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PubMed1999

Additive triple DMARD combination therapy of a low dose of sulfhydryl compounds, sulfasalazine and methotrexate in the treatment of rheumatoid arthritis: a clinical trial.

To evaluate the efficacy and safety of additive triple disease modifying anti-rheumatic drug (DMARD) combination therapy of a low dose of sulfhydryl compounds ¿D-penicillamine, bucillamine or tiopronin¿, sulfasalazine (SSZ) and methotrexate (MTX) as a treatment for rheumatoid arthritis (RA) patients, we studied a total of 33 Japanese RA patients (6 males, 27 females). At 1 or 2 months after simultaneous administration of the 3 above-mentioned DMARDs was begun, significant improvements were seen in markers of joint inflammation, i.e., erythrocyte sedimentation rate and C-reactive protein in sera. At 6 months, clinical improvement judged by the physicians' overall assessment of joint symptoms and laboratory data was observed in 29 (88%) of the 33 RA patients. No marked effect was observed in the other 4 (12%) patients, however. We observed no significant adverse reaction to this therapy. This suggests that additive triple DMARD combination therapy of a low dose of sulfhydryl compounds, SSZ and MTX could be a useful drug therapy for the treatment of RA patients, even those who are refractory.

Adult↗
PubMed1991

Effect of sulfhydryl compounds on ATP-stimulated H+ transport and Cl- uptake in rabbit renal cortical endosomes.

The vacuolar H+ ATPase is inhibited by N-ethylmaleimide (NEM), a sulfhydryl compound, suggesting the involvement of a sulfhydryl group in this transport process. We have examined the effects of several sulfhydryl-containing compounds on the vacuolar H+. ATPase of rabbit renal cortical endosomes. A number of such compounds were effective inhibitors of endosomal H+ transport at 10(-5)-10(-6) M, including NEM, mersalyl, aldrithiol, 5,5' dithiobis (2-nitrobenzoic acid), p-chloromercuribenzoic acid (PCMB) and p-chloromercuriphenyl sulfonic acid (PCMBS). NEM, mersalyl, aldrithiol and PCMBS had no effect on pH-gradient dissipation, whereas PCMB decreased the pH gradient faster than control. In the absence of ATP, PCMB (10(-4) M) stimulated endosomal 36Cl- uptake, particularly in the presence of an inside-alkaline pH gradient (pHin = 7.6/pHout = 5.5). This result was not an effect of PCMB on the Cl(-)-conductive pathway. The less permeable PCMBS did not stimulate 36Cl- uptake. The effects of PCMB were concentration dependent and were prevented by dithioerithritol. ATP-dependent 36Cl- uptake was decreased by addition of PCMB. Finally, PCMB had no effect on 45Ca2+ uptake. These results support the presence of two functionally important sulfhydryl groups in this endosomal preparation. One such group is involved with ATP-driven H+ transport and must be located on the cytoplasmic surface of the endosomal membrane. The second sulfhydryl group must reside on the internal surface of the endosomal membrane and relates to a PCMB-activated Cl-/OH- exchanger that is functional both in the presence and absence of ATP. This endosomal transporter is similar to the PCMB-activated Cl-/OH- exchanger recently described in rabbit renal brush-border membranes.

Animals↗
PubMed1993

Acute effects of nitroglycerin depend on both plasma and intracellular sulfhydryl compound levels in vivo. Effect of agents with different sulfhydryl-modulating properties.

BACKGROUND: Changes in sulfhydryl (SH) compound availability may alter the hemodynamic effect of nitroglycerin (NTG). Data on the relation between NTG effect and thiol levels are, however, limited to in vitro experiments. The present study investigates how intracellular and extracellular changes in SH group concentrations (cysteine and glutathione [GSH]) affect the responsiveness to NTG in vivo. METHODS AND RESULTS: GSH and cysteine levels in plasma, vena cava, and aorta were measured after administration of N-acetylserine (placebo, n = 6), N-acetylcysteine (NAC, extracellular and intracellular SH donor, n = 6), oxothiazolidine (OXO, intracellular SH donor, n = 6), buthionine sulfoximine (BSO, intracellular GSH-depleting agent, n = 6), BSO+NAC (n = 6), and BSO+OXO (n = 6) in chronically catheterized conscious rats. In addition, the effect of 2.5 mg NTG/kg i.v. on mean arterial pressure (MAP) was determined before and after the same treatment. NAC (5 mmol/kg i.v. for 2 hours) significantly (p < 0.05) increased extracellular cysteine and GSH levels and potentiated the hypotensive effect of NTG (from 26 +/- 3 to 31 +/- 4 mm Hg [mean +/- SEM], p < 0.05). OXO (5 mmol.kg-1 x hr-1 i.v. for 2 hours) significantly increased intracellular cysteine and GSH levels but had no effect on NTG responsiveness (p > 0.05). BSO (1 g i.p. three times within 24 hours) significantly decreased intracellular GSH levels (p < 0.05) and attenuated the effect of NTG (from 28 +/- 3 to 16 +/- 2 mm Hg). CONCLUSIONS: The results suggest that the acute hypotensive effect of NTG in vivo is: 1) increased by high extracellular GSH and/or cysteine levels (NAC), 2) decreased by low intracellular GSH levels (BSO), and 3) unaffected by high intracellular levels of cysteine and GSH (OXO).

Animals↗
PubMed1991

Roles of sulfhydryl compounds in the gastric mucosal protection of the herb drugs composing oren-gedoku-to (a traditional herbal medicine).

We investigated the involvement of sulfhydryl compounds in the cytoprotective effect of each component herb drug composing Oren-gedoku-to (OGT) against ethanol-induced gastric lesions and potential difference (PD) reduction in comparison with that of OGT in rats. Pretreatment with N-ethylmaleimide (NEM) significantly blocked the cytoprotective effects of OGT, Coptidis rhizoma and Phellodendri cortex, but did not block the cytoprotective effects of Gardeniae fructus and Scutellariae radix. The inhibitory effects of OGT, Coptidis rhizoma and Phellodendri cortex against the PD reduction disappeared in the presence of NEM or diethyldithiocarbamate (DDC), whereas NEM or DDC had little or no effect with Gardeniae fructus and Scutellariae radix. These results suggest that the gastric mucosal protection of Coptidis rhizoma and Phellodendri cortex may be ascribed to the reinforcement of mucosal barrier resistance through endogenous sulfhydryl compounds and DDC-sensitive compounds, but those of Gardeniae fructus and Scutellariae radix may be independent of NEM- or DDC-sensitive compounds.

Animals↗
PubMed1994

Sulfhydryl compounds, captopril, and MPG inhibit complement-mediated myocardial injury.

Factors including complement activation, neutrophil infiltration, and oxygen-derived free radicals have been implicated in the pathogenesis of myocardial tissue injury during ischemia and reperfusion. Certain sulfhydryl-containing compounds have been shown to inhibit complement activation. The sulfhydryl compounds captopril and N-(2-mercaptopropionyl)-glycine (MPG) are antioxidant compounds that previously have been shown to protect the myocardium from ischemia and reperfusion-induced damage. In this study, captopril (an angiotensin-converting-enzyme inhibitor; ACEI) and MPG, and the non-sulfhydryl compound enalaprilat (also an ACEI) were tested for their ability to protect the isolated perfused rabbit heart against complement-induced injury. Both captopril and MPG protected hearts against complement-mediated increases in left ventricular end-diastolic pressure and increases in coronary arterial perfusion pressure in a concentration-dependent manner, whereas enalaprilat was not protective. The ability of these compounds to inhibit complement activation also was tested using an in vitro complement-mediated red blood cell hemolysis assay. These findings offer additional insight as to the mechanism whereby captopril, MPG, and possibly other sulfhydryl compounds, may be acting to provide cytoprotection during myocardial ischemia and reperfusion.

Animals↗
PubMed1982

Role of sulfhydryl compounds in the control of tyrosinase activity in Neurospora crassa.

It is known that Neurospora crassa mycelia cultured in standard concentrations (76 to 190 micrograms/ml) of sulfate accumulate a low molecular weight inhibitor of tyrosinase (monophenol, dihydroxyphenylalanine: oxygen oxidoreductase; EC 1.14.1.18.1.). This is not observed in cultures grown under sulfate-limiting conditions. The chemical nature of tyrosinase inhibition was investigated. It was shown to be due to the low molecular weight sulfhydryl fraction of the extracts, in which glutathione is predominant. The concentration of low molecular weight sulfhydryl compounds decreased sharply in mycelia submitted to various treatments which also derepressed tyrosinase, such as (i) starvation in phosphate buffer, (ii) treatment with cycloheximide, and (iii) mating. These results suggest that the concentration of sulfhydryl compounds may be of physiological significance in the control of tyrosinase activity in N. crassa.

Catechol Oxidase↗
PubMed1984

Effects on red blood cell choline transport induced by different sulfhydryl compounds.

The uptake of choline was studied in different types of paroxysmal nocturnal hemoglobinuria (PNH)-like RBC obtained from normal human erythrocytes by the action of different sulfhydryl compounds. The results were compared with the uptake of choline in true PNH cells and in normal reticulocytes. The PNH-like cells which better mimicked true PNH were those prepared using acetylcysteine. Indeed these erythrocytes displayed a capacity to incorporate choline against a concentration gradient exactly as PNH cells exposed to either acetylcholine or choline. The uptake of choline by by the other PNH-like cells differed from that of PNH erythrocytes in several ways. The results suggest that every sulfhydryl compound induces a different damage on RBC membrane.

Biological Transport, Active↗
PubMed1990

Thioureas react with superoxide radicals to yield a sulfhydryl compound. Explanation for protective effect against paraquat.

Thiourea and superoxide dismutase were effective antidotes to paraquat toxicity in an HL60 cell culture system, whereas other hydroxyl scavengers were ineffective. The efficacy of thioureas was not due to blockage of intracellular paraquat uptake, inhibition of NADPH-P-450 reductase, or reaction with the paraquat radical. Thiourea also competitively inhibited the reduction of cytochrome c by the xanthine/xanthine oxidase superoxide-generating system, and the release of iron from ferritin by superoxide radicals. The reaction of superoxide with thiourea produced a sulfhydryl compound distinct from products formed by hydrogen peroxide or hydroxyl radicals. Spectrophotometric and chromatographic studies indicated the carbon-sulfide double bond was converted to a sulfhydryl group which reacted with Ellman's reagent. Additional confirmatory evidence for the sulfhydryl compound was obtained with carbon-13 NMR and mass spectroscopies. Thus, thioureas are direct scavengers of superoxide radicals as well as hydroxyl radicals and hydrogen peroxide. The rate constant for the reduction of thiourea by superoxide was estimated at 1.1 x 10(3) M-1 s-1. The implication of this finding on free radical studies, the mechanism of paraquat toxicity, and the metabolism of thioureas is discussed.

Acetonitriles↗
PubMed2004

Mechanisms of gastroprotection by lansoprazole pretreatment against experimentally induced injury in rats: role of mucosal oxidative damage and sulfhydryl compounds.

This study investigated the mechanisms involved in the protective actions exerted by lansoprazole against experimental gastric injury. Following the intraluminal injection of ethanol-HCl, the histomorphometric analysis of rat gastric sections demonstrated a pattern of mucosal lesions associated with a significant increase in the mucosal contents of malondialdehyde and 8-iso-prostaglandin F(2alpha) (indices of lipid peroxidation), as well as a decrease in the levels of mucosal sulfhydryl compounds, assayed as reduced glutathione (GSH). Pretreatment with lansoprazole 90 micromol/kg, given intraduodenally as single dose or once daily by intragastric route for 8 days, significantly prevented ethanol-HCl-induced gastric damage. The concomitant changes in the mucosal levels of malondialdehyde, 8-iso-prostaglandin F(2alpha) and GSH elicited by ethanol-HCl were also counteracted by lansoprazole. In separate experiments, performed on animals undergoing 2-h pylorus ligation, lansoprazole did not enhance the concentration of prostaglandin E(2), bicyclo-prostaglandin E(2), or nitric oxide (NO) metabolites into gastric juice. Western blot analysis revealed the expression of both type 1 and 2 cyclooxygenase (COX) isoforms in the gastric mucosa of pylorus-ligated rats. These expression patterns were not significantly modified by single-dose or repeated treatment with lansoprazole. Lansoprazole also exhibited direct antioxidant properties by reducing 8-iso-prostaglandin F(2alpha) generation in an in vitro system where human native low-density lipoproteins were subjected to oxidation upon exposure to CuSO(4). The present results suggest that the protective effects of lansoprazole can be ascribed to a reduction of gastric oxidative injury, resulting in an increased bioavailability of mucosal sulfhydryl compounds. It is also proposed that lansoprazole does not exert modulator effects on the gastric expression of COX isoforms as well as on the activity of NO pathways.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1994

Sulfhydryl compounds and antioxidants inhibit cytotoxicity to outer hair cells of a gentamicin metabolite in vitro.

Aminoglycoside antibiotics such as gentamicin have long been known to destroy cochlear and vestibular hair cells in vivo. In the cochlea outer hair cells are preferentially affected. In contrast, gentamicin will not damage outer hair cells in vitro unless it has been enzymatically converted to a cytotoxic metabolite. Several potential inhibitors of this enzymatic reaction were tested in an in vitro assay against outer hair cells isolated from the guinea pig cochlea. Viability of hair cells (viable cells as per cent of total number of cells observed) averaged about 70% under control conditions. Addition of metabolized gentamicin significantly reduced viability to less than 50% in one hour. Sulfhydryl compounds (glutathione, dithioerythritol) and antioxidants (vitamin C, phenylene diamine, trolox) prevented the cytotoxic actions of the gentamicin metabolite. Inhibitors of amine oxidases and compounds reportedly protective against renal and acute lethal toxicity of aminoglycosides (poly-L-aspartate and pyridoxal phosphate, respectively) were ineffective as protectants. The results reinforce the hypothesis that gentamicin is enzymatically converted to a cytotoxin and imply the participation of sulfhydryl-sensitive groups or free radicals in this reaction. Alternatively or additionally, sulfhydryl compounds or antioxidants may participate in detoxification reactions.

Animals↗
PubMedDate not supplied

The effect of immunostimulatory drugs on sulfhydryl compounds in plasma, liver and brain after ethanol-induced liver injury in rats.

Sulfhydryl compounds in plasma, liver and brain of rats treated with two immunostimulant drugs, isoprinosine and levamisole, after alcoholic liver injury have been investigated. After use of both drugs for 6 days we found partially beneficial effect on the SH-groups in plasma and liver. No changes in nonprotein SH compounds were observed in rat brain after treatment with isoprinosine, levamisole or ethanol. Furthermore, levamisole shortens the time necessary for the return of AlAT activity to normal value.

Animals↗
PubMedDate not supplied

Dynamics of nonprotein and protein sulfhydryl compounds in rat gastric mucosa: possible implication for cytoprotection and ulcerogenesis.

The hypothesis that nonprotein and protein sulfhydryls in gastric mucosa may play some role in the defensive and offensive processes of gastric epithelium was tested in this study in the intact rat gastric mucosa. Both sulfhydryl compounds presented statistically significant changes during the 24-hour day. The content of nonprotein sulfhydryls was less during the dark span than during the light span, while the circadian acrophase of protein sulfhydryls occurred during dark span. These results may offer a new interpretation of the greater vulnerability to ulcerogenic agents of the gastric mucosa of rats during their usual activity span.

Animals↗
PubMed1985

The effect of sulfhydryl compounds on the catalytic activity of Cu, Zn-superoxide dismutase purified from rat liver.

Sulfhydryl compounds such as reduced glutathione, cysteine and 2-mercaptopropionylglycine, a hepato-protective agent, activated Cu, Zn-superoxide dismutase purified from rat liver at low concentrations (below 10 microM). Furthermore we found evidence indicating that this activation is achieved by reducing Cu2+ present in the catalytic site of the dismutase, and thereby promoting the dismutation of superoxide anions.

Animals↗
PubMed1990

Ethanol decreases the level of sulfhydryl compounds in red blood cells and changes their hematological pattern in rats.

The level of sulfhydryl compounds in red blood cells (RBCs) and plasma and some haematological parameters were investigated in rats treated with ethanol for 4 weeks (daily dose of 6g/kg, 30% w/v, p.o.). After ethanol ingestion, the significant decrease of non-protein - SH groups were observed in RBCs and plasma. In treated rats, the mean corpuscular haemoglobin concentration (MCHC) was decreased and the mean corpuscular volume (MCV) was increased. There is a positive correlation between these two parameters and decreased content of sulfohydryl groups in RBCs.

Animals↗
PubMed1985

Efficacy of sulfhydryl compounds as inhibitors of iron-dependent doxorubicin-enhanced lipid peroxidation.

The ability of sulfhydryl compounds to inhibit doxorubicin enhanced lipid peroxidation in the presence of added iron was evaluated. Optimal conditions for doxorubicin-enhanced lipid peroxidation were 25 microM doxorubicin, 2 mM ADP and 250 microM ferric chloride at pH 8.0. Lipid peroxidation was inhibited by EDTA (500 microM), SKF 525 A (100 microM) and vitamin E (0.1 unit/ml). Cysteamine (1 mM) stimulated basal lipid peroxidation but produced net inhibition of lipid peroxidation with doxorubicin. Cysteamine (10 mM) was more efficacious at inhibiting lipid peroxidation. N-acetylcysteine at 1 and 10 mM was a potent stimulator of lipid peroxidation and was ineffective at inhibiting lipid peroxidation in the presence of doxorubicin either at optimal or suboptimal concentrations of iron. In contrast, glutathione (1 mM) was a potent inhibitor of lipid peroxidation. The data suggests that N-acetylcysteine protects against doxorubicin by prior conversion to glutathione.

Acetylcysteine↗
PubMed1976

Metabolic transformation of colchicine, IV[1]. On the interaction of colchicine and colchiceine with sulfhydryl compounds.

The interaction of colchicine and one of its metabolites, O10-demethylcolchicine (colchiceine), with sulfhydryl compounds was studied in several experimental systems. Colchiceine protects reduced glutathione from oxidation by atmospheric oxygen. Inactivation of enzymes with catalytically essential sulfhydryl groups is prevented by colchiceine. In affinity chromatographic experiments, Agarose-bound colchiceine adsorbs sulfhydryl enzymes which may be eluted specifically by SH-compounds like mercaptoethanol. No such effects are shown by colchicine. The data demonstrate a novel type of biochemical reactivity in the metabolite colchiceine with potential biological relevance.

Adenosine Deaminase↗
PubMed1988

Changes in sulfhydryl compounds in plasma, liver and brain after acute and chronic acetaldehyde administration in rats.

The content of sulfhydryl compounds in proteins and non-proteins of plasma, liver and brain after acute and chronic administration of acetaldehyde (ACH) was investigated in rats. After ACH 1.5% w/v ingestion for 1 and 4 weeks (0.3 ml/kg) daily, proteins and non-proteins in plasma and liver were decreased significantly. After acute ACH administration SH-groups in brain proteins were not significantly decreased, but in the brain non-proteins these groups were increased significantly.

Acetaldehyde↗