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Results for “Sulfhydryl Compounds”

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PubMed1995

The role of non-protein sulfhydryl compounds in gastric adaptive cytoprotection against ethanol-induced mucosal damage in rats.

The contribution of the endogenous nonprotein sulfhydryl compounds (SH) in gastric adaptive cytoprotection was investigated in rats. N-ethylmaleimide (NEM) treatment significantly reduced mucosal SH level, and aggravated the mucosal injury induced by absolute ethanol. Oral administration of the mild irritants, 20% ethanol, 5% NaCl or 0.3 M HCl, significantly increased the basal mucosal SH level. These agents also showed a cytoprotective action against the necrotizing effect of absolute ethanol. Administration of NEM did not alleviate this cytoprotective potential, although it abolished the increased SH level evoked by these mild irritants. Thus, it is concluded that modulation of endogenous SH by mild irritants perhaps only plays a minor role in the gastric adaptive cytoprotection.

Administration, Oral↗
PubMed2000

Effects of sulfhydryl compounds on interleukin-1-induced vascular endothelial growth factor production in human synovial stromal cells.

We investigated the effects of various sulfhydryl compounds on interleukin-1 (IL-1)-induced vascular endothelial growth factor (VEGF) production in human synovial stromal cells (HSSC). HSSC stimulated by IL-1beta (100 ng/ml) produced VEGF and interleukin-6 (IL-6) in vitro. Monosulfhydryl compounds, N-acetylcysteine, D-penicillamine, tiopronin and the bucillamine-like disulfhydryl compound, compound A scarcely affected VEGF or IL-6 production at concentrations of 10(-5) and 10(-4) M. However, the disulfhydryl compound, bucillamine inhibited VEGF production but not IL-6 production at concentrations of 10(-5) and 10(-4) M. These results suggest that bucillamine may be a selective inhibitor of IL-1-induced VEGF production in HSSC, and that inhibition of VEGF production may require not only SH groups but also a specific chemical structure.

Acetylcysteine↗
PubMed1985

Reversal of antisecretory activity of omeprazole by sulfhydryl compounds in isolated rabbit gastric glands.

We have examined the interaction of omeprazole, a gastric antisecretory agent, with endogenous or exogenous sulfhydryl compounds in isolated rabbit gastric glands. The glands exposed to omeprazole (2 microM for 50 min) could recover acid secretory response to dibutyryl-cAMP upon addition of dithiothreitol, cysteine or glutathione. Washing the omeprazole-exposed glands free of the extracellular drug also led to a similar recovery of the acid secretory response. Depletion of cellular glutathione with 2-cyclohexen-1-one had no considerable effect on the secretory response of the glands to dibutyryl-cAMP, but prevented the reversal of the antisecretory effect of omeprazole upon washing or adding exogenous cysteine. Also, the antisecretory potency of omeprazole increased several fold in the glutathione-depleted glands. These observations indicate that cellular glutathione is essential to reactivate the omeprazole-modified enzyme(s), possibly (H+ + K+)-ATPase, in acid secretory process and led us to propose that omeprazole is an agent reacting with sulfhydryl groups.

Animals↗
PubMed1984

Influence of some sulfhydryl compounds on the antineoplastic effectiveness of 5-fluorouracil and 6-mercaptopurine.

The influence of three chosen model sulfhydryl groups containing compounds, characterized by increasing size of molecule--cysteine, glutathione and insulin on antineoplastic activity of 5-fluorouracil (5-FU) and 6-mercaptopurine (6-MP) against murine leukemia L-1210 5-FU and 6-MP and murine sarcoma Sa 180, was studied. Sulfhydryl compounds failed to change in most cases the therapeutic (antineoplastic) effect of 5-FU and 6-MP. However, certain doses of these sulfhydryl compounds enhanced the cytostatic effect of 6-MP in respect to Sa-180.

Animals↗
PubMed1995

Effects of sulfhydryl compounds on the accumulation, removal and cytotoxicity of inorganic mercury by primary cultures of rat renal cortical epithelial cells.

The effects of sulfhydryl compounds on the accumulation, removal and cytotoxicity of inorganic mercury (Hg) were investigated in primary cultures of rat renal cortical epithelial cells. The compounds investigated were 2,3-dimercaptosuccinic acid, 2,3-dimercapto-1-propanol, D-penicillamine, glutathione (GSH) and L-cysteine. In the accumulation experiment, the cells were co-incubated with Hg and the above compounds for 30 min. (short-term) or 18 hr (long-term). In the removal experiment, cells incubated with Hg were further incubated with the above compounds for 30 min. In both experiments, the alleviative effect of the compounds on the cytotoxicity was estimated by the uptake of neutral red or by cell growth. 2,3-Dimercaptosuccinic acid had the highest antidotal effects except for Hg removal. 2,3-Dimercapto-1-propanol exerted the least antidotal effects in the short-term, as well as in the long-term experiments, 2,3-dimercapto-1-propanol increased the Hg accumulation and the cytotoxicity despite its removal of most of the Hg. Although D-penicillamine, L-cysteine and GSH did not increase the Hg removal in the long-term experiment other antidotal effects were seen.

Animals↗
PubMed1982

Protective role of endogenous pulmonary glutathione and other sulfhydryl compounds against lung damage by alkylating agents. Investigations with 4-ipomeanol in the rat.

Because endogenous glutathione is known to participate in the detoxification of highly reactive, hepatotoxic drug metabolites, we studied the role of this substance in the pulmonary toxicity of 4-ipomeanol [1-(3-furyl)-4-hydroxypentanone] in rats. 4-Ipomeanol was an appropriate model for these studies since previous investigations have indicated that an alkylating metabolite, formed in situ, is responsible for selective lung damage by 4-ipomeanol. Toxic doses of 4-ipomeanol preferentially depleted rat lung glutathione. Pretreatment of animals with piperonyl butoxide, an inhibitor of the metabolic activation of 4-ipomeanol, prevented both the depletion of lung glutathione and the pulmonary toxicity of 4-ipomeanol. Prior depletion of lung glutathione by diethylmaleate increased both the pulmonary covalent binding and the toxicity of 4-ipomeanol, whereas administration of cysteine and cysteamine decreased both the covalent binding and the toxicity. These in vivo studies, in conjunction with previous in vitro studies which showed inhibitory effects of sulfhydryl compounds on the covalent binding of 4-ipomeanol, are consistent with the view that pulmonary glutathione plays a protective role against pulmonary alkylation and lung toxicity by 4-ipomeanol, probably by reacting with the toxic metabolite(s) to form nontoxic conjugate(s). Pulmonary glutathione may similarly provide protection against other electrophilic drugs or metabolites that can damage the lungs.

Animals↗
PubMedDate not supplied

Protection against radiation induced chromosome injury by sulfhydryl compounds.

The radiation induced changes in a critically radiation-sensitive tissue, bone marrow of Swiss albino mice and its modification by two sulfhydryl compounds, MPG and WR-2721, were studied cytogenetically after whole body exposure to 0.5, 1.5, 3.0, 4.5 and 6.0 Gy of 60Co gamma radiation. The changes in the structural arrangements of chromosomes in the bone marrow were studied at various post-irradiation times from 1 to 28 days. Both the control (irradiated) and experimental (drug + irradiation) animals showed qualitatively similar types of aberrations; the severity of lesions increased with the radiation dose. The maximum damage in all the groups was seen on day 1, post-irradiation. Both the drugs afforded better protection at lower doses of exposure, their effectiveness decreasing with an increasing radiation dose. Of the two drugs, WR-2721 was more effective than MPG against initial aberration yield but the former, at the present drug dose, showed some toxic effect at the later post-irradiation intervals (2 weeks onward) as manifested by an increase in the chromatid breaks and polyploidy.

Animals↗
PubMed1996

Effect of the sulfhydryl compound cysteamine on gamma-radiation-induced mutations in double-stranded M13 DNA.

Sulfhydryl compounds can protect DNA against free-radical-induced DNA damages not only by scavenging of radicals, but also by chemical non-enzymatic repair or modification of such damages by hydrogen-donation. To investigate the influence of chemical repair and modification on mutations, induced by gamma-radiation-generated free radicals (.OH, .H), phosphate-buffered aqueous solutions of double-stranded (ds) M13 DNA were exposed to gamma-rays under N2 in the presence of 5 mM cysteamine. The exposed DNA was subsequently transfected to wild-type E. coli and mutations in the mutational target were characterized. This target in fact contains three different target sequences, i.e., the lac promoter/operator, the lacZ alpha gene and a 144 bp inframe insert. The mutation spectrum obtained was compared with those in the absence of cysteamine under N2 and N2O. In the latter case, the ratio of .OH and .H available for reacting with DNA is about the same as under N2 + cysteamine. The results show that chemical repair and/or modification by cysteamine of potentially lethal lesions takes place, leading to a much higher survival of ds M13 DNA in the presence of cysteamine than could be expected on basis of scavenging of .OH and .H alone. This higher survival appeared to be accompanied with a higher mutation induction. However, the N2 + cysteamine mutation spectrum shows a remarkable resemblance with the N2O-spectrum. This holds for the total mutation target, as well as each of the three targets, although the mutations obtained in each of the three targets under the same irradiation conditions are quite different. Thus, it can be concluded that cysteamine is mainly effective on radiation-induced potentially lethal DNA lesions, and not so much on (pre)mutagenic damages. Moreover, the type of mutation appeared to be strongly dependent on the mutational target sequence.

Bacteriophage M13↗
PubMed1989

Irreversible inhibition of v-src tyrosine kinase activity by herbimycin A and its abrogation by sulfhydryl compounds.

Herbimycin A, an antibiotic which reverses Rous sarcoma virus transformation, inhibited irreversibly the auto- and trans-phosphorylation activities of p60v-src in in vitro immune complex kinase assays. The addition of a sulfhydryl compound such as dithiothreitol, 2-mercaptoethanol, glutathione (reduced form) or cysteine abolished the ability of herbimycin A to inactivate p60v-src kinase as well as the ability to reverse transformed cell morphology, whereas the addition of oxidized glutathione, cystine or methionine showed no effect. The sulfhydryl alkylating reagent N-ethylmaleimide also, although less effectively, inactivated p60v-src kinase activity in vitro. These results suggest the likelihood that sulfhydryl groups of p60v-src are involved in the inactivation of v-src tyrosine kinase activity by herbimycin A.

Benzoquinones↗
PubMed1977

Total lactate dehydrogenase and its isoenzymes in serum in the presence of penicillamine and other sulfhydryl compounds.

Toward delineation of changes in total lactate dehydrogenase (LDH) and in the distribution of LDH isoenzymes as assessed by polyacrylamide disc electrophoresis, we inbucated human and rat sera with various agents, notably sulfhydryl compounds. Although artefacts were apparent when these agents were used without preliminary adjustment of pH, we saw little alteration in total unitage when one or two volumes of serum was mixed with one volume of any of several thiols, especially penicillamine, at an initial concentration of 0.4 mol/liter and pH 7.0-7.5. Under these conditions, penicillamine caused a loss in LDH-5 after incubation for 1 h at 25 degrees C together with small decreases in mobility of the other four isoenzymes toward the anode. A zymosan region appeared below the albumin and tracking dye area. With longer periods of incubation of rat serum with penicillamine or alpha-mercaptosuccinate, a novel band in the zymogram was noted just above the LDH-4 peak. The observations are discussed in terms of allosteric effectors.

Animals↗
PubMed1980

[Pharmacological studies of new sulfhydryl compounds 2-mercapto-2-methylpropanoyl-L-cysteine (SA96). I. Evaluation of anti-rheumatic action (author's transl)].

Oral administration of 2-mercapto-2-methylpropanoyl-L-cysteine (SA 96), a newly synthesized sulfhydryl compound, showed protective and curative effects on adjuvant-induced arthritis in rats similarly to those seen with D-penicillamine (D-PA). However, the effects of these compounds were not dose-dependent, and the maximum effects of SA96 were observed at 10 mg/kg/day. On the contrary, SA96 and D-PA had little effect on the various acute and subacute inflammatory responses induced in rat and mice. Formation of hemolytic plaque forming cells in the spleen of mice immunized with 5 X 10(8) sheep red blood cells was potentiated by the oral administration of both compounds. These stimulatory effects of SA96 and D-PA on the humoral immune responses were also not dose-dependent, and the maximum effects of SA96 were observed with 10 mg/kg/day, as in the case of adjuvant-induced arthritis in rats. In in vitro experiments, the inactivation of rheumatoid factor and the inhibition of collagenase and bone alkaline phosphatase activities were observed with both compounds, but these effects of SA96 were more potent than those of D-PA. As there is a similarity in the pharmacological profiles of SA96 and D-PA, SA96 may prove to be clinically effective for rheumatoid arthritis.

Acute Disease↗
PubMed2003

Alteration in plasma levels of nonprotein sulfhydryl compounds and S-nitrosothiols in chronic renal failure patients.

BACKGROUND: Uremia is accompanied by the elevated nitric oxide (NO) synthesis, and it has not yet been established how this influences the levels of nonprotein sulfhydryl compounds (NPSH) and formation of S-nitrosothiols (SNT). METHODS: Our study was designed to determine plasma levels of SNT and NPSH in chronic renal failure (CRF) patients, who were hemodialysed (HD) or were not on hemodialysis treatment (ND), and in the control group. RESULTS: In ND patients, the plasma levels of SNT were significantly increased (11.25+/-2.08 nmol/ml, p<0.01), while NPSH levels were simultaneously decreased (66.67+/-15.0 nmol/ml, p<0.05) in comparison with the control subjects (SNT: 8.75+/-2.08 nmol/ml, NPSH: 86.66 nmol/ml). In HD patients, plasma concentration of SNT before hemodialysis was significantly lower than in the control group (0.150+/-0.042 nmol/mg protein vs. control: 0.175+/-0.075 nmol/mg protein), and no significant change was observed after dialysis (0.142+/-0.058 nmol/mg protein, p<0.05). The level of NPSH in HD patients before dialysis was significantly decreased in comparison with the control subjects, both, when the results were calculated per 1 ml of plasma (45.96+/-17.87 nmol/ml) and per 1 mg of protein (0.70+/-0.25 nmol/mg protein). In the postdialysis samples, NPSH rose (79.15+/-22.9 nmol/ml, p<0.001 which corresponds to 1.30+/-0.55 nmol/mg protein, p<0.001) as compared to the level before dialysis. CONCLUSIONS: Firstly, plasma SNT level was found to be increased in CRF patients who were not treated with hemodialysis, while in HD patients, it dropped below the control values. It indicates that hemodialysis disturbs an equilibrium of reactions involved in S-nitrosothiols formation most probably by removing low molecular weight S-nitrosylating compounds. Secondly, the increased level of NPSH after each hemodialysis session indicates reestablished antioxidant capacity of plasma and suggests the existence of dialysable compounds, which via unknown mechanism become responsible for the decreased level of thiols.

Adult↗
PubMed2002

The gamma-glutamyltransferase activity and non-protein sulfhydryl compounds levels in rat kidney of different age groups.

The present work was aimed to obtain information about age-dependent changes of gamma-glutamyltransferase (GGT) activity and the levels of non-protein sulfhydryl compounds (NPSH) in rat kidneys. In addition, protein-bound cysteine (PB-Cys), sulfane sulfur compounds and reactive oxygen species (ROS) were estimated. The results indicate that the activity of GGT and NPSH levels in the kidneys are reduced with age. At the same time, a significant increase in the level of protein-bound cysteine was observed. Simultaneously, the content of sulfane sulfur compounds was increased in the group of the oldest animals. These findings indicate that the capacity for extracellular glutathione degradation and, in consequence, the availability of cysteine for intracellular glutathione biosynthesis may be impaired. The increased PB-Cys level indicates potentiation of the thiolation reaction, i.e. development of protein-mixed disulfides. These results reveal age dependent disturbances in the thiol-disulfide equilibrium in the kidneys which leads to an imbalance between pro- and antioxidatory processes.

Aging↗
PubMed1990

Oxygen radicals mediate depletion of pancreatic sulfhydryl compounds in rats with cerulein-induced acute pancreatitis.

Acute edematous pancreatitis was induced in conscious rats by intravenous infusion of cerulein at a supramaximal dose of 7.5 micrograms/kg/h during 6 h. The most important finding of our study was a marked decrease in the protein and non-protein content of sulfhydryl groups parallel to an evident elevation in the malondialdehyde concentration in pancreatic tissue. The presented data suggest that in cerulein-induced acute pancreatitis in rats, oxygen radicals mediate increased peroxidation reactions which are accompanied by depletion of nonenzymatic sulfhydryl-containing free radical scavengers. The above phenomenon contributes to a disturbance in thiol metabolism resulting in serious diminution of pancreatic protein sulfhydryl compounds.

Acute Disease↗