic compounds probably would explain the antiulcerogenic effect of the polar extract of Mouriri pusa leaves.

Animals↗