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PubMed1997

Cloning and characterization of sulfite dehydrogenase, two c-type cytochromes, and a flavoprotein of Paracoccus denitrificans GB17: essential role of sulfite dehydrogenase in lithotrophic sulfur oxidation.

A 13-kb genomic region of Paracoccus dentrificans GB17 is involved in lithotrophic thiosulfate oxidation. Adjacent to the previously reported soxB gene (C. Wodara, S. Kostka, M. Egert, D. P. Kelly, and C. G. Friedrich, J. Bacteriol. 176:6188-6191, 1994), 3.7 kb were sequenced. Sequence analysis revealed four additional open reading frames, soxCDEF. soxC coded for a 430-amino-acid polypeptide with an Mr of 47,339 that included a putative signal peptide of 40 amino acids (Mr of 3,599) with a RR motif present in periplasmic proteins with complex redox centers. The mature soxC gene product exhibited high amino acid sequence similarity to the eukaryotic molybdoenzyme sulfite oxidase and to nitrate reductase. We constructed a mutant, GBsoxC delta, carrying an in-frame deletion in soxC which covered a region possibly coding for the molybdenum cofactor binding domain. GBsoxC delta was unable to grow lithoautotrophically with thiosulfate but grew well with nitrate as a nitrogen source or as an electron acceptor. Whole cells and cell extracts of mutant GBsoxC delta contained 10% of the thiosulfate-oxidizing activity of the wild type. Only a marginal rate of sulfite-dependent cytochrome c reduction was observed from cell extracts of mutant GBsoxC delta. These results demonstrated that sulfite dehydrogenase was essential for growth with thiosulfate of P. dentrificans GB17. soxD coded for a periplasmic diheme c-type cytochrome of 384 amino acids (Mr of 39,983) containing a putative signal peptide with an Mr of 2,363. soxE coded for a periplasmic monoheme c-type cytochrome of 236 amino acids (Mr of 25,926) containing a putative signal peptide with an Mr of 1,833. SoxD and SoxE were highly identical to c-type cytochromes of P. denitrificans and other organisms. soxF revealed an incomplete open reading frame coding for a peptide of 247 amino acids with a putative signal peptide (Mr of 2,629). The deduced amino acid sequence of soxF was 47% identical and 70% similar to the sequence of the flavoprotein of flavocytochrome c of Chromatium vinosum, suggesting the involvement of the flavoprotein in thiosulfate oxidation of P. denitrificans GB17.

Amino Acid Sequence↗

PubMed1967

Yield coefficients of Thiobacillus neapolitanus in continuous culture.

Thiobacillus neapolitanus, when grown in continuous culture with thiosulfate limiting growth, possessed an apparent maximal molar growth yield of 8.0 g (dry weight) per mole of thiosulfate. The substrate requirement for energy of maintenance was the highest yet reported, amounting to 21.8 mmoles of thiosulfate per g per hr. The molar growth yield, corrected for this maintenance energy requirement, was 13.9 g (dry weight) per mole of thiosulfate. It was concluded that substrate-level phosphorylation during sulfite oxidation accounted for about 45% of the adenosine triphosphate (ATP) requirement for CO(2) assimilation and maintenance during growth on limiting thiosulfate, that three sites of energy conservation exist in the electron-transport chain terminating in oxygen, and that 7.8 moles of ATP are required to fix and assimilate 1 mole of CO(2) into cell material.

Adenosine Triphosphate↗

PubMed1985

Treatment of acute cyanide intoxication with hemodialysis.

A dramatic response was noted in a patient at our hospital who received hemodialysis therapy for severe acidosis secondary to an unknown toxin, subsequently identified as cyanide. We were unable to find any information concerning the hemodialysis clearance and extraction ratio of cyanide; thus, we studied the effect of hemodialysis in dogs receiving a constant infusion of cyanide with and without a simultaneous infusion of thiosulfate. The hemodialysis clearance of cyanide in the presence of thiosulfate was 38.3 +/- 5.4 ml/min with an extraction ratio of 0.43 +/- 0.06 (n = 4). Hemodialysis was found to increase the lethal dose of cyanide without thiosulfate infusion, and a further increase was noted with the thiosulfate infusion. Thiosulfate promotes mitochondrial metabolism of cyanide to thiocyanate. The end product, thiocyanate, is quickly removed by hemodialysis. We believe that the demonstrated effectiveness of hemodialysis in the treatment of acute cyanide intoxication is related not only to the hemodialysis clearance of cyanide, but also to the removal of its metabolic end product, thiocyanate. Based on our observations, we feel that hemodialysis is an effective adjunct in the treatment of acute cyanide intoxication.

Acidosis↗

PubMedDate not supplied

[The functional role of reduced inorganic sulfur compounds in the metabolism of the microaerophilic bacterium Spirillum winogradskii].

Oxidation of reduced sulfur compounds by microaerophilic sulfur bacterium Spirillum winogradskii was found to occur only concomitantly with consumption of an organic substrate and was not linked to their utilization as electron donors in energy metabolism. No enzymes of dissimilatory sulfur metabolism were found in the cells of the sulfur bacterium oxidizing thiosulfate to tetrathionate; oxidation of thiosulfate and sulfide was caused by their reaction with reactive oxygen species (ROS), mostly H2O2 produced in the course of aerobic growth. Decreased lytic effect of ROS in the presence of thiosulfate resulted in a twofold increase in the cell yield under aerobic conditions and more efficient substrate utilization. The latter effect was caused by decreased expense of energy for the biosynthesis of oxygen-protecting polysaccharides. The stimulatory effect of thiosulfate on the growth processes was due to the activation of a number of TCA cycle enzymes producing the intermediates for constructive metabolism, especially of the NADP-dependent malic enzyme. As a result of thiosulfate-induced synthesis of SH-containing cell components, the integral antioxidative activity increased 1.5-fold.

Adenosine Triphosphate↗

PubMed1990

Effects of various known and potential cyanide antagonists and a glutathione depletor on acute toxicity of cyanide in mice.

To compare the protective potencies of a large number of known and potential cyanide antagonists in one stock of mice, groups (N = 10) of male CF-1 Swiss-Webster mice were given a single maximal or near-maximal intraperitoneal injection of each substance. Ethyl maleate, a glutathione (GSH) depletor and potential enhancer of cyanide toxicity, was given to other groups. Thirty min later, the mice were given subcutaneous injections of graded doses of KCN. In untreated control mice, the 24-hr median lethal dose (LD50) of KCN was 11 mg/kg of body weight (potency ratio, PR = 1.0). In comparison, protective effects of traditional antagonists thiosulfate and nitrite produced PR values of 1.48 and 2.95, respectively. Tetrathionate, sulfate, dithionite, methionine, hydroxocobalamin, ascorbate, pyridoxal phosphate, alpha-ketoglutarate, alpha-ketobutyrate, GSH, GSH disulfide (GSSG) and selenite were similar in efficacy to thiosulfate (P less than 0.05; PR values 1.35-1.59). Cysteine, diethyldithiocarbamate (DEDC), and cobaltous chloride were more effective than thiosulfate (PR values 1.68, 1.69, and 1.85, respectively). Phentolamine and dicobalt EDTA were ineffective, whereas papaverine enhanced toxicity (PR 0.72). Agents with significant PR values (greater than or equal to 1.14) but which were less effective than thiosulfate included sulfite, dimercaptosuccinic acid, pyruvate, citrate, alpha-ketovalerate, naloxone, and corn oil. Ethyl maleate in corn oil markedly enhanced KCN lethality (PR 0.57 compared to corn oil alone), and caused prolonged illness in several mice. Vitamin E in corn oil had no effect. Dual mixtures of thiosulfate with other selected substances were also tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1981

Cyanide intoxication in sheep; therapeutics.

Various cyanide antidotes were evaluated by comparing the effects of delay in time of therapy following oral administration of sodium cyanide in sheep. Successful therapy of lethal doses of sodium cyanide could be accomplished with the more potent antidotes for up to 30 minutes following administration of sodium cyanide. Either 660 mg/kg sodium thiosulfate or 1 mg/kg p-aminopropriophenone were effective antidotes for moderate lethal doses (7.6 mg/kg) of sodium cyanide. The conventional low dosage nitrite/thiosulfate (6.7 mg/kg and 67 mg/kg) was much less effective. Larger doses (15.2 mg/kg) of sodium cyanide were effectively antagonized by either 660 mg/kg sodium thiosulfate alone or in combination with 1.5 mg/kg p-aminopropriophenone or 22 mg/kg sodium nitrite. At high cyanide dosage, p-aminopropriophenone alone was less effective than sodium thiosulfate alone. Sodium thiosulfate at high dosage appears to be the antidote of choice. This more closely satisfies the requirements of high efficacy and low toxicity for an antidote. Sodium nitrate or other antidotes may be used in conjunction with sodium thiosulfate, but their use is not necessary for high efficacy.

Animals↗

PubMed1998

Effect of procaine hydrochloride on cyanide intoxication and its effect on neuronal calcium in mice.

Cyanide intoxication in mice can be antagonized by the local anesthetic, procaine HCI, either alone or in combination with sodium nitrite and/or sodium thiosulfate. Antitoxic potency, derived from LD50 values, was compared in groups of mice pretreated with sodium nitrite (43.9 mg/kg i.p.), sodium thiosulfate (1 g/kg i.p.), and procaine HCI (37.0 mg/kg i.p.) either alone or in various combinations. The results of present study indicated that procaine HCI provides a significant protection against the lethal effects of potassium cyanide. Dose-response studies revealed procaine hydrochloride pretreated 3 min before KCN, at doses of 18.48-73.9 mg/kg, produced significant elevation of KCN LD50, moreover it has a good dose-effect relationship, but its antidotal effect was weaker than sodium nitrite or sodium thiosulfate when they were administered alone. The protective effect of sodium nitrite and sodium thiosulfate was enhanced with procaine HCI. When procaine was administered in combination both with sodium nitrite and sodium thiosulfate, its protective effects were further enhanced. Its antitoxic potency is 6.22. The effects of procaine on antagonizing the cyanide-induced whole-brain total calcium increase were also studied. KCN (7 mg/kg i.p.) significantly increased whole-brain total calcium level from 28.37 +/- 0.75 to 48.05 +/- 1.06 mg/g dry wt within 30 min, which can be prevented by procaine pretreated 15 min before KCN. One of the possible mechanism of procaine on antagonizing cyanide toxicity seems, at least, related to its effect on inhibiting the cyanide-induced neuronal calcium increase and maintaining the homeostasis of neuronal calcium.

Anesthetics, Local↗

PubMed2007

Denitrification in a binary culture and thiocyanate metabolism in Thiohalophilus thiocyanoxidans gen. nov. sp. nov. - a moderately halophilic chemolithoautotrophic sulfur-oxidizing Gammaproteobacterium from hypersaline lakes.

Anaerobic enrichment culture with thiocyanate as electron donor and nitrate as electron acceptor at 2 M NaCl inoculated with a mixture of sediments from hypersaline lakes in Kulunda Steppe (Altai, Russia) resulted in a selection of a binary consortium of moderately halophilic, obligately chemolithoautotrophic sulfur-oxidizing bacteria (SOB) capable of complete denitrification of nitrate with thiosulfate as the electron donor. One consortium member, strain HRhD 3sp, was isolated into pure culture with nitrate and thiosulfate using a density gradient. This strain was responsible for the reduction of nitrate to nitrite in the consortium, while a second strain, HRhD 2, isolated under microoxic conditions with thiosulfate as substrate, was capable of anaerobic growth with nitrite and thiosulfate. Nitrite, either as substrate or as product, was already toxic at very low concentrations for both strains. As a result, optimal growth under anaerobic conditions could only be achieved within the consortium. On the basis of phylogenetic analysis, both organisms were identified as new lineages within the Gammaproteobacteria. As well as thiosulfate, strain HRhD 2 can also use thiocyanate as electron donor, representing a first halophilic SOB capable of growth with thiocyanate at 2-4 M NaCl. Product and enzymatic analysis identified the "carbonyl sulfide (COS) pathway" of primary thiocyanate degradation in this new species. On the basis of phenotypic and genetic analysis, strain HRhD 2 is proposed to be assigned to a new genus and species Thiohalophilus thiocyanoxidans.

Aerobiosis↗

PubMed2006

Isolation of a carbon disulfide utilizing Thiomonas sp. and its application in a biotrickling filter.

The carbon disulfide (CS2)-oxidizing bacterium Thiomonas sp. WZW was enriched and isolated using activated sewage sludge as inoculum. Growth of Thiomonas sp. WZW was observed on CS2, thiosulfate, dimethylsulfide (DMS), dimethyldisulfide (DMDS), and H2S. No growth occurred on dimethylsulfoxide, methanol, acetate, and on complex media with glucose, yeast extract, or tryptone. DMDS-grown cells respired CS2, DMS, and DMDS, while thiosulfate-grown cells did not respire CS2. Chemostat cultures growing on thiosulfate could be rapidly adapted to growth on CS2. Growth was observed between pH 6 and 8. The Ks values for CS2, thiosulfate, and sulfide of CS2-grown cells were between 5 and 10 microM. CS2 was inhibitory above 0.3 mM. A lab-scale biotrickling filter with lava stone as carrier material for treatment of CS2-polluted air was inoculated with Thiomonas sp. WZW. A rapid start up (95% removal in 1 week) was obtained at an inlet CS2 concentration of 2 cmol l(-1) and an initial space velocity (SV) of 54 h(-1). Subsequent thiosulfate addition for a week during start up increased the removal to 99%. The step-wise increase of SV to 130 h(-1) and a CS2 concentration to 3 micromol l(-1) resulted in a stable performance with a removal efficiency of 95%. Feeding mixtures of volatile sulfur compounds showed simultaneous conversion of H2S, CS2, dimethyldisulfide (DMDS), and DMS, with a preference in this order.

Betaproteobacteria↗

PubMed2002

Response of Ceriodaphnia dubia to ionic silver: discrepancies among model predictions, measured concentrations and mortality.

Silver thiosulfate, often a waste product of photoprocessing, is less bioavailable or toxic to aquatic organisms than is ionic silver. We conducted duplicate 48-h Ceriodaphnia dubia tests in reconstituted laboratory water using treatments of 92.7 nM Ag+ with various concentrations of thiosulfate. Expected Ag+ concentrations were generated for thiosulfate treatment levels using MINEQL + chemical equilibrium modeling. Ag+ concentrations in treatments were determined using a novel silicon-based sensor. Based on predicted Ag+ and published 48-h LC50 values for C. dubia, we did not expect to observe adverse effects. Yet, 100% mortality was observed at low thiosulfate treatments, whereas > 85% and > 95% survival was observed at higher thiosulfate treatment levels, respectively. Our results indicate that biotic responses match the sensor-based Ag+ concentrations. However, there is a discrepancy between these empirical results and responses expected to occur with Ag+ concentrations as predicted by MINEQL + chemical modeling. By correlating silicon sensor data with toxicity results obtained from our laboratory, our work clearly relates a specific chemical form (Ag+) to toxicity results.

Animals↗

PubMed1981

Factors affecting oxidation of thiosalts by thiobacilli.

The effects of temperature, initial pH, and the concentrations of ammonium, phosphate, and heavy metals on the oxidation of thiosalts by an authentic strain of Thiobacillus thiooxidans (ATCC 8085) and by a mixed culture isolated from a base metal-processing mill effluent pond were studied. The optimum temperature was 30 degrees C and the optimum initial pH was 3.75 for both cultures using thiosulfate and for the mixed culture using tetrathionate. T. thiooxidans ATCC 8085 did not oxidize tetrathionate. For a thiosalt concentration of 2,000 ppm (2,000 mg/liter), maximal rates of destruction occurred at concentrations of ammonium ion above 2 mg/liter and in the presence of 1 mg of phosphate per liter. Under optimal conditions, the rate of thiosulfate oxidation by the pure culture was 55 +/- 3 mg/liter per h; the mixed culture oxidized thiosulfate at the rate of 40 +/- 1 mg/liter per h and tetrathionate at the rate of 50 +/- 2 mg/liter per h. Metal ions caused normal inhibition kinetics in the oxidation of thiosulfate by T. thiooxidans ATCC 8085. K(i) values were calculated for cadmium (16 mg/liter), copper (0.46 mg/liter), lead (2 mg/liter), silver (3.1 mg/liter), and zinc (33 mg/liter). Only a slight additive effect was apparent in the presence of all of these metal ions. The mixed culture of thiosalt-oxidizing bacteria was less sensitive to heavy metal inhibition; the order of inhibition of thiosulfate oxidation was Cd < Zn < Pb < Ag < Cu, and that of tetrathionate oxidation was Zn < Cd < Pb < Ag < Cu.

Journal Article↗

PubMed2002

Low molecular mass dinitrosyl nonheme-iron complexes up-regulate noradrenaline release in the rat tail artery.

BACKGROUND: Dinitrosyl nonheme-iron complexes can appear in cells and tissues overproducing nitric oxide. It is believed that due to their chemical nature these species may be implicated in certain pathophysiological events. We studied the possible role of low molecular mass dinitrosyl iron complexes in the control of noradrenaline release in electrically stimulated rat tail artery. RESULTS: A model complex, dinitrosyl-iron-thiosulfate (at 1-10 microM) produced a concentration-dependent enhancement of electrical field stimulated [3H]noradrenaline release (up to 2 fold). At the same time, dinitrosyl-iron-thiosulfate inhibited neurogenic vasoconstriction, consistent with its nitric oxide donor properties. A specific inhibitor of cyclic GMP dependent protein kinase, Rp-8pCPT-cGMPS, partially inhibited the effect of dinitrosyl-iron-thiosulfate on neurogenic vasoconstriction, but not on [3H]noradrenaline release. Another model complex, dinitrosyl-iron-cysteine (at 3 microM) elicited similar responses as dinitrosyl-iron-thiosulfate. Conventional NO and NO+ donors such as sodium nitroprusside, S-nitroso-L-cysteine or S-nitroso-glutathione (at 10 microM) had no effect on [3H]noradrenaline release, though they potently decreased electrically-induced vasoconstriction. The "false complex", iron(II)-thiosulfate showed no activity. CONCLUSIONS: Low molecular mass iron dinitrosyl complexes can up-regulate the stimulation-evoked release of vascular [3H]noradrenaline, apparently independently of their NO donor properties. This finding may have important implications in inflammatory tissues.

Animals↗

PubMed2003

Do antidotes for acute cyanide poisoning act on mercaptopyruvate sulfurtransferase to facilitate detoxification?

A well-known combined therapy for acute cyanide poisoning is intravenous administration of sodium nitrite, sodium thiosulfate and cobalt EDTA. Sodium nitrite oxidizes oxy-hemoglobin, resulting in methemoglobin, which has a high affinity for cyanide. Sodium thiosulfate is a substrate of thiosulfate: cyanide sulfurtransferase (rhodanese, EC.2.8.1.1), and facilitates catalytic metabolism of cyanide to less toxic thiocyanate. Cobalt EDTA combines with cyanide to reduce cyanide in the blood. Here, we focus on cytosolic and mitochondrial mercaptopyruvate sulfurtransferase (MST, EC. 2.8.1.2), which detoxifies cyanide more effectively than rhodanese, because rhodanese is localized only in mitochondria. Thiosulfate also serves as a substrate of MST and cyanide can be metabolized to thiocyanate. However, the K(m) value for thiosulfate is so large that it is not expected to contribute much to the detoxification of cyanide. On the other hand, nitrite and cobalt EDTA did not affect MST. Thus, combined therapy only slightly acts on MST to detoxify cyanide. Some investigators have attempted a new therapy in which mercaptopyruvate, a substrate of MST was administered intravenously, but this was not effective for detoxification due to the rapid decomposition of mercaptopyruvate in the blood. There are two possible strategies to facilitate MST activities: development of modified mercaptopyruvate with a longer half time and development of a chemical compound which indirectly increases transcription of MST via regulation of a DNA binding protein.

Acute Disease↗

PubMed1991

Acetonitrile serum concentrations and cyanide blood levels in a case of suicidal oral acetonitrile ingestion.

Acute acetonitrile toxicity is mainly dependent on the release of cyanide via hepatic metabolism. Although evaluated in animals, few data are available concerning the toxicokinetic parameters of acetonitrile and acetonitrile-liberated cyanide in human. This paper reports a case of suicidal oral acetonitrile ingestion of about 5 mL without severe symptoms of intoxication in a previously healthy adult male with a body weight of 60 kg. Acetonitrile serum concentrations as well as cyanide blood levels were determined over the whole hospitalization. The elimination half-lives calculated from these data were 32 h for acetonitrile and 15 h for cyanide. After sodium thiosulfate bolus application, the cyanide blood level rapidly decreased to 10% of the initial value, indicating that sodium thiosulfate sufficiently detoxifies acetonitrile-liberated cyanide. Since cyanide levels again increased to maximal values about 4.5 h after sodium thiosulfate application, continued thiosulfate therapy is required as predicted by the long elimination half-lives of acetonitrile and acetonitrile-liberated cyanide. Determination of cyanide and acetonitrile concentrations is recommended for the estimation of optimal individual sodium thiosulfate dosage.

Acetonitriles↗

PubMed1989

Cyanide poisoning: pathophysiology and current approaches to therapy.

Considering the difficulties following the administration of nitrites (or aminophenols) or cobalt-EDTA as well as the ineffectivenes of hydroxycobalamin and pyruvate, we feel that a more sensible treatment for acute cyanide intoxication is hemodialysis combined with the intravenous administration of sodium thiosulfate. The addition of hemodialysis to such a regimen is helpful in three ways. First, it removes the small extracellular reservoir of cyanide, particularly if the poison is still being absorbed from the gastrointestinal tract. Second, it corrects the severe lactic acidosis seen in virtually all cases of cyanide toxicity. As with most poisons death from metabolic acidosis alone is likely. Third, the removal of thiocyanate, the end product of cyanide metabolism, results in a maneuver which should decrease both tissue and plasma cyanide levels. The immediate treatment of acute cyanide intoxication is supportive, as it is with most all drugs and poisons. Gastric lavage using activated charcoal should be initiated immediately to remove any remaining cyanide in the gastrointestinal tract. Simultaneously, high flow oxygen should be administered either by nasal cannula or by endotracheal intubation. Correction of the metabolic acidosis should be instituted with bicarbonate. Immediate hemodialysis should be performed with the concomitant administration of thiosulfate. Animal studies suggest that continuous infusion of thiosulfate (12 mg/kg/hr) is more effective for treating cyanide intoxication than is bolus administration (41, 51). Bolus administration is the currently recommended form of thiosulfate therapy in humans. The Lilly kit contains a 50 ml ampule of thiosulfate having 12.5 gm, which in adults may be repeated once at one-half the dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Cyanides↗

PubMed1962

Reduction of inorganic compounds with molecular hydrogen by Micrococcus lactilyticus. II. Stoichiometry with inorganic sulfur compounds.

Woolfolk, C. A. (University of Washington, Seattle). Reduction of inorganic compounds with molecular hydrogen by Micrococcus lactilyticus. II. Stoichiometry with inorganic sulfur compounds. J. Bacteriol. 84:659-668. 1962.-Extracts of Micrococcus lactilyticus (Veillonella alcalescens) are capable of utilizing molecular hydrogen for the reduction of metabisulfite (pyrosulfite) to thiosulfate via dithionite as an intermediate. The first step of metabisulfite reduction (i.e., to dithionite) is reversible, and, when dithionite is added as a substrate, there is an evolution of molecular hydrogen accompanied by the formation of equilibrium concentrations of metabisulfite. Kinetic studies indicate that dithionite may be directly reduced to thiosulfate without the formation of sulfoxylate as an intermediate. Although tetrathionate is reduced to thiosulfate with an uptake of hydrogen, polythionates probably are not formed as intermediates in the reduction of metabisulfite to thiosulfate.

Hydrogen↗

PubMed1996

Antidotal effect of dihydroxyacetone against cyanide toxicity in vivo.

Potassium cyanide (CN) intoxication in mice was found to be effectively antagonized by dihydroxyacetone (DHA), particularly if administered in combination with another CN antidote, sodium thiosulfate. Cyanide-induced convulsions were also prevented by DHA treatment, either alone or in combination with thiosulfate. Injection (i.p.) of DHA (2 g/kg) 2 min after or 10 min before CN (s.c.) increased LD50 values of CN(8.7 mg/kg) by factors of 2.1 and 3.0, respectively. Treatment with a combination of DHA and thiosulfate after CN increased the LD50 by a factor of 2.4. Pretreatment with a combination of DHA and thiosulfate (1 g/kg) increased the LD50 of CN to 83 mg/kg. Administration of alpha-ketoglutarate (2.0 g/kg), but not pyruvate, 2 min after CN increased the LD50 of CN by a factor of 1.6. Brain, heart and liver cytochrome oxidase activities were also measured following in vivo CN treatment with and without DHA. Pretreatment with DHA prevented the inhibition of cytochrome oxidase activity by CN and treatment with DHA after CN accelerated the recovery of cytochrome oxidase activity, especially in brain and heart homogenates. DHA is a physiological agent and, therefore, could prove to be a safe and effective antidote for CN, particularly in cases of fire smoke inhalation in which a combination of CN and carbon monoxide is present. In these cases the normally used antidote, sodium nitrite, to induce methemoglobin so as to trap the CN, is contraindicated because some of the oxygen-carrying capacity of the blood will have already been diminished by carbon monoxide.

Animals↗

PubMed2001

Denitrification at extremely high pH values by the alkaliphilic, obligately chemolithoautotrophic, sulfur-oxidizing bacterium Thioalkalivibrio denitrificans strain ALJD.

Thioalkalivibrio denitrificans is the first example of an alkaliphilic, obligately autotrophic, sulfur-oxidizing bacterium able to grow anaerobically by denitrification. It was isolated from a Kenyan soda lake with thiosulfate as electron donor and N2O as electron acceptor at pH 10. The bacterium can use nitrite and N2O, but not nitrate, as electron acceptors during anaerobic growth on reduced sulfur compounds. Nitrate is only utilized as nitrogen source. In batch culture at pH 10, rapid growth was observed on N2O as electron acceptor and thiosulfate as electron donor. Growth on nitrite was only possible after prolonged adaptation of the culture to increasing nitrite concentrations. In aerobic thiosulfate-limited chemostats, Thioalkalivibrio denitrificans strain ALJD was able to grow between pH values of 7.5 and 10.5 with an optimum at pH 9.0. Growth of the organism in continuous culture on N2O was more stable and faster than in aerobic cultures. The pH limit for growth on N2O was 10.6. In nitrite-limited chemostat culture, growth was possible on thiosulfate at pH 10. Despite the observed inhibition of N2O reduction by sulfide, the bacterium was able to grow in sulfide-limited continuous culture with N2O as electron acceptor at pH 10. The highest anaerobic growth rate with N2O in continuous culture at pH 10 was observed with polysulfide (S8(2-)) as electron donor. Polysulfide was also the best substrate for oxygen-respiring cells. Washed cells at pH 10 oxidized polysulfide to sulfate via elemental sulfur in the presence of N2O or O2. In the absence of the electron acceptors, elemental sulfur was slowly reduced which resulted in regeneration of polysulfide. Cells of strain ALJD grown under anoxic conditions contained a soluble cd1-like cytochrome and a cytochrome-aa3-like component in the membranes.

Aerobiosis↗