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Streptomyces sioyaensis, which produces the antibiotic siomycin, oxidizes elemental sulfur when added to the culture medium and accumulates thiosulfate in the fermented broth. The accumulated thiosulfate was isolated as the ammonium salt and was identified by melting point, IR spectrum, and paper chromatography. A variety of other streptomycetes also oxidized elemental sulfur and accumulated thiosulfate.
Mutants carrying defects in cysteine synthase A or B or both were isolated from Salmonella typhimurium LT2. Parent strains were able to grow on minimal media containing sulfate, sulfite, sulfide, or thiosulfate as sulfur sources. Mutants lacking cysteine synthase B were unable to grow on thiosulfate, whereas mutants lacking cysteine synthase A grew on the four inorganic sulfur sources described above with little difference in their growth rates. Mutants lacking both cysteine synthases failed to grow on media containing any of the inorganic sulfur sources tested. Purification of cysteine synthase B resulted in the copurification of S-sulfocysteine synthase. In addition, the two activities were also cotransduced. These activities appear to be associated with the cysM gene, and this is able to be cotransducted with the cysK gene at a high frequency. From these results, it may be concluded that thiosulfate is assimilated via S-sulfocysteine exclusively with the aid of S-sulfocysteine synthase.
Many photosynthetic bacteria use inorganic sulfur compounds as electron donors for carbon dioxide fixation. A thiosulfate-induced cytochrome c has been purified from the photosynthetic alpha-proteobacterium Rhodovulum sulfidophilum. This cytochrome c(551) is a heterodimer of a diheme 30-kDa SoxA subunit and a monoheme 15-kDa SoxX subunit. The cytochrome c(551) structural genes are part of an 11-gene sox locus. Sequence analysis suggests that the ligands to the heme iron in SoxX are a methionine and a histidine, while both SoxA hemes are predicted to have unusual cysteine-plus-histidine coordination. A soxA mutant strain is unable to grow photoautotrophically on or oxidize either thiosulfate or sulfide. Cytochrome c(551) is thus essential for the metabolism of both these sulfur species. Periplasmic extracts of wild-type R. sulfidophilum exhibit thiosulfate:cytochrome c oxidoreductase activity. However, such activity can only be measured for a soxA mutant strain if the periplasmic extract is supplemented with purified cytochrome c(551). Gene clusters similar to the R. sulfidophilum sox locus can be found in the genome of a green sulfur bacterium and in phylogenetically diverse nonphotosynthetic autotrophs.
Two studies were conducted to determine whether sodium thiosulfate (THS) can estimate extracellular water (ECW) in beef cattle in conjunction with empty body water (EBW) estimation by urea space. Experiment 1 used 24 steers (366 kg) to determine the clearance parameters for THS and urea. Blood samples were taken over 1 h. A two-component curve, Y = A1ek1(t) + A2ek2(t), (t = hours after infusion) fit the clearance of both markers; intercepts (A1, A2) and clearance coefficients (k1, k2) were 44.8, 44.4, -25.8, and -2.24 mg/dL, respectively, for THS (r2 = .98, Sy.x = 2.72, animal effects removed and 24.4, 10.5, -21.7, and -.71 mg/dL, respectively, for urea (r2 = .98, Sy.x = 1.49). Sodium thiosulfate equilibrated with ECW 5 to 10 min after infusion. Experiment 2 consisted of 22 steers (483 kg) infused with a combination solution of 20% urea, 10% THS, and 4% sodium thiocyanate (SCN; equilibration time = 28 min); half the steers were implanted with estradiol. Empty body water increased with implantation (P less than .01). Extracellular water tended to increase in implanted steers as measured by THS (12 min, P = .14) and SCN (P = .10). The estimation of ECW at 12 min was not different (P greater than .2) from the SCN estimate at 28 min (SCN = 3.7 + .873 THS; r2 = .70; P less than .001). Sodium thiosulfate gave reasonable estimates of ECW (22 to 26% of BW) and required only 0- and 12-min blood samples.(ABSTRACT TRUNCATED AT 250 WORDS)
Potassium chloride was subjected to various kinds of pretreatments and irradiated in a nuclear reactor. Irradiated potassium chloride was dissolved in deaerated aqueous solution of several sulfur-salts. A portion of the solution was chromatographed on a thin layer chromatographic plate and the distribution of 35S-chemical species was determined. Irradiation of potassium chloride degassed at 3x10(-4)Torr resulted in the formation of about 60% of 35S in the form of thiosulfate and remainder was distributed among sulfide, sulfate and elementary sulfur. Thiosulfate[35S] was converted to elementary sulfur[35S] first by reducing to hydrogen sulfide [35S] with nascent hydrogen and then by oxidizing the latter to elementary sulfur[35S] with hexacyanoferrate(III). Elementary sulfur[35S] was finally extracted into benzene. Radiochemically pure elementary sulfur[35S] could be produced by simple procedures with a yield of about 60%. Thiosulfate[35S] was decomposed with acid to elementary sulfur[35S] and sulfur[35S] dioxide. The former was separated by centrifuging and dispersed in boiling water to form colloidal suspension of elementary sulfur[35S]. Approximately 40% of 35S was recovered as colloid.
OBJECTIVE: To evaluate if parenteral gold-therapy with Sodium gold thiosulfate is effective and safe for the treatment of rheumatoid arthritis we began an open, multicenter trial. METHODS: 126 rheumatoid arthritis patients were treated with Sodium gold thiosulfate for two years. Efficacy, quality of life, progression of joint damage, inflammatory parameters and side effects were evaluated. RESULTS: Gold salts reduced joint inflammation and improved subjective and objective symptoms, quality of life and activity of illness within 6 months. Side effects appeared in 13,8% of all cases and regressed, promptly, when gold therapy stopped. The poor efficacy caused the interruption and the change from the gold therapy to others disease-modifying anti-rheumatic drugs (DMRDs) in 17,8 % of the patients. CONCLUSIONS: The follow-up showed Sodium gold thiosulfate was effective in Rheumatoid Arthritis and the survival in therapy was of 77,8% to one year and of 68,4% to two years.
Vascular calcification is common among hemodialysis (HD) patients and contributes to the development of peripheral arterial disease. A 57-year-old Japanese man who had been on HD for 30 years was referred to us for severe pain with multiple ulcers on his toes and fingers. He was an ex-smoker and had no diabetes mellitus. On admission, he had ulcers on his big toes bilaterally and right 2nd - 4th fingers. Peripheral pulses were strong and his ankle-brachial pressure index was above 1.3. Laboratory data were as follows: calcium 9.9 mg/dl, albumin 3.3 g/dl, phosphate 3.0 mg/dl, Ca x P product 30, and parathyroid hormone 98 pg/ml. He had a parathyroidectomy in 1998 and 1999. X-rays of his hands and legs showed diffuse subcutaneous arteriolar calcification. Angiography revealed no local stenotic lesions. Despite intensive therapies including hyperbaric oxygen therapy, painful gangrene developed on his right big toe and the pain was so intense that he could not go to sleep in a supine position. We infused intravenous sodium thiosulfate (20 g) 3 times weekly, based on previous reports. Within 4 - 5 days, he experienced rapid and dramatic symptom relief. The score of the visual analogue pain scale improved from 10/10 - 2/10. The signs of ischemia, measured by transcutaneous partial oxygen pressure and thermography, improved significantly. During the infusion of sodium thiosulfate, the patient complained of nausea, vomiting and hyperosmia. These adverse symptoms were resolved after discontinuation of the infusion. Pain relief was sustained and he could walk after 2 weeks of infusion. Our case supports the use of sodium thiosulfate as a novel therapeutic choice for critical limb ischemia with severe vascular calcification in chronic HD patients.
Sodium nitroprusside is an antihypertensive agent used frequently in the critical care setting. Recently, the Food and Drug Administration (FDA) published a report that led to a labeling change emphasizing the pharmacokinetics of nitroprusside with metabolism to highly toxic cyanide. Although evidence validates that cyanogenesis occurs with nitroprusside administration, prevention and treatment of cyanide poisoning is rarely instituted in clinical practice. Simultaneous infusion of thiosulfate with nitroprusside provides the sulfur donor necessary to prevent cyanide accumulation. Cyanide combines with thiosulfate to form the less toxic sodium thiocyanate, which is then excreted. A 10:1 ratio of nitroprusside to thiosulfate in the infusion eliminates the possibility of cyanide intoxication without altering the efficacy of nitroprusside.
Experiments were made in dogs weighing 15-25 kg with experimental tourniquet shock (35 dogs) and experimental myocardial infarction (29 dogs). Intravenous injection of sodium thiosulfate (500 mg/kg) exerted a marked therapeutic effect on cardio- and central hemodynamics under acute circulatory disturbances both in tourniquet shock and myocardial infarction. Sodium thiosulfate increased cardiac discharge, minute blood flow volume, the first derivative, the threshold of ventricular fibrillation, improved the heart work, decreased and normalized the general peripheral resistance. This effect is likely to be related to the stimulation of intracellular metabolism and antidote action of sodium thiosulfate against ischemic toxin.
In order to invalidate or confirm the affirmation that non antithyroid sulphide molecules alter the measure of the thyroid fixation rate of iodine 131 we undertook on the rat: on one hand a kinetic study of thyroid fixation of sodium thiosulfate labelled with sulphur 35, which showed a very low captation not exceeding 0,01% of injected radioactivity; on the other hand the study of the effects of some sulphide molecules on thyroid fixation of iodine 131 in the rat: sodium thiosulfate, association of sodium thiosulfate + metalloidal sulphur + methionine, carbutamide and dimethylsulfoxyde in various kinds of dose administration and periods. None of the products used in our work conditions produced a significant decrease of the fixation rate of iodine 131. In three different experimental protocols (sulfur association and dimethylsulfoxide), we showed a significant light increase of the fixation rate.
Thermoanaerobacter brockii fermented serine to acetate and ethanol. It oxidized leucine to isovalerate, isoleucine to 2-methylbutyrate, and valine to isobutyrate only in the presence of thiosulfate, or when co-cultured with Methanobacterium sp. This oxidative deamination was rendered thermodynamically possible by the ability ofT. brockii to reduce thiosulfate to sulfide or the transfer of reducing equivalents to the hydrogenotrophic methanogen. The results suggest that T. brockii may be of ecological significance in thermal environments in the turnover of amino acids, especially with thiosulfate or H(2)-utilizing methanogens are present.
Sulfur isotope fractionation during reduction of thiosulfate was investigated with growing batch cultures of Desulfovibrio desulfuricans CSN (DSM 9104) at 30 degreesC. The sulfide produced was depleted in 34S by 10 per thousand as compared to total thiosulfate sulfur. The depletion was equal to that during sulfate reduction under similar conditions. The two sulfur atoms of the thiosulfate molecule were affected differently by fractionation. Sulfide produced from sulfonate sulfur was depleted by 15.4 per thousand, sulfide produced from sulfane sulfur by 5.0 per thousand.
Thiosulfate reductase purified 900-fold from an extract of baker's yeast by a new procedure consisted of three charge-isomeric species, all with catalytic activity. Amino acid analysis of thiosulfate reductase and titrations with 5,5'-dithiobis(2-nitrobenzoate) and iodo[14C]acetate indicated only one cysteine residue per enzyme molecule. Alkylation of this cysteine with either iodoacetate or iodoacetamide did not inactivate the enzyme, indicating that sulfur-sulfur bond cleavage in the thiosulfate substrate does not require an enzymic sulfhydryl group as attacking nucleophile.
In this paper, a capillary zone electrophoretic (CZE) method was developed for the separation of the sulfur species dithionite (S2O4(2-)), sulfite (SO3(2-)), sulfate (SO4(2-)) and thiosulfate (S2O3(2-)). A carrier electrolyte (pH 7.0) containing 1.5 mmol L(-1) pyromellitic (PM) acid, 10 mmol L(-1) Tris(hydroxymethyl)-aminomethane (Tris), 0.5 mmol L(-1) diethylenetriamine (DETA) and 0.1% (v/v) formaldehyde (as stabilizer for S2O4(2-) and SO3(2-)) allowed the determination of the sulfur anions after 9 min CZE separation with indirect UV detection at 214 nm. The addition of 0.1% (v/v) formaldehyde to the sample solution stabilizes dithionite and sulfite as HOCH2SO2- and HOCH2SO3- anions. The procedure was applied for the determination of dithionite and its decomposition products sulfite, sulfate and thiosulfate in commercial formulations of bleaching agents. Dithionite was found to be the major component of the commercial formulations in concentrations between 30.80 and 33.30% (w/w). As anticipated, sulfite, sulfate and thiosulfate were found to be present as decomposition or by-products in the commercial formulations at concentrations of 14.30-14.80, 5.20-5.70 and 0.30-0.40% (w/w), respectively. The results were found to be in good agreement with those of polarographic and spectrophotometric determinations.
New analogs of dUMP, dTMP and 5-fluoro-dUMP, including the corresponding 5'-thiophosphates (dUMPS, dTMPS and FdUMPS), 5'-dithiophosphates (dUMPS2, dTMPS2 and FdUMPS2), 5'-H-phosphonates (dUMP-H, dTMP-H and FdUMP-H) and 5'-S-thiosulfates (dUSSO3, dTSSO3 and FdUSSO3), have been synthesized and their interactions studied with highly purified mammalian thymidylate synthase. dUMPS and dUMPS2 proved to be good substrates, and dTMPS and dTMPS2 classic competitive inhibitors, only slightly weaker than dTMP. Their 5-fluoro congeners behaved as potent, slow-binding inhibitors. By contrast, the corresponding 5'-H-phosphonates and 5'-S-thiosulfates displayed weak activities, only FdUMP-H and FdUSSO3 exhibiting significant interactions with the enzyme, as weak competitive slow-binding inhibitors versus dUMR The pH-dependence of enzyme time-independent inhibition by FdUMP and FdUMPS was found to correlate with the difference in pKa values of the phosphate and thiophosphate groups, the profile of FdUMPS being shifted (approximately 1 pH unit) toward lower pH values, so that binding of dUMP and its analogs is limited by the phosphate secondary hydroxyl ionization. Hence, together with the effects of 5'-H-phosphonate and 5'-S-thiosulfate substituents, the much weaker interactions of the nucleotide analogs (3-5 orders of magnitude lower than for the parent 5'-phosphates) with the enzyme is further evidence that the enzyme's active center prefers the dianionic phosphate group for optimum binding.
OBJECTIVE: To assess the incidence and magnitude of ototoxicity in patients undergoing an experimental targeted chemoradiation protocol incorporating extremely high-dose intra-arterial cisplatin therapy with systemic sodium thiosulfate neutralization for the treatment of advanced carcinomas of the head and neck. DESIGN: Inception cohort study. SETTING: University-based, tertiary care referral center for advanced head and neck malignant disease. PATIENTS: The first 70 patients with advanced carcinomas of the head and neck consecutively entered in the protocol. INTERVENTION: Patients received up to 4 weekly courses of intra-arterial cisplatin (150 mg/m2 per infusion), together with systemic sodium thiosulfate and external beam radiation (68-70 Gy). Audiometric analysis was performed before the initiation of therapy, and subsequent to the second and fourth cisplatin infusions. MAIN OUTCOME MEASURES: Audiometric thresholds. Ototoxicity was defined as an increase in pure-tone threshold of 15 dB at 1 frequency or 10 dB at 3 frequencies, between 250 and 4000 Hz. RESULTS: The incidence of ototoxicity was 25% at 150 mg/m2, 50% at 300 mg/m2, 64% at 450 mg/m2, and 60% at 600 mg/m2. Hearing at frequencies of 2000 Hz or less was minimally or not affected. Previous hearing loss did not appear to affect the incidence of ototoxicity. A plateau of hearing loss at 60-dB hearing level, as noted by other authors, was not observed. There were no cases of debilitating tinnitus or of vestibular loss. CONCLUSIONS: Ototoxicity did occur but was largely confirmed to the higher frequencies. Hearing losses resulting from this chemoradiation protocol were not sufficiently severe to alter its application.
Recent published reports have suggested that cisplatin administered in high doses or in certain combination chemotherapy can cause serious neurotoxicity in a large percentage of patients treated. In several high-dose cisplatin-based intracavitary chemotherapy trials with the simultaneous intravenous administration of sodium thiosulfate, the incidence of clinically relevant neurotoxicity has been extremely low. In addition, several patients with serious preexisting cisplatin-induced neurologic dysfunction were treated without worsening of their clinical condition. It is suggested that thiosulfate might have been responsible for the low incidence of neurotoxicity in this patient population. Further experimental and clinical investigation of the potential of this agent to protect against cisplatin-induced neuropathy appears warranted.
Binding parameters for a series of N-heterocyclic aminoethyl disulfides and thiosulfates to DNA were determined at different ionic strengths and pH values. None of the thiosulfates showed any binding ability, but the disulfides revealed DNA binding abilities that were suppressed both by increased ionic strength and hydrogen-ion concentration. No correlation between DNA binding ability and radiation protective activity in mice was evident.