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PubMed1989

Activity of polymorphonuclear leukocytes in the presence of sulfide.

Polymorphonuclear leukocytes (PMN) isolated from human blood were exposed to various levels of hydrogen sulfide. The effect on respiratory burst, myeloperoxidase activity, and capacity to phagocytose and kill bacteria were studied. A 1-h exposure of the PMN to 1 mM sulfide did not decrease their myeloperoxidase activity or their capacity to initiate a respiratory burst. Actually the products of the respiratory burst rapidly oxidized sulfide. The phagocytosis and killing of bacteria in the presence of 1 mM sulfide was only decreased to a minor extent. Myeloperoxidase in cell extract was, however, almost completely inhibited by 1 microM sulfide. These results indicate that hydrogen sulfide does not easily permeate PMN. PMN may be able to function in infected sites with high sulfide levels such as in the gingival pockets of periodontal disease. In the oxygenated areas of these sites the PMN may actually help in the detoxification of sulfide.

Blood Bactericidal Activity↗
PubMed1991

Effects of hydrogen sulfide exposure on surface properties of lung surfactant.

Hydrogen sulfide is an irritant and chemical asphyxiant gas that exerts its primary toxic effects on the respiratory and neurological systems. Exposure to hydrogen sulfide above a threshold value of 200-300 ppm is characterized by the sudden onset of hemorrhagic pulmonary edema. The purpose of this study was to determine whether this response is associated with changes in the surface properties of pulmonary surfactant. Bronchoalveolar lavage fluid was retrieved from the lungs of Fischer 344 rats exposed to two concentrations of hydrogen sulfide or fresh air for 4 h. Surface tension-lowering properties were assayed using a captive bubble surface tensiometer. Lung injury was assessed by histopathology and measurements of total protein and lactate dehydrogenase activity in the lavagate. Marked abnormalities in surfactant activity were demonstrated in the lavagates from rats exposed to the highest concentration (300 ppm) of hydrogen sulfide. These involved the properties of adsorption to the air-water interface and surface tension lowering under quasi-static interfacial compression. Exposure to 200 ppm hydrogen sulfide had no effect on minimum surface tension despite a significant increase in protein and lactate dehydrogenase in the lavagate. This would suggest a threshold-type response for the inhibition of surfactant activity by hydrogen sulfide. In vitro studies using normal rat surfactant showed that the abnormalities in surfactant activity were due to inhibitors in the edema fluid and not to a direct effect of sulfide on surfactant. The pathophysiological consequences of increased alveolar surface tension after hydrogen sulfide exposure may need to be considered in the clinical setting.

Adsorption↗
PubMed1995

Sulfide-induced perturbations of the neuronal mechanisms controlling breathing in rats.

The effects of sulfide on neonatal rat respiration were studied. Two in vitro experimental models were utilized: the isolated brain stem-spinal cord preparation and the medullary slice preparation containing respiratory rhythm-generating regions from neonatal rats. Plethysmographic measurements of the effects of sulfide on the breathing patterns of unanesthetized neonatal rats were also made to compare the sensitivities of neonatal and adult rats to sulfide toxicity. In vitro, sulfide acted at sites within the ventrolateral medulla to depress the frequency of respiratory rhythmic discharge by approximately 50-60%. However, the neuronal network underlying respiratory rhythmogenesis continued to function in the presence of concentrations of sulfide far beyond those deemed to be lethal in vivo. Intraperitoneal administration of sulfide caused a dose-dependent decrease in the frequency and amplitude of breathing of neonatal rats of all ages (0-19 days postnatal), although the sensitivity to sulfide increased with age. We hypothesize that the rapid suppression of breathing caused by sulfide is due to changes in neuronal excitability within respiratory rhythm-generating centers rather than, as previously hypothesized, to perturbations of cellular oxidative metabolism.

Aging↗
PubMed1997

Sulfide acquisition by the vent worm Riftia pachyptila appears to be via uptake of HS-, rather than H2S.

Deep-sea hydrothermal vents are home to a variety of invertebrate species, many of which host chemosynthetic bacteria in unusual symbiotic arrangements. The vent tubeworm Riftia pachyptila (Vestimentifera) relies upon internal chemolithoautotrophic bacterial symbionts to support its large size and high growth rates. Because of this, R. pachyptila must supply sulfide to the bacteria, which are far removed from the external medium. Internal H2S ([H2S+HS-+S2-]) can reach very high levels in R. pachyptila (2-12mmoll-1 in the vascular blood), most of which is bound to extracellular hemoglobins. The animal can potentially take up sulfide from the environment via H2S diffusion or via mediated uptake of HS-, or both. It was expected that H2S diffusion would be the primary sulfide acquisition mechanism, paralleling the previously demonstrated preferential uptake of CO2. Our data show, however, that the uptake of HS- is the primary mechanism used by R. pachyptila to obtain sulfide and that H2S diffusion into the worm apparently proceeds at a much slower rate than expected. This unusual mechanism may have evolved because HS- is less toxic than H2S and because HS- uptake decouples sulfide and inorganic carbon acquisition. The latter occurs via the diffusion of CO2 at very high rates due to the maintenance of an alkaline extracellular fluid pH. H2S accumulation is limited, however, to sulfide that can be bound by the hemoglobins, protecting the animal from sulfide toxicity and the symbionts from sulfide inhibition of carbon fixation.

Animals↗
PubMed2005

Measuring sulfide accumulation in diffusive gradients in thin films by means of purge and trap followed by ion-selective electrode.

A procedure for measuring in situ sulfide concentrations by coupling diffusive gradients in thin films (DGT) to solid-state ion-selective electrodes (ISE) is described and evaluated. Laboratory tests were performed to evaluate the coupling of these techniques, and these results were compared to the previously used methods of computer imaging densitometry (CID) and methylene blue. An average elution efficiency of 89%, as detected by ISE, was determined for a series of solutions containing amounts of sulfide ranging from 0.009 to 2.50 micromol. The validity of the standard mass-transfer equation for sulfide accumulation by DGT probes and subsequent detection by ISE was tested by measuring the mass of sulfide collected over time and with respect to varying diffusive gel thicknesses. Regressions of the sulfide mass accumulation versus the independent variables of time and inverse diffusive thickness proved to be linear. The use of DGT coupled to ISE provides a preconcentration method for sulfide that improves the detection limit (DL) over other techniques. This alternative method provides quantitative measurements of DGT-captured sulfide from solutions with a detection limit of at least 0.1 micromol/L for a 24-h deployment. The DGT technique also provides potential advantages in understanding sulfide speciation over existing methods.

Densitometry↗
PubMed2006

Recent findings on sinks for sulfide in gravity sewer networks.

Sulfide buildup in sewer networks is associated with several problems, including health impacts, corrosion of sewer structures and odor nuisance. In recent years, significant advances in the knowledge of the major processes governing sulfide buildup in sewer networks have been made. This paper summarizes this newly obtained knowledge and emphasizes important implications of the findings. Model simulations of the in-sewer processes important for the sulfur cycle showed that sulfide oxidation in the wetted biofilm is typically the most important sink for dissolved sulfide in gravity sewers. However, sulfide emission and thereby potential hydrogen sulfide buildup in the sewer atmosphere is of particular importance in sewers constructed with large diameter pipes, in sewers constructed with steep slopes and in sewers conveying low pH wastewater. Precipitation of metal sulfides is only important when the sulfide concentration in the wastewater is low; i.e. less than 1 g Sm(-3).

Computer Simulation↗
PubMed2003

Introducing the emission process of hydrogen sulfide to a sewer process model (WATS).

Emission of hydrogen sulfide in sewer networks results in odor, health and corrosion problems. These problems generally occur when wastewater is transported under anaerobic and turbulent conditions. Studies on integrated aerobic/anaerobic processes in sewers have led to a conceptual sewer process model, WATS (Wastewater Aerobic/anaerobic Transformations in Sewers). The WATS model accounts for the carbon cycle, reaeration and sulfide formation. However, to handle odor, health and corrosion problems more efficiently, other aspects of the sulfur cycle need to be included. Emphasis in this study is on an extension of the WATS model in terms of hydrogen sulfide emission. A fundamental concept of this extended model is related to emission of the molecular form of hydrogen sulfide and thereby to pH of wastewater. An engineering application of the extended WATS model includes different scenarios of sewer performance concerning hydrogen sulfide emission under dissolved oxygen-limited conditions. By applying the extended WATS model, users can more realistically cope with the fate of hydrogen sulfide. Consequently, when dealing with the sulfur cycle, users need no longer be restricted to the sulfide formation process but can also take transfer of hydrogen sulfide across the air-water interface into account.

Bacteria, Aerobic↗
PubMed2004

Biological removal of air loaded with a hydrogen sulfide and ammonia mixture.

The nuisance impact of air pollutant emissions from wastewater pumping stations is a major issue of concern to China. Hydrogen sulfide and ammonia are commonly the primary odor and are important targets for removal. An alternative control technology, biofiltration, was studied. The aim of this study is to investigate the potential of unit systems packed with compost in terms of ammonia and hydrogen sulfide emissions treatment, and to establish optimal operating conditions for a full-scale conceptual design. The laboratory scale biofilter packed with compost was continuously supplied with hydrogen sulfide and ammonia gas mixtures. A volumetric load of less than 150 gH2S/(m3 x d) and 230 gNH3/(m3 x d) was applied for about fifteen weeks. Hydrogen sulfide and ammonia elimination occurred in the biofilter simultaneously. The removal efficiency, removal capacity and removal kinetics in the biofilter were studied. The hydrogen sulfide removal efficiency reached was very high above 99%, and ammonia removal efficiency was about 80%. Hydrogen sulfide was oxidized into sulphate. The ammonia oxidation products were nitrite and nitrate. Ammonia in the biofilter was mainly removed by adsorption onto the carrier material and by absorption into the water fraction of the carrier material. High percentages of hydrogen sulfide or ammonia were oxidized in the first section of the column. Through kinetics analysis, the presence of ammonia did not hinder the hydrogen sulfide removal. According to the relationship between pressure drop and gas velocity for the biofilter and Reynolds number, non-Darcy flow can be assumed to represent the flow in the medium.

Air Pollutants↗
PubMed2005

Calculations on the group 15 intraring substituted benzenes (pyridine to bismin series) and their datively bonded oxides and sulfides.

The series of heterocyclic compounds pyridine, phosphorin, arsenin, antimonin, bismin, and the related series of pyridine oxide, etc., and pyridine sulfide, etc., were investigated using density functional theory. In addition to molecular geometries and energies, the nucleus independent chemical shift (NICS) values were calculated for each ring, and the CHELPG atomic charges were calculated. Calculated heats of formation are: pyridine +133, phosphorin +181, arsenin +231, antimonin +329, bismin +468, pyridine oxide +143, phosphorin oxide +1, arsenin oxide +183, antimonin oxide +344, bismin oxide +570, pyridine sulfide +252, phosphorin sulfide +205, arsenin sulfide +328, antimonin sulfide +435, and bismin sulfide + 642 kJ/mol. The question of aromaticity for these heterocycles was discussed. On the basis of hydrogenation energies, NICS values, and lack of bond alternation, the entire series from pyridine to bismin appears to be aromatic and to a roughly equal degree. The situation for the oxides and sulfides of pyridine, phosphorin, and arsenin is much the same, but bismin oxide and bismin sulfide are nonplanar and according to NICS nonaromatic. Antimonin oxide is aromatic by some of the criteria and nonaromatic by others.

Journal Article↗
PubMed2003

Gene modulation by the cyclooxygenase inhibitor, sulindac sulfide, in human colorectal carcinoma cells: possible link to apoptosis.

The mechanisms underlying the anti-tumorigenic properties of cyclooxygenase inhibitors are not well understood. One novel hypothesis is alterations in gene expression. To test this hypothesis sulindac sulfide, which is used to treat familial adenomatous polyposis, was selected to detect gene modulation in human colorectal cells at physiological concentrations with microarray analysis. At micromolar concentrations, sulindac sulfide stimulated apoptosis and inhibited the growth of colorectal cancer cells on soft agar. Sulindac sulfide (10 microm) altered the expression of 65 genes in SW-480 colorectal cancer cells, which express cyclooxygenase-1 but little cyclooxygenase-2. A more detailed study of 11 genes revealed that their expression was altered in a time- and dose-dependent manner as measured by real-time RT-PCR. Northern analysis confirmed the expression of 9 of these genes, and Western analysis supported the conclusion that sulindac sulfide altered the expression of these proteins. Cyclooxygenase-deficient HCT-116 cells were more responsive to sulindac sulfide-induced gene expression than SW-480 cells. However, this response was diminished in HCT-116 cells overexpressing cyclooxygenase-1 compared with normal HCT-116 cells suggesting the presence of cyclooxygenase attenuates this response. However, prostaglandin E2, the main product of cyclooxygenase, only suppressed the sulindac sulfide-induced expression of two genes, with little known biological function while it modulated the expression of two more. The most likely explanation for this finding is the metabolism of sulindac sulfide to inactive metabolites by the peroxidase activity of cyclooxygenase. In conclusion, this is the first report showing sulindac sulfide, independent of cyclooxygenase, altered the expression of several genes possibly linked to its anti-tumorigenic and pro-apoptotic activity.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1986

Adaptation to Hydrogen Sulfide of Oxygenic and Anoxygenic Photosynthesis among Cyanobacteria.

Four different types of adaptation to sulfide among cyanobacteria are described based on the differential toxicity to sulfide of photosystems I and II and the capacity for the induction of anoxygenic photosynthesis. Most cyanobacteria are highly sensitive to sulfide toxicity, and brief exposures to low concentrations cause complete and irreversible cessation of CO(2) photoassimilation. Resistance of photosystem II to sulfide toxicity, allowing for oxygenic photosynthesis under sulfide, is found in cyanobacteria exposed to low H(2)S concentrations in various hot springs. When H(2)S levels exceed 200 muM another type of adaptation involving partial induction of anoxygenic photosynthesis, operating in concert with partially inhibited oxygenic photosynthesis, is found in cyanobacterial strains isolated from both hot springs and hypersaline cyanobacterial mats. The fourth type of adaptation to sulfide is found at H(2)S concentrations higher than 1 mM and involves a complete replacement of oxygenic photosynthesis by an effective sulfide-dependent, photosystem II-independent anoxygenic photosynthesis. The ecophysiology of the various sulfide-adapted cyanobacteria may point to their uniqueness within the division of cyanobacteria.

Journal Article↗
PubMed1986

Effect of nitrate on biogenic sulfide production.

The addition of 59 mM nitrate inhibited biogenic sulfide production in dilute sewage sludge (10% [vol/vol]) amended with 20 mM sulfate and either acetate, glucose, or hydrogen as electron donors. Similar results were found when pond sediment or oil field brines served as the inoculum. Sulfide production was inhibited for periods of at least 6 months and was accompanied by the oxidation of resazurin from its colorless reduced state to its pink oxidized state. Lower amounts of nitrate (6 or 20 mM) and increased amounts of sewage sludge resulted in only transient inhibition of sulfide production. The addition of 156 mM sulfate to bottles with 59 mM nitrate and 10% (vol/vol) sewage sludge or pond sediment resulted in sulfide production. Nitrate, nitrite, and nitrous oxide were detected during periods where sulfide production was inhibited, whereas nitrate, nitrite, and nitrous oxide were below detectable levels at the time sulfide production began. The oxidation of resazurin was attributed to an increase in nitrous oxide which persisted in concentration of about 1.0 mM for up to 5 months. The numbers of sulfate-reducing organisms decreased from 10 CFU ml sludge to less than detectable levels after prolonged incubation of oxidized bottles. The addition of 10 mM glucose to oxidized bottles after 14.5 weeks of incubation resulted in rereduction of the resazurin and subsequent sulfide production. The prolonged inhibition of sulfide production was attributed to an increase in oxidation-reduction potential due to biogenic production of nitrous oxide, which appeared to have a cytotoxic effect on sulfate-reducing populations.

Journal Article↗
PubMed1997

Formation of dimethyl sulfide and methanethiol in anoxic freshwater sediments.

Concentrations of volatile organic sulfur compounds (VOSC) were measured in water and sediment columns of ditches in a minerotrophic peatland in The Netherlands. VOSC, with methanethiol (4 to 40 nM) as the major compound, appeared to be mainly of sediment origin. Both VOSC and hydrogen sulfide concentrations decreased dramatically towards the water surface. High methanethiol and high dimethyl sulfide concentrations in the sediment and just above the sediment surface coincided with high concentrations of hydrogen sulfide (correlation factors, r = 0.91 and r = 0.81, respectively). Production and degradation of VOSC were studied in 32 sediment slurries collected from various freshwater systems in The Netherlands. Maximal endogenous methanethiol production rates of the sediments tested (up to 1.44 (mu)mol per liter of sediment slurry (middot) day(sup-1)) were determined after inhibition of methanogenic and sulfate-reducing populations in order to stop VOSC degradation. These experiments showed that the production and degradation of VOSC in sediments are well balanced. Statistical analysis revealed multiple relationships of methanethiol production rates with the combination of methane production rates (indicative of total anaerobic mineralization) and hydrogen sulfide concentrations (r = 0.90) or with the combination of methane production rates and the sulfate/iron ratios in the sediment (r = 0.82). These findings and the observed stimulation of methanethiol formation in sediment slurry incubations in which the hydrogen sulfide concentrations were artificially increased provided strong evidence that the anaerobic methylation of hydrogen sulfide is the main mechanism for VOSC formation in most freshwater systems. Methoxylated aromatic compounds are likely a major source of methyl groups for this methylation of hydrogen sulfide, since they are important degradation products of the abundant biopolymer lignin. Increased sulfate concentrations in several freshwater ecosystems caused by the inflow of water from the river Rhine into these systems result in higher hydrogen sulfide concentrations. As a consequence, higher fluxes of VOSC towards the atmosphere are conceivable.

Journal Article↗
PubMed1980

Bioassay of Selenium Sulfide (Gavage) for Possible Carcinogenicity (CAS No. 7446-34-6).

Selenium sulfide is an ingredient in dandruff shampoos used in concentrations of 1% in products sold over-the-counter and 2.5% in products which are available by prescription only. Prescription shampoos have been shown in clinical studies to be of therapeutic value against dandruff. An antimitotic mechanism of action is suggested by data showing that selenium sulfide decreases the rate of incorporation of radioactively labeled thymidine into the DNA of dermal epithelial cells. Approximately 200 kg of selenium sulfide is estimated to be used annually for this purpose. A bioassay of selenium sulfide for possible carcinogenicity was conducted by administering this substance by gavage to F344 rats and B6C3F1 mice. Groups of 50 rats and 50 mice of each sex were administered selenium sulfide suspended in 0.5% aqueous carboxymethylcellulose 7 days per week for 103 weeks at either 3 or 5 mg/kg/day for rats and 20 or 100 mg/kg/day for mice. As vehicle controls, groups of 50 rats and 50 mice of each sex were administered only the 0.5% aqueous carboxymethylcellulose. Similar groups of untreated controls also were used. All surviving rats and mice were killed and necropsied at week 104 or 105. The significant effects that could be related to administration of selenium sulfide at the doses used were decreased body weight and increased tumor formation in female mice and in rats of each sex. Dosed rats and female mice had an increased incidence of hepatocellular carcinomas and adenomas. Dosed female mice also had an increased incidence of alveolar/bronchiolar carcinomas and adenomas. Under the conditions of this bioassay, selenium sulfide was carcinogenic for F344 rats and female B6C3F1 mice, including hepatocellular carcinomas in male and female rats and female mice and alveolar/bronchiolar carcinomas and adenomas in female mice. Selenium sulfide was not carcinogenic for male mice; but they have been able to tolerate higher doses. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Positive Male Mice: Negative Female Mice: Positive

Journal Article↗
PubMed2006

Sulfide oxidation under chemolithoautotrophic denitrifying conditions.

Chemolithoautotrophic denitrifying microorganisms oxidize reduced inorganic sulfur compounds coupled to the reduction of nitrate as an electron acceptor. These denitrifiers can be applied to the removal of nitrogen and/or sulfur contamination from wastewater, groundwater, and gaseous streams. This study investigated the physiology and kinetics of chemolithotrophic denitrification by an enrichment culture utilizing hydrogen sulfide, elemental sulfur, or thiosulfate as electron donor. Complete oxidation of sulfide to sulfate was observed when nitrate was supplemented at concentrations equal or exceeding the stoichiometric requirement. In contrast, sulfide was only partially oxidized to elemental sulfur when nitrate concentrations were limiting. Sulfide was found to inhibit chemolithotrophic sulfoxidation, decreasing rates by approximately 21-fold when the sulfide concentration increased from 2.5 to 10.0 mM, respectively. Addition of low levels of acetate (0.5 mM) enhanced denitrification and sulfate formation, suggesting that acetate was utilized as a carbon source by chemolithotrophic denitrifiers. The results of this study indicate the potential of chemolithotrophic denitrification for the removal of hydrogen sulfide. The sulfide/nitrate ratio can be used to control the fate of sulfide oxidation to either elemental sulfur or sulfate.

Acetates↗
PubMed1990

Dithiothreitol liberates non-acid labile sulfide from brain tissue of H2S-poisoned animals.

Acid-labile sulfide measured by conventional gas dialysis and ion chromatography with electrochemical detection accounts for only a proportion of the total sulfide present in brain tissue after poisoning with NaHS, an H2S precursor. Dithiothreitol (DTT) displaced additional measurable sulfide not detectable by the conventional techniques from NaHS-poisoned brain tissue. Sulfide liberation by DTT was dose-dependent and maximal at higher DTT concentration (10 and 30 mM) and was thought to represent non-acid labile sulfide. Dithiothreitol was also found to be significantly protective against H2S poisoning. Furthermore, in vitro inhibition by sulfide of monoamine oxidase (MAO) was reversed by DTT, thus suggesting a molecular mechanism consistent with known persulfide chemistry. Persulfide formation may thus underlie some aspects of hydrogen sulfide neurotoxicity. The rational development of antidotes for use in H2S poisoning may thus have to be centered on strategies concentrating on known thiol, disulfide and persulfide chemistry.

Animals↗
PubMed1983

Origin of the labile sulfide in the iron-sulfur proteins of Escherichia coli.

A method has been devised for measuring the abundance of sulfur-34 in the hydrogen sulfide released upon the acidification of Escherichia coli cells. Evidence is presented, based on the rate at which the hydrogen sulfide is released from the cells as well as the total amount released, that this hydrogen sulfide originates from the iron-sulfur proteins present in the cells. The sulfur-34 abundance in this hydrogen sulfide which was isolated from cells grown with [sulfane-34S] thiocystine, a compound which can differentially label in vivo the sulfur-34 abundance of cysteine and hydrogen sulfide, shows cysteine sulfur and not hydrogen sulfide to be the origin of the sulfide sulfur of iron-sulfur proteins in aerobically grown E. coli.

Bacterial Proteins↗
PubMed1997

Colonic sulfide in pathogenesis and treatment of ulcerative colitis.

A role for colonic sulfide in the pathogenesis and treatment of ulcerative colitis (UC) has emerged based on biochemical, microbiological, nutritional, toxicological, epidemiological, and therapeutic evidence. Metabolism of isolated colonic epithelial cells has indicated that the bacterial short-chain fatty acid n-butyrate maintains the epithelial barrier and that sulfides can inhibit oxidation of n-butyrate analogous to that observed in active UC. Sulfur for fermentation in the colon is essential for n-butyrate formation and sulfidogenesis aids disposal of colonic hydrogen produced by bacteria. The numbers of sulfate-reducing bacteria and sulfidogenesis is greater in UC than control cases. Sulfide is mainly detoxified by methylation in colonic epithelial cells and circulating red blood cells. The enzyme activity of sulfide methylation is higher in red blood cells of UC patients than control cases. Patients with UC ingest more protein and thereby sulfur amino acids than control subjects. Removing foods rich in sulfur amino acids (milk, eggs, cheese) has proven therapeutic benefits in UC. 5-Amino salicylic acid reduces fermentative production of hydrogen sulfide by colonic bacteria, and aminoglycosides, which inhibit sulfate-reducing bacteria, are of therapeutic benefit in active UC. Methyl-donating agents are a category of drugs of potential therapeutic use in UC. A correlation between sulfide production and mucosal immune responses in UC needs to be undertaken. Control of sulfidogenesis and sulfide detoxification may be important in the disease process of UC, although whether their roles is in an initiating or promoting capacity has yet to be determined.

Bacteria↗