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PubMed1983

Reversible interconversion between sulfo and desulfo xanthine oxidase in a system containing rhodanese, thiosulfate, and sulfhydryl reagent.

The desulfo form of milk xanthine oxidase (xanthine: oxygen oxidoreductase, EC 1.2.3.2) was reactivated by incubation with rhodanese (thiosulfate: cyanide sulfurtransferase, EC 2.8.1.1), thiosulfate, and sulfhydryl reagent; 50% of full activity was recovered. No further reactivation occurred with additional incubation. It was also found that native enzyme in the sulfo form with full activity was inactivated by incubation with the same system, down to half of full activity and no further inactivation occurred. After these incubations the enzyme was found to be a mixture of functional and nonfunctional enzymes based on spectral changes with xanthine, on [14C]oxipurinol equilibration, and on steady-state kinetics. The 35S of [35S]thiosulfate was incorporated into desulfo xanthine oxidase in parallel with an increase in catalytic activity. Most of the 35S was cyanolysable but was protected from cyanolysis by pretreatment with allopurinol. The 35S was released from 35S-labeled reconstituted xanthine oxidase upon incubation with the rhodanese system containing unlabeled thiosulfate. However, catalytic activity remained unchanged, indicating that the sulfur atom was exchanged during the incubation.

Dithiothreitol↗
PubMed1975

The efficiency of aquocobalamine as an antidote in cyanide poisoning when given alone or combined with sodium thiosulfate.

The antidotal activities of aquocobalamineacetates and sodium thiosulfate were tested in guinea pigs and cats. The animals were attached to artificial respirators throughout the experiment and were poisoned with a continuous infusion of sodium cyanide solution (4.1 muMol/kg.min NaCN). The rate of action of each antidote was determined from the time taken for the HCN exhalation to drop below the level of 100 nMol/kg.min in quinea pigs, and to values below 25 nMol/kg.min in cats; the detoxifying capacity of each antidote was determined from the time taken for the HCN exhalation to rise above the said values and the time interval for normal function of heart activity to be restored. Aquobalamine was characterized by its rapid rate of reaction in both the animal species; its detoxifying capacity showed, however, according to our expectations, variations corresponding to the applied doses. The combination of the antidotes aquocobalamine (100 mg/kg) and thiosulfate (500 mg/kg) proved to possess high rate of reaction and a large detoxifying capacity in guinea pigs. Similar results were obtained in cats with antidote doses of 200 mg/kg aquocobalamine combined with 500 mg/kg thiosulfate. The slow rate of reaction and large detoxifying capacity of thiosulfate were confirmed in our experiments. It combination with aquocobalamine showed no undesirable change in its antidotal action providing a time interval of 1 min was maintained between the 2 injections.

Animals↗
PubMed1988

Effects of fosfomycin, mesna, and sodium thiosulfate on the toxicity and antitumor activity of cisplatin.

Fosfomycin and mesna were investigated in rats and mice concerning their detoxifying effects on cisplatin toxicity in comparison to sodium thiosulfate, a known protector against cisplatin nephrotoxicity. After separate i.p. injection of cisplatin and fosfomycin (500 mg/kg) or mesna (800 mg/kg) a slight increase in the 50% lethal dose of cisplatin was found in all animals. In mice sodium thiosulfate proved to be far more effective in preventing lethal toxicity and nephrotoxicity as measured by blood urea nitrogen increase. Fosfomycin and mesna were almost without influence on cisplatin treatment of L-1210 leukemia whereas their inhibition of the antitumor effect against S-180 ascites sarcoma (increase of in cisplatin dose to cure 50% of animals from 2.0 mg/kg to 3.5/4.7 mg/kg cisplatin) was similar to thiosulfate, which showed a strong inhibiting effect in the treatment of both tumors. In rats fosfomycin distinctively reduced the antitumor efficacy of cisplatin against Yoshida ascites sarcoma. Thus the concurrent injection of fosfomycin and mesna reduced both the toxicity and the antitumor activity of cisplatin. Therefore their simultaneous administration in addition to cisplatin via the same injection route should be avoided. Due to the weak detoxifying efficacy of fosfomycin and mesna they cannot be used instead of sodium thiosulfate for renal protection against cisplatin toxicity in local i.p. treatment modalities.

Animals↗
PubMed1989

Protection of gastric mucosa against hypertonic sodium chloride by 16,16-dimethyl prostaglandin E2 or sodium thiosulfate in the rat: evidence for decreased mucosal penetration of damaging agent.

Protection of the gastric mucosa may be the result of either increased cellular resistance to injury (cytoprotection) or, alternatively, decreased exposure of mucosal cells to the damaging agent. To determine whether decreased exposure of mucosal cells to damaging agents plays a role in mucosal protection by 16,16-dm PGE2 or sodium thiosulfate, we estimated the intramucosal concentration of 22NaCl and measured its absorption from the gastric lumen into the systemic circulation 1 and 5 min after intragastric administration of hypertonic (25% w/v) 22NaCl. In an attempt to explain the differences observed, we also measured the net transmucosal water flux in control animals and rats pretreated with the protective agents. Administration of hypertonic NaCl rapidly (within 1 min) induced extensive hemorrhagic mucosal lesions that were significantly reduced by pretreatment with 16,16-dm PGE2 or sodium thiosulfate. Ultra-low temperature autoradiography indicated that luminal hypertonic 22NaCl penetrates the upper layers of the mucosa in relatively high concentrations (12.5% w/v) within 1 min but its concentration decreases rapidly and reached low levels (3.12% w/v) by 5 min. Absorption of NaCl from the gastric lumen into the systemic circulation 1 and 5 min after hypertonic NaCl was lower in both pretreatment groups than in the control. Net gastric transmucosal water flux (from serosa to mucosa) increased (P less than 0.05) from 100 +/- 2 in controls, to 1470 +/- 8 and 715 +/- 9 microliters in rats pretreated with 16,16-dm PGE2 and sodium thiosulfate, respectively. We conclude that 16,16-dm PGE2 and sodium thiosulfate protect the gastric mucosa against hypertonic NaCl, diminish mucosal penetration of NaCl, decrease mucosal absorption of NaCl, and significantly increase serosal to mucosal transmucosal water flux.(ABSTRACT TRUNCATED AT 250 WORDS)

16,16-Dimethylprostaglandin E2↗
PubMed1991

Phase-1 trial of high-dose intravenous cisplatin with simultaneous intravenous sodium thiosulfate.

Previous pharmacological and clinical data have suggested that it is possible to increase significantly the dose of "active" cisplatin delivered systemically by the simultaneous administration of intravenous sodium thiosulfate. In order to define more critically the toxicity and potential efficacy of this therapeutic approach, 36 patients with a variety of solid tumors and limited pretreatment were entered into a phase-1 trial of high-dose intravenous cisplatin plus sodium thiosulfate. The maximally tolerated dose of cisplatin was found to be 200 mg/m2, excessive renal toxicity being observed at a dose of 225 mg/m2 (6/14 courses associated with serum creatinine rise to greater than 2.0 mg-%). Following several courses of high-dose cisplatin, peripheral neuropathy becomes the limiting toxicity (9/15 patients receiving at least three courses of cisplatin at greater than or equal to 150 mg/m2 experienced at least grade-1 neuropathy). Significant ototoxicity developed after only one or two treatment courses, but with continued treatment hearing loss appeared to stabilize in the moderately severe range in most patients. Major responses (PR/CR) were observed in 7/27 evaluable patients. We conclude that cisplatin can be administered at a dose at 200 mg/m2 as a 2-h infusion (with simultaneous sodium thiosulfate) with significant but acceptable toxicities and without evidence of loss of anti-neoplastic activity (secondary to the presence of thiosulfate). However, owing to the development of neurotoxicity most patients will be unable to receive more than three courses of this high-dose treatment regimen.

Adult↗
PubMed2000

Stable sulfur isotope fractionation during the reduction of thiosulfate by Dethiosulfovibrio russensis.

Stable sulfur isotope fractionation was investigated during reduction of thiosulfate by growing batch cultures of Dethiosulfovibrio russensis at a cell-specific reduction rate of 2.4 +/- 0.72 fmol cell(-1) d(-1) (28 degrees C). Citrate was used as carbon and energy source. The hydrogen sulfide produced by this sulfur- and thiosulfate-reducing bacterium was depleted in 34S by 11% compared to total thiosulfate sulfur, in agreement with previous results observed for sulfate-reducing bacteria. This indicates the operation of a similar pathway for thiosulfate reduction in these phylogenetically different bacteria.

Anaerobiosis↗
PubMed2005

Oxidation of thiosulfate to tetrathionate by an haloarchaeon isolated from hypersaline habitat.

A novel, extremely halophilic, neutrophilic archaeon was isolated from a mixed sediment sample from different hypersaline lakes in Kulunda steppe (Altai, Russia) at 4 M NaCl with acetate and thiosulfate as substrates. The enrichment culture developed in two phases. During the first phase, a rapid growth of heterotrophic, red-colored, polymorphic rods occurred with the concomitant oxidation of thiosulfate to tetrathionate. The latter was subsequently oxidized to sulfate during a second, slower phase by extremely halophilic, chemolithoautotrophic bacteria belonging to the gamma subdivision of the Proteobacteria. The archaeal strain HG 1 was isolated from the first phase of the enrichment culture using acetate as substrate. It was able to oxidize thiosulfate to tetrathionate during heterotrophic growth with acetate-a property not yet demonstrated for any of the known haloarchaea. The presence of tetrathionate synthase, the enzyme responsible for thiosulfate oxidation, was detected in strain HG 1. The activity was associated with membranes and depended specifically on Cl-, in contrast to the similar activity in extremely halophilic sulfur-oxidizing Gammaproteobacteria from the same enrichment, which was soluble and demanded both Na+ and Cl- . Strain HG 1 was identified as a member of the genus Natronorubrum.

Archaea↗
PubMed1975

The use of thiosulfate to increase polymerization of IgM subunits.

Sodium thiosulfate was used to enhance in vivo the polymerization of myeloma IgM, deficient in disulfide cross-links. The therapy sharply decreased the amount of low molecular weight IgM fractions, while increasing the serum content of molecules of higher molecular weight. The degree of disulfide cross-linking in IgM increased under the influence of thiosulfate. The rate of secretion into the serum and urine of some membrane-related glycopeptides and species rich in sialic acid was reduced. Also, the discharge of L chains to the urine was lowered during the thiosulfate trial. All these changes were attributed to enhancement of disulfide-interchanging enzyme activity by thiosulfate.

Binding Sites↗
PubMed1982

The specificity of active-site alkylation by iodoacetic acid in the enzyme thiosulfate sulfurtransferase.

The active-site sulfhydryl group in the enzyme thiosulfate sulfurtransferase (rhodanese; thiosulfate:cyanide sulfurtransferase; EC 2.8.1.1) is alkylated rapidly by iodoacetic acid in the free enzyme form, E, with complete loss of sulfurtransferase activity. Iodoacetic acid is completely ineffective with the sulfur-substituted form of the enzyme, ES. Iodoacetamide, on the other hand, has no effect on either enzyme form. The competitive enzyme inhibitor, toluenesulfonic acid, protects against inactivation in a strictly competitive way and analysis gives an apparent binding constant for toluenesulfonic acid of 12.5 mM, which is in agreement with studies of its effect on the catalyzed reaction. These results are taken to indicate that iodoacetic acid is an affinity analog for the substrate, thiosulfate, and inactivates because it can use the specific thiosulfate binding interactions, correctly orient its reactive center and displace intraprotein interactions which appear to protect the active-site sulfhydryl group in the E form.

Alkylation↗
PubMed1985

Nephrotoxicity of high-dose intracavitary cisplatin with intravenous thiosulfate protection.

Sodium thiosulfate has been shown experimentally to protect against cisplatin-induced renal insufficiency by inactivating the nephrotoxic as well as cytotoxic properties of the agent. However, significant plasma levels of 'active' cisplatin have been demonstrated following high-dose intracavitary cisplatin administration with simultaneous intravenous thiosulfate delivery. At the UCSD Cancer Center 131 patients have been treated with a total of 485 courses (median per patient, 3; range 1-18) of intrapleural or intraperitoneal cisplatin with intravenous thiosulfate protection. Seventy-six patients (58%) had previously been treated with intravenous cisplatin. A total of 14 courses (2.9%) of intracavitary therapy were complicated by a serum creatinine rise to greater than 1.5 mg% which, in all but three cases, returned to the normal range within 1 month following treatment. All but one patient demonstrating clinical evidence of nephrotoxicity had been heavily pretreated with cisplatin. We conclude that thiosulfate can protect against clinically significant cisplatin-induced nephrotoxicity by cisplatin delivered in high doses via the intracavitary route.

Acute Kidney Injury↗
PubMed2004

Growth inhibitory effect of alk(en)yl thiosulfates derived from onion and garlic in human immortalized and tumor cell lines.

Two alk(en)yl thiosulfates, sodium n-propyl thiosulfate (NPTS) and sodium 2-propenyl thiosulfate (2PTS), are natural constituents of onion and garlic, respectively, which were identified originally as causative agents of onion- and garlic-induced hemolytic anemia in dogs. As a continuation of our studies on the beneficial functions of NPTS and 2PTS, in the present study, we investigated the antitumor effects of these compounds. They were shown to inhibit the in vitro proliferation of three human tumorigenic cell lines, WiDr, 293 and HL-60, in a dose-dependent manner. Overall, NPTS seemed to have weak activity for inhibiting cell growth compared with 2PTS, though not in WiDr cells, which were sensitive to both compounds. NPTS and 2PTS caused oxidative damage to HL-60 cells and induced apoptosis. The extent of apoptosis was approximately proportional to that of the oxidative damage and also to that of the cytotoxicity caused by these compounds. These results suggest that the alk(en)yl thiosulfates have an antitumor effect through the induction of apoptosis initiated by oxidative stress.

Allyl Compounds↗
PubMed2004

Persulfate oxidation for in situ remediation of TCE. I. Activated by ferrous ion with and without a persulfate-thiosulfate redox couple.

The objective of the laboratory study is to examine the conditions under which transition metal ions (e.g., ferrous ion, Fe2+) could activate the persulfate anion (S2O8(2)-) to produce a powerful oxidant known as the sulfate free radical (SO4-*) with a standard redox potential of 2.6 V. The SO4-* is capable of destroying groundwater contaminants in situ such as trichloroethylene (TCE). Experiments using Fe2+ as an activator under various molar ratios of S2O8(2)-/Fe2+/TCE in an aqueous system indicated that partial TCE degradation occurred almost instantaneously and then the reaction stalled. Either destruction of SO4-* in the presence of excess Fe2+ or the rapid conversion of all Fe2+ to Fe3+ limited the ultimate oxidizing capability of the system. Sequential addition of Fe2+ in small increments resulted in an increased TCE removal efficiency. Therefore, it appeared that Fe2+ played an important role in generating SO4-*. An observation of oxidation-reduction potential (ORP) variations revealed that the addition of sodium thiosulfate (Na2S2O3) to the ferrous ion activated persulfate system could significantly decrease the strong oxidizing conditions. It was hypothesized that the thiosulfate induced reducing conditions might convert Fe3+ to a lower valence state of Fe2+, making the Fe2+ available to activate persulfate decomposition. The sequential addition of thiosulfate (S2O3(2)-), after the initial stalling of ferrous ion activated persulfate oxidation of TCE, resulted in an improvement in TCE removal. The ferrous ion activated persulfate-thiosulfate redox couple resulted in fairly complete TCE degradation in aqueous systems in a short time frame. In soil slurry systems, TCE degradation was slower in comparison to aqueous systems.

Chromatography, Gas↗
PubMed2005

Deletion of flavoredoxin gene in Desulfovibrio gigas reveals its participation in thiosulfate reduction.

The gene encoding Desulfovibrio gigas flavoredoxin was deleted to elucidate its physiological role in the sulfate metabolism. Disruption of flr gene strongly inhibited the reduction of thiosulfate and exhibited a reduced growth in the presence of sulfite with lactate as electron donor. The growth with sulfate was not however affected by the lack of this protein. Additionally, flr mutant cells revealed a decrease of about 50% in the H2 consumption rate using thiosulfate as electron acceptor. Altogether, our results show in vivo that during sulfite respiration, trithionate and thiosulfate are produced and that flavoredoxin is specific for thiosulfate reduction.

Bacterial Proteins↗
PubMed2002

SoxV, an orthologue of the CcdA disulfide transporter, is involved in thiosulfate oxidation in Rhodovulum sulfidophilum and reduces the periplasmic thioredoxin SoxW.

Proteins of the CcdA/DsbD family have previously been found to be involved in the protein disulfide isomerase and cytochrome c maturation pathways of bacteria. SoxV is a CcdA homologue encoded by a genetic locus involved in lithotrophic thiosulfate oxidation in Rhodovulum sulfidophilum. Mutagenesis studies demonstrate an essential and specific role for SoxV in thiosulfate oxidation. Another protein encoded by the same locus, SoxW, is a periplasmic thioredoxin. SoxW was found to be in the reduced state during growth of R. sulfidophilum in the presence of thiosulfate. Maintenance of SoxW in the reduced state was shown to require SoxV. Nevertheless, SoxW was found to be dispensible for thiosulfate oxidation suggesting that SoxV reduces more than one periplasmic partner protein.

Alphaproteobacteria↗
PubMed2002

Dechlorination of chloroacetanilide herbicides by thiosulfate salts.

Halogenated organic compounds (XOCs) are among the most widely used synthetic chemicals. Many XOCs are recalcitrant to natural degradation and have become prominent environmental contaminants. One group of such XOCs are the heavily used chloroacetanilide herbicides. We have found that chloroacetanilide herbicides are rapidly dechlorinated in water, sand, and soil by thiosulfate salts under ambient conditions. Structural and kinetics analysis suggests that the reaction occurred by S(N)2 nucleophilic substitution, in which the chlorine was replaced by thiosulfate and the herbicide was detoxified. Laboratory studies showed that this reaction could be used for removing residues of chloroacetanilide herbicides in water, soil, and sand. Our findings also suggest that some other XOCs may be subject to this reaction. Because common thiosulfate salts are innocuous products (e.g., fertilizers) and the reaction selectively detoxifies XOCs at low thiosulfate levels, this discovery may lead to a new way for safe removal of certain XOCs from the environment.

Acetamides↗
PubMed1975

Biochemical studies on sulfate-reducing bacteria. XIV. Enzyme levels of adenylylsulfate reductase, inorganic pyrophosphatase, sulfite reductase, hydrogenase, and adenosine triphosphatase in cells grown on sulfate, sulfite, and thiosulfate.

Sulfate-reducing bacteria, Desulfovibrio vulgaris, strain Miyazaki, were grown on either sulfate, sulfite, or thiosulfate as the terminal electron acceptor. Better growth was observed on sulfite and less growth on thiosulfate than on sulfate. Enzyme levels of adenylylsulfate (APS) reductase [EC 1.8.99.2], reductant-activated inorganic pyrophosphatase [EC 3.6.1.1], sulfite reductase [EC 1.8.99.1] (desulfoviridin), hydrogenase [EC 1.12.2.1], and Mg2+-activated ATPase [EC 3.6.1.3] were compared in crude extracts of these cells at various stages of growth. 1) The specific activity of APS reductase in sulfite-grown cells was only one-fourth that in sulfate-grown cells throughout growth. Thiosulfate-grown cells had an activity intermediate between those of sulfate- and sulfite-grown cells. 2) Cells grown on sulfite had lower specific activity of reductant-activated inorganic pyrophosphatase than cells grown on sulfate or thiosulfate. 3) The specific activity of sulfite reductase (desulfoviridin) was highest in sulfite-grown cells. The sulfite medium gave the enzyme in high yield as well as with high specific activity. 4) The specific activities of hydrogenase and Mg2+-ATPase were not significantly altered by electron acceptors in the growth medium.

Adenosine Monophosphate↗
PubMed2000

Validation of thiosulfate for neutralization of acidified sodium chlorite in microbiological testing.

At low pH, acidified sodium chlorite (ASC) has antimicrobial activity against a variety of foodborne contaminants. To evaluate the antimicrobial efficacy of ASC at specific time points posttreatment, it is necessary to halt the action of the disinfectant by removing residual chlorite or by increasing the pH. In this study, thiosulfate was investigated at varying concentrations for its effect on microbial survival and was investigated at a concentration of 0.1% in the presence of ASC for its effect on the antimicrobial and chemical activity of the test solution. Additionally, sodium thiosulfate was tested in two buffering systems, buffered peptone water (BPW) and Butterfield's phopshate buffer (BPB), for its ability to inactivate ASC chemistry. The results of this study show that, at a concentration of 0.1%, sodium thiosulfate has no deleterious effect on Escherichia coli survival and is effective in halting the antimicrobial action of ASC by eliminating the production of residual chlorite. The BPW alone and BPB in combination with thiosulfate were found to be effective inactivators of ASC chemistry.

Bacteria↗
PubMed1986

Hypomagnesemia following high-dose intracavitary cisplatin with systemically administered sodium thiosulfate.

Seventy-one patients receiving a minimum of two courses of high-dose intracavitary cisplatin (100-200 mg/m2/course) with i.v. thiosulfate administered to protect against cisplatin-induced renal insufficiency were retrospectively evaluated to examine the influence of thiosulfate and large cumulative doses of cisplatin on the incidence of hypomagnesemia. Only 8% of 50 patients who had normal serum magnesium levels prior to the initiation of the experimental program became hypomagnesemic during the therapeutic trial. Similarly, while 67% of the 21 patients with low initial serum magnesium levels remained hypomagnesemic, 33% had normal serum levels at the completion of therapy. It is suggested that the intravenous administration of thiosulfate might have been responsible for the strikingly low incidence of hypomagnesemia in this patient population. A prospective evaluation of the utility of sodium thiosulfate in preventing cisplatin-induced renal magnesium wasting appears indicated.

Adult↗