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PubMed2001

Mechanistic study of microbial control of hydrogen sulfide production in oil reservoirs.

Microbial control of biogenic production of hydrogen sulfide in oil fields was studied in a model system consisting of pure cultures of the nitrate-reducing, sulfide-oxidizing bacterium (NR-SOB) Thiomicrospira sp. strain CVO and the sulfate-reducing bacterium (SRB) Desulfovibrio sp. strain Lac6, as well as in microbial cultures enriched from produced water of a Canadian oil reservoir. The presence of nitrate at concentrations up to 20 mM had little effect on the rate of sulfate reduction by a pure culture of Lac6. Addition of CVO imposed a strong inhibition effect on production of sulfide. In the absence of added nitrate SRB we were able to overcome this effect after an extended lag phase. Simultaneous addition of CVO and nitrate stopped the production of H2S immediately. The concentration of sulfide decreased to a negligible level due to nitrate-dependent sulfide oxidation activity of CVO. This was not prevented by raising the concentration of Na-lactate, the electron donor for sulfate reduction. Similar results were obtained with enrichment cultures. Enrichments of produced water with sulfide and nitrate were dominated by CVO, whereas enrichments with sulfate and Na-lactate were dominated by SRB. Addition of an NR-SOB enrichment to an SRB enrichment inhibited the production of sulfide. Subsequent addition of sufficient nitrate caused the sulfide concentration to drop to zero. A similar response was seen in the presence of nitrate alone, although after a pronounced lag time, it was needed for emergence of a sizable CVO population. The results of the present study show that two mechanisms are involved in microbial control of biogenic sulfide production. First, addition of NR-SOB imposes an inhibition effect, possibly by increasing the environmental redox potential to levels which are inhibitory for SRB. Second, in the presence of sufficient nitrate, NR-SOB oxidize sulfide, leading to its complete removal from the environment. Successful microbial control of H2S in an oil reservoir is crucially dependent on the simultaneous presence of NR-SOB (either indigenous population or injected) and nitrate in the environment.

Bacteria↗
PubMed2001

Sulfide oxidation coupled to ATP synthesis in chicken liver mitochondria.

Chicken liver mitochondria consumed O2 at an accelerated rate when supplied with low concentrations of hydrogen sulfide. Maximum respiration occurred in 10 microM sulfide, and continued more slowly up to concentrations as high as 60 microM. Sulfide oxidation was coupled to adenosine triphosphate (ATP) synthesis, as shown by firefly luciferase luminescence and by measurement of the mitochondrial membrane electrochemical gradient. Synthesis of ATP required low, steady-state concentrations of sulfide (< 5 microM), which were maintained by use of a syringe pump. The ratio of consumed O2 to sulfide changed at low sulfide and O2 concentrations, indicating alternative metabolic reactions and products. In low concentrations of sulfide, presumably most similar to physiological, the O2/sulfide ratio was 0.75. This is the first report of sulfide oxidation linked to ATP synthesis in any organism not specifically adapted to a sulfide-rich environment. We suggest that this may be a widespread mitochondrial trait, and that it is consistent with the hypothesis that mitochondria originated from sulfide-oxidizing symbionts.

Adenosine Triphosphate↗
PubMed2004

Performance of a substratum-irradiated photosynthetic biofilm reactor for the removal of sulfide from wastewater.

The performance of a sulfide-removal system based on biofilms dominated by green sulfur bacteria (GSB) has been investigated. The system was supplied with radiant energy in the band 720-780 nm, and fed with a synthetic wastewater. The areal net sulfide removal rate and the efficacy of the incident radiant energy for sulfide removal have been characterized over ranges of bulk sulfide concentration (1.6-11.5 mg L(-1)) and incident irradiance (0.21-1.51 W m(-2)). The areal net sulfide removal rate increased monotonically with both increasing incident irradiance and increasing bulk sulfide concentration. The efficacy of the radiant energy for sulfide removal (the amount of sulfide removed per unit energy supplied) also increased monotonically with rising bulk sulfide concentration, but exhibited a maximum value with respect to incident irradiance. The maximum observed values of this net removal rate and this efficacy were, respectively, 2.08 g m(-2) d(-1) and 2.04 g W(-1) d(-1). In-band changes in the spectral composition of the radiant energy affected this efficacy only slightly. The products of sulfide removal were sulfate and elemental-S. The elemental-S was scarcely released into the liquid, however, and reasons for this, such as sulfur reduction and polysulfide formation, are considered. Between 1.45 and 3.85 photons were needed for the net removal of one electron from S-species. Intact samples of the biofilm were characterized by microscopy, and their thicknesses lay between 39 +/- 9 and 429 +/- 57 microm. The use of the experimentally determined rates and efficacies for the design of a pilot-scale system is illustrated.

Biodegradation, Environmental↗
PubMed2005

Kinetics and stoichiometry of sulfide oxidation by sewer biofilms.

Oxidation of sulfide under aerobic conditions by biofilms grown on municipal wastewater in 6 identical pipe reactors was investigated. The biofilms were grown at pH 7.6 and temperatures of 20 and 25 degrees C under aerobic-anaerobic transient conditions with pulse dosing of sulfide in the bulk water. The pulse dosing of sulfide served to simulate conditions in a gravity sewer located downstream of a pressure main. During growth of the biofilms, sulfide was pulse dosed in concentrations of 0, 0.5, 2.0 and 5.0 g Sm(-3) with a frequency of 1h(-1). Based on a series of batch experiments, kinetics and stoichiometry of sulfide oxidation by the sewer biofilms was investigated and a rate equation and a stoichiometric constant proposed. Sulfide oxidation kinetics was significantly faster for biofilms grown at sulfide loadings of 0.5, 2.0 and 5.0 g Sm(-3)h(-1) than for biofilms grown in the absence of sulfide. However, the kinetics of sulfide oxidation was relatively constant for biofilms grown at sulfide loadings above 0.5 g Sm(-3)h(-1). Mass balance calculations of dissolved oxygen and sulfur compounds suggested the oxidation product to be elemental sulfur. Further oxidation of elemental sulfur could not be documented.

Biofilms↗
PubMed2003

Simultaneous release of metals and sulfide in lacustrine sediment.

A single DGT (diffusive gradient in thin films) probe that could measure metals and sulfide simultaneously and at the same location was deployed in the surface sediment of a productive lake (Esthwaite Water). It contained a layer of AgI that binds sulfide overlying a layer of chelating resin that binds metals. Analysis for sulfide in two dimensions showed local sources of sulfide, 1-5 mm in diameter, at 8-11 cm depth within the sediment. A transect of trace metals measured at 100-microm intervals through the largest sulfide "hot spot" demonstrated concomitant release of Fe, Mn, Cu, Ni, and Co. Substantial supersaturation with respect to metal sulfides was observed for Fe and Co at the site of metal generation, but at a distance of less than 1 mm, solution concentrations were consistent with equilibration with amorphous FeS and CoS phases. Simple mass balance calculations were consistent with Fe being supplied from reductive dissolution of its oxides and with sulfide being supplied from reduction of sulfate. The observed concentrations of Cu, Ni, Co, and Mn could be accounted for by their release from iron oxides without invoking Mn reduction. The metals are removed rapidly (approximately 1 min) at the edge of the hot spot. These first observations of the simultaneous release of trace metals and sulfide are consistent with the known removal of metals by formation of their insoluble sulfides if the in situ kinetics of metal sulfide formation is on this time scale. The coproduction of reduced Fe and S suggests that iron- and sulfate-reducing bacteria may exist together in the same localized zone of actively decomposing organic matter.

Environmental Monitoring↗
PubMed2002

Mechanism of the oxidation of sulfides by dioxiranes. 1. Intermediacy of a 10-S-4 hypervalent sulfur adduct.

Earlier studies established that dimethyldioxirane (1a) reacts with sulfides 2 in two consecutive concerted electrophilic oxygen-transfer steps to give first sulfoxides 3 and then sulfones 4. The same sequential electrophilic oxidation model was assumed for the reaction of sulfides 2 with the strongly electrophilic methyl(trifluoromethyl)dioxirane (1b). In this paper we report on a systematic and general study on the mechanism of the reaction of simple sulfides 2 with DMDO (1a) and TFDO (1b) which provides clear evidence for the involvement of hypervalent sulfur species in the oxidation process. In the oxidation of sulfides 2a-c, diphenyl sulfide (2d), para-substituted aryl methyl sulfides 2e-i, and phenothiazine 2k with 1b, the major product was the corresponding sulfone 4, even when a 10-fold excess of sulfide relative to 1b was used. The sulfone:sulfoxide 4:3 ratio depends among other factors on the dioxirane 1a or 1b used, the sulfide substitution pattern, the polar, protic, or aprotic character of the solvent, and the temperature. The influence of these factors and also deuterium and (18)O tracer experiments performed allow a general mechanism to be depicted for these oxidations in which the key step is the reversible cyclization of a zwitterionic intermediate, 6, to form a hypervalent sulfur species, 7. The classical sequential mechanism which establishes that sulfides are oxidized first to sulfides and then to sulfones can be enclosed in our general picture of the process and represents just those particular cases in which the zwitterionic intermediate 6 decomposes prior to undergoing ring closure to afford the hypervalent sulfurane intermediate 7.

Epoxy Compounds↗
PubMedDate not supplied

Sulfide binding in the body fluids of hydrothermal vent alvinellid polychaetes.

Dissolved H2S is a major environmental factor in hydrothermal vent ecosystems. In a study of adaptations to sulfide by alvinellid polychaetes, the sulfide-binding capacity of body fluids was examined in Paralvinella palmiformis from northeast Pacific ridges and Alvinella species from the East Pacific Rise. Sulfide concentrations in vascular blood and coelomic fluid of freshly collected animals were notably variable. Separation of P. palmiformis body-fluid components revealed that most sulfide (ca. 77%) was accumulated in the dissolved fraction. In P. palmiformis, both vascular blood and coelomic fluid could reversibly bind sulfide in vitro with a low affinity, saturating only at high dialysate concentrations (ca. 2 mmol L-1). No sulfide-binding activity was observed in the vascular blood from Alvinella species. A dissolved protein component of greater than 90 kDa appears to be involved in sulfide binding in Paralvinella, probably a vascular extracellular high-molecular-weight hemoglobin. Some sulfide may also adsorb onto a 15.38-kDa intracellular hemoglobin present in the coelomic erythrocyte fraction. In the absence of epibiotic bacteria, Paralvinella body fluids may function as a sulfide buffer to protect tissues from deleterious effects of sulfide exposure.

Animals↗
PubMed1990

Biosynthesis and urinary excretion of methyl sulfonium derivatives of the sulfur mustard analog, 2-chloroethyl ethyl sulfide, and other thioethers.

Thioether methyltransferase was previously shown to catalyze the S-adenosylmethionine-dependent methylation of dimethyl selenide, dimethyl telluride, and various thioethers to produce the corresponding methyl onium ions. In this paper we show that the following thioethers are also substrates for this enzyme in vitro: 2-hydroxyethyl ethyl sulfide, 2-chloroethyl ethyl sulfide, thiodiglycol, t-butyl sulfide, and isopropyl sulfide. To demonstrate thioether methylation in vivo, mice were injected with [methyl-3H]methionine plus different thioethers, and extracts of lungs, livers, kidneys, and urine were analyzed by high-performance liquid chromatography for the presence of [3H]methyl sulfonium ions. The following thioethers were tested, and all were found to be methylated in vivo: dimethyl sulfide, diethyl sulfide, methyl n-propyl sulfide, tetrahydrothiophene, 2-(methylthio)ethylamine, 2-hydroxyethyl ethyl sulfide, and 2-chloroethyl ethyl sulfide. This supports our hypothesis that the physiological role of thioether methyltransferase is to methylate seleno-, telluro-, and thioethers to more water-soluble onium ions suitable for urinary excretion. Conversion of the mustard gas analog, 2-chloroethyl ethyl sulfide, to the methyl sulfonium derivative represents a newly discovered mechanism for biochemical detoxification of sulfur mustards, as this conversion blocks formation of the reactive episulfonium ion that is the ultimate alkylating agent for this class of compounds.

Animals↗
PubMed1980

Dimethyl sulfide in milk of lactating dairy cows fed various sulfur compounds.

Mature dairy cows in late lactation were given capsules containing 26, 40, 60, or 80 g of D,L-methionine; 32, 49, 69, or 90 g of methionine hydroxy analog; or 1, 2, or 4 ml of dimethyl sulfide. Animals used as controls received capsules containing water. Milk was collected at hourly intervals for 5 h and analyzed for dimethyl sulfide content by gas chromatography. All experimental cows were managed and fed (mainly corn silage plus concentrate with some hay and pasture) with the rest of the herd but were limited to water and clover hay during the 5-h experimental periods. Administration of 60 or 80 g of D,L-methionine or 1, 2, or 4 ml of dimethyl sulfide resulted in the appearance of dimethyl sulfide in the milk. The concentration of dimethyl sulfide in milk from cows receiving orally administered dimethyl sulfide (2 or 4 ml) was greatest at 1 h. When D,L-methionine (60 or 80 g) was given, dimethyl sulfide concentrations were lower and peaked later in the sampling period. The maximum concentration of dimethyl sulfide in the milk was 4.5 ppb when 4 ml of dimethyl sulfide were administered orally. No dimethyl sulfide was in the milk for any amount of methionine hydroxy analog, for 26 or 40 g of D,L-methionine, or for control capsules.

Animals↗
PubMed2002

Evaluation of the effect of reactive sulfide on the acute toxicity of silver (I) to Daphnia magna. Part 1: description of the chemical system.

Experiments were designed to assess the potential protective effect of the presence of sulfide against the acute (48-h) toxicity of silver(I) to Daphnia magna. Tests were conducted in borosilicate glass beakers (250 ml) in moderately hard synthetic water. Toxicity solutions were replaced after 24 h by static renewal method. This paper describes the chemical system, and the acute toxicity results are presented in a companion paper. Sulfide was below detection limit (<5 nM) in controls with no sulfide added. Sulfide, added as zinc sulfide clusters at approximately 35- or approximately 350-nM concentration, dropped in concentration to approximately 25 and 250 nM, respectively, over the 24-h period of measurements. Silver also decreased in concentration during the experiment (up to 59%), and the rate of loss was greater in the absence of sulfide compared with the presence of sulfide. A filtration experiment indicated a 1:1 binding ratio of silver to sulfide and a conditional stability constant for the Ag(I)-zinc sulfide complex of log K' = 8.9. The losses of sulfide and silver during the experiments highlighted the need for regular monitoring of the important chemical components of the system, even during short (48-h) toxicity tests.

Animals↗
PubMed2002

Evaluation of the effect of reactive sulfide on the acute toxicity of silver (I) to Daphnia magna. Part 2: toxicity results.

The protective effect of reactive sulfide against AgNO3 toxicity to Daphnia magna neonates was studied. Acute (48-h) toxicity tests were performed in the absence (<5 nM) and presence of low (approximately 25 nM) and high (approximately 250 nM) concentrations of zinc sulfide clusters under oxic conditions. In both the presence and the absence of sulfide, lower mean lethal concentration (LC50) values were observed when measured as opposed to nominal silver concentrations were used in calculations. This reflected the fact that measured total silver concentrations were lower than nominal concentrations due to losses of silver from solution observed during the experiment. High concentration (approximately 250 nM) of sulfide completely protected against toxicity up to the highest silver concentration tested (2 microg/L [19 nM]) with measured silver data. In the presence of environmentally realistic levels of sulfide (approximately 25 nM) in receiving waters, acute silver toxicity was reduced by about 5.5-fold. However, when filtered (0.45 microm) silver concentrations alone were considered, toxicity (48-h LC50) was similar in the absence (0.22 microg/L) and presence (0.28 microg/L) of sulfide. The difference between measured total and filtered silver was attributed to chemisorption of the metal sulfide onto the membrane filter and provides evidence that the toxic fraction of silver is that which is unbound to sulfide. Accumulation of silver was greater in daphnids exposed to silver in the presence of sulfide than in its absence, even though a toxic effect was not observed under these conditions. In this case, silver appears to be incorporated by daphnids rather than merely adsorbed on the surface. Our results point out the need to incorporate sulfide into the acute biotic ligand model and to assess its potentially large role in preventing chronic toxicity.

Adsorption↗
PubMed1998

Sulfide oxidation in the phototrophic sulfur bacterium Chromatium vinosum.

Sulfide oxidation in the phototrophic purple sulfur bacterium Chromatium vinosum D (DSMZ 180(T)) was studied by insertional inactivation of the fccAB genes, which encode flavocytochrome c, a protein that exhibits sulfide dehydrogenase activity in vitro. Flavocytochrome c is located in the periplasmic space as shown by a PhoA fusion to the signal peptide of the hemoprotein subunit. The genotype of the flavocytochrome-c-deficient Chr. vinosum strain FD1 was verified by Southern hybridization and PCR, and the absence of flavocytochrome c in the mutant was proven at the protein level. The oxidation of thiosulfate and intracellular sulfur by the flavocytochrome-c-deficient mutant was comparable to that of the wild-type. Disruption of the fccAB genes did not have any significant effect on the sulfide-oxidizing ability of the cells, showing that flavocytochrome c is not essential for oxidation of sulfide to intracellular sulfur and indicating the presence of a distinct sulfide-oxidizing system. In accordance with these results, Chr. vinosum extracts catalyzed electron transfer from sulfide to externally added duroquinone, indicating the presence of the enzyme sulfide:quinone oxidoreductase (EC 1.8.5.-). Further investigations showed that the sulfide:quinone oxidoreductase activity was sensitive to heat and to quinone analogue inhibitors. The enzyme is strictly membrane-bound and is constitutively expressed. The presence of sulfide:quinone oxidoreductase points to a connection of sulfide oxidation to the membrane electron transport system at the level of the quinone pool in Chr. vinosum.

Base Sequence↗
PubMed2002

Photoreduction of bicarbonate catalyzed by supported cadmium sulfide.

Cadmium sulfide supported on silica (CdS-chi/SiO2, chi = 4, 11, 17, 25%) and zinc sulfide (CdS-chi/ZnS, chi = 5, 10, 20, 30%) was prepared by impregnation with cadmium sulfate and subsequent addition of sodium sulfide. The specific surface areas of the silica and zinc sulfide supported powders are in the range o f 188-280 and 95-104 m2 g(-1), respectively. After sonication of an aqueous suspension of CdS-17/SiO2 the particle size distribution exhibited two maxima at 22 and 57 microm. In the presence of sodium sulfite the supported cadmium sulfides photocatalyze the reduction of bicarbonate to formate, formaldehyde, and oxalate. Upon polychromatic irradiation (lambda > or = 290 nm) the C1-products formate and formaldehyde were obtained in concentrations of 30-130 microM whereas the C2-product oxalate reached only 1-8 microM. Formaldehyde is not formed through reduction of intermediate formate whereas oxalate is produced via oxidation of the latter. The linear increase of oxalate concentration with coverage can be rationalized by the assumption that dimerization of the intermediate carbon dioxide radical anion does not occur on the cadmium sulfide but in solution or on the silica surface. For zinc sulfide supported samples the coverages of 10, 20, and 30% do not change the photocatalytic activity significantly whereas a loading of 5% induces a 40-fold and 16-fold increase as compared to unmodified cadmium and zinc sulfide, respectively. This strong enhancement suggests that in CdS-05/ZnS the efficiency of charge separation is strongly improved through interparticle electron transfer. The results demonstrate that both silica and zinc sulfide supports increase the photocatalytic activity of cadmium sulfide through the presence of a recently found electronic semiconductor-support interaction (SEMSI effect). Additionally, the low coverage sample CdS-05/ZnS combines this novel effect with the higher charge separation efficiency of a coupled semiconductor system.

Journal Article↗
PubMed2004

Effect of sulfide structure on enantioselectivity in catalytic asymmetric epoxidation of aldehydes: mechanistic insights and implications.

Bridged bicyclic sulfide 1 was originally found to provide high levels of asymmetric induction in sulfur ylide-mediated epoxidations. This sulfide possesses chirality in the [2.2.1] thioether moiety and the [2.2.1] camphor-derived carbocyclic moiety. To determine whether the optimal sulfide had been used, a diastereomer of sulfide 1 in which the stereochemistry of the [2.2.1] carbocycle was reversed (sulfide 5) was prepared and studied as an epoxidation catalyst. This diastereomer gave considerably lower levels of asymmetric induction than the original sulfide 1. From computational and x-ray studies it was found that sulfide 5 gave rise to a more hindered ylide, which reacted more reversibly with aldehydes leading to lower enantioselectivity. Conditions that reduced reversibility were also tested and high enantioselectivities were returned for sulfide 5 (similar to sulfide 1). The implications for the synthesis of chiral sulfides for asymmetric epoxidations are discussed.

Journal Article↗
PubMed1995

Antineoplastic drugs sulindac sulfide and sulfone inhibit cell growth by inducing apoptosis.

The nonsteroidal anti-inflammatory drug sulindac is known to inhibit chemical carcinogenesis in rodent models and cause regression of adenomas in patients with adenomatous polyposis coli. Sulindac is a prodrug that is metabolized to a pharmacologically active sulfide derivative that potently inhibits prostaglandin synthesis. Recent studies, however, have shown that a sulfone derivative of sulindac, which essentially lacks prostaglandin synthesis inhibitory activity, also inhibits chemical carcinogenesis, suggesting that reduction of prostaglandin levels is not necessary for the antineoplastic activity of this class of drugs. Both sulindac sulfide and the sulfone inhibit the growth of cultured tumor cells, although the cellular mechanism(s) responsible for the antineoplastic activity of sulindac derivatives is unknown. In this study, we investigated the effects of sulindac sulfide and sulfone on the proliferation, differentiation, and apoptosis of HT-29 human colon carcinoma cells. Sulindac sulfide and sulfone significantly reduced cell number in both preconfluent and confluent cultures of HT-29 cells with the sulfide showing approximately 4-fold greater potency. In addition to HT-29 cells, both drugs inhibited the growth of a variety of tumor cell lines derived from other tissues, as well as normal epithelial cells and fibroblasts. Neither sulindac sulfide nor sulfone inhibited cell proliferation under conditions where the drugs were growth inhibitory. Only under specific conditions involving mitogenic stimulation did sulindac sulfide and sulfone cause cell cycle arrest. Neither sulindac sulfide nor the sulfone induced differentiation of HT-29 cells, but both drugs strongly induced apoptosis. The apoptotic response to sulindac sulfide and sulfone was both time- and dose-dependent and involved a mechanism independent of their inhibitory effect on cell cycle progression. These data suggest that apoptosis is responsible for the cell growth inhibitory activity of sulindac sulfide and sulfone and represents a potential mechanism for the antineoplastic activity of these drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

The usefulness of thiosulfate as an indicator of hydrogen sulfide poisoning: three cases.

We examined the usefulness of thiosulfate as an indicator of hydrogen sulfide poisoning by analysing sulfide and thiosulfate in three cases. In the first (non-fatal) case sulfide and thiosulfate were not detected in the blood samples from any of the four workers involved in the accident. In the urine samples, only thiosulfate was detected in three out of the four workers at a concentration of 0.12-0.43 micromol/ml, which was 4-14 times higher than the level in a healthy person. In the second (fatal) case sulfide and thiosulfate were detected in the blood sample at concentrations of 0.007 micromol/ml for sulfide, and 0.025 micromol/ml for thiosulfate. The thiosulfate concentration was at least 8 times higher than the level in a healthy person. In the third (fatal) case sulfide and thiosulfate were detected in the blood sample at concentrations of 0.95 micromol/ml for sulfide, and 0.12 micromol/ml for thiosulfate. Based on the above results, we concluded that thiosulfate in urine is the only indicator to prove hydrogen sulfide poisoning in non-fatal cases, while the analysis of sulfide in fatal cases should be accompanied by the measurement of thiosulfate in blood.

Adult↗
PubMed1998

Colonic luminal hydrogen sulfide is not elevated in ulcerative colitis.

It has been proposed that the reduction in n-butyrate oxidation by colonic epithelial cells observed in ulcerative colitis may be related to exposure to reduced forms of sulfur derived from dissimilatory sulfate reduction by luminal microflora. This study aims to compare stool sulfide concentrations in control and colitic subjects. Control subjects had significant colorectal disease excluded by virtue of their selection. Patients with ulcerative colitis were stratified by disease extent and activity, and by salicylate drug use. Stool sulfide was measured using a direct spectrophotometric method on NaOH (free sulfide) and zinc acetate (total sulfide) stool slurries. Fifteen control and 19 colitic subjects were studied. There was no significant difference in stool sulfide between control and colitic patients (free sulfide, control = 0.52 (0.17), colitic = 0.45 (0.10), t = 0.36, P = 0.71, total sulfide, control = 1.33 (0.21), colitic = 0.96 (0.15), t = 1.44, P = 0.16). Disease extent or activity did not significantly influence stool sulfide. These results do not support a primary etiologic role for luminal sulfide in ulcerative colitis.

Colitis, Ulcerative↗
PubMed2005

Silver accumulation in Daphnia magna in the presence of reactive sulfide.

Previously, we demonstrated a higher silver body burden when Daphnia magna were exposed to silver in the presence of environmentally relevant concentrations (25 nM) of reactive sulfide, but the explanation was unclear. In the present study, D. magna were exposed to AgNO3 (0.93 microg Ag/L=8.6 nM as a mixture of cold Ag and (110m)Ag) in synthetic water in either the presence or absence of 25 nM sulfide as zinc sulfide clusters. After 1-h exposure, daphnids were transferred to clean water for up to 5-h depuration. At different times of Ag exposure and depuration, daphnids were randomly sampled for whole body silver burden. Also, after 1 h, daphnids were sampled for silver accumulation in "gills" (small organs on the thoracic appendages), digestive tract, and carcass. Other groups were exposed to the same silver and sulfide concentrations for 1 h and then sampled for whole-body autoradiography. Silver body burden was about two-fold higher in the presence of sulfide. A two-fold increase in silver burden in "gills" and digestive tract, but not in carcass, was also observed in the presence of sulfide. Absolute differences due to sulfide were greatest in digestive tract and explained most of the difference in whole body burden. Transfer to clean water caused a significant drop in silver concentration in whole body and all compartments to similar levels in the two groups after 5-h depuration. These results indicate that the higher silver body burden observed in the presence of sulfide is mainly due to sulfide-bound silver in the digestive tract of the daphnids. This conclusion is supported by autoradiography, which showed a high concentration of silver in the digestive tract of daphnids exposed to Ag/sulfide.

Animals↗