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At least 19 recordsLinked to original sources
PubMed1989

Acute hydrogen sulfide poisoning. Demonstration of selective uptake of sulfide by the brainstem by measurement of brain sulfide levels.

The possibility of measuring sulfide levels in the central nervous system (CNS) opens up many avenues for exploration. In acute hydrogen sulfide (H2S) poisoning, death results from loss of central respiratory drive. To date, however, measurement of brain sulfide has not been possible. By employing gas dialysis and ion chromatography coupled to electrochemical detection, rat brain sulfide levels could be measured either following inhalation of H2S or after injection of sodium hydrosulfide (median lethal dose, [LD50] = 14.6 +/- 1.00 mg/kg). Accumulation of brain sulfide was linearly proportional to the dose over the range 0.50 LD50 to 3.33 LD50 units, and was strongly correlated with mortality data (R = 0.947). Furthermore, analysis of untreated (control) brain showed an endogenous sulfide level of 1.57 +/- 0.04 micrograms/g (mean +/- SE; N = 16). Studies on various rat brain regions (brainstem, cerebellum, hippocampus, striatum and cortex) showed that the endogenous sulfide level of brainstem, 1.23 +/- 0.06 micrograms/g, was significantly lower than that of the other brain regions. Net uptake of sulfide was greatest in the brainstem (3.02 micrograms/g) compared to the other regions as was the selective accumulation of sulfide as calculated from normalized blood flow rates. The results of subcellular fractionation demonstrated that sulfide was detectable in fractions enriched in myelin, synaptosomes and mitochondria. Approximately one-quarter of the endogenous sulfide content of whole rat brain was found in the mitochondrial fraction. The sulfide content of these fractions increased 2- to 3-fold after 50 mg/kg NaHS, the greatest increases occurring in myelin- and mitochondrial-enriched fractions.

Analysis of Variance↗
PubMed2004

Sulfide consumption by mussel gill mitochondria is not strictly tied to oxygen reduction: measurements using a novel polarographic sulfide sensor.

Some organisms that survive in environments rich in hydrogen sulfide possess specific metabolic pathways for sulfide oxidation and subsequent use of reducing equivalents in oxidative phosphorylation, a process called chemolithoheterotrophy. This process is dependent on ambient oxygen partial pressure and environmental sulfide exposure. To define accurately the kinetics of sulfide metabolism and its dependence on cellular conditions, we have developed a polarographic sulfide sensor (PSS) to measure sulfide concentrations directly and continuously under physiological conditions. The ribbed mussel Geukensia demissa, an inhabitant of sulfide-rich coastal sediments, consumes sulfide in a chemolithoheterotrophic metabolic strategy. Gill mitochondria use sulfide as respiratory substrate for ATP production, and sulfide consumption is sufficiently rapid and so kinetically complex that only continuous real-time detection captures these events. Under normoxic conditions, oxygen and sulfide consumption are matched. Under hypoxic to anoxic conditions, however, sulfide consumption continues without commensurate oxygen consumption, and these results can be duplicated at higher oxygen conditions by selective blockade of terminal oxidases. These metabolic capabilities depend on prior environmental sulfide exposure, which suggests substantial mitochondrial metabolic plasticity. The recent finding that endogenous sulfide is a critical cell signaling molecule in all organisms suggests that the metabolic pathways that tightly control cellular sulfide levels are widespread. Sensors that accurately report sulfide concentrations under physiologically relevant conditions are valuable tools with which to explore the expanding role of sulfide in biological systems.

Alabama↗
PubMed2005

Mitochondrial depolarization following hydrogen sulfide exposure in erythrocytes from a sulfide-tolerant marine invertebrate.

Sulfide-tolerant marine invertebrates employ a variety of mechanisms to detoxify sulfide once it has entered their bodies, but their integumentary, respiratory epithelium and circulatory cells may still be exposed to toxic sulfide concentrations. To investigate whether sulfide exposure is toxic to mitochondria of a sulfide-tolerant invertebrate, we used the fluorescent dyes JC-1 and TMRM to determine the effect of sulfide exposure on mitochondrial depolarization in erythrocytes from the annelid Glycera dibranchiata. In erythrocytes exposed to 0.11-1.9 mmol l-1 sulfide for 1 h, the dyes showed fluorescence changes consistent with sulfide-induced mitochondrial depolarization. At the highest sulfide concentration, the extent of depolarization was equivalent to that caused by the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP). Even when induced by as little as 0.3 mmol l-1 sulfide, the depolarization was not reversible over a subsequent 5 h recovery period. The mechanism of toxicity was likely not via inhibition of cytochrome c oxidase (COX), since other COX inhibitors and other mitochondrial electron transport chain inhibitors did not produce similar effects. Furthermore, pharmacological inhibition of the mitochondrial permeability transition pore failed to prevent sulfide-induced depolarization. Finally, increased oxidation of the free radical indicators H2DCFDA and MitoSOX in erythrocytes exposed to sulfide suggests that sulfide oxidation increased oxidative stress and superoxide production, respectively. Together, these results indicate that sulfide exposure causes mitochondrial depolarization in cells of a sulfide-tolerant annelid, and that this effect, which differs from the actions of other COX inhibitors, may be via increased free radical damage.

Analysis of Variance↗
PubMed2002

Physiology of sulfide in the rat colon: use of bismuth to assess colonic sulfide production.

Colonic bacteria produce hydrogen sulfide, a toxic compound postulated to play a pathogenetic role in ulcerative colitis. Colonic sulfide exposure has previously been assessed via measurements of fecal sulfide concentration. However, we found that <1% of fecal sulfide of rats was free, the remainder being bound in soluble and insoluble complexes. Thus fecal sulfide concentrations may reflect sulfide binding capacity rather than the toxic potential of feces. We utilized bismuth subnitrate to quantitate intracolonic sulfide release based on observations that bismuth 1) avidly binds sulfide; 2) quantitatively releases bound sulfide when acidified; and 3) does not influence fecal sulfide production by fecal homogenates. Rats ingesting bismuth subnitrate excreted 350 +/- 18 micromol/day of fecal sulfide compared with 9 +/- 1 micromol/day in control rats. Thus the colon normally absorbs approximately 340 micromol of sulfide daily, a quantity that would produce local and systemic injury if not efficiently detoxified by the colonic mucosa. Studies utilizing bismuth should help to clarify the factors influencing sulfide production in the human colon.

Animal Feed↗
PubMed1991

Sulfide-induced sulfide-quinone reductase activity in thylakoids of Oscillatoria limnetica.

Sulfide-dependent partial electron-transport reactions were studied in thylakoids isolated from cells of the cyanobacterium Oscillatoria limnetica, which had been induced to perform sulfide-driven anoxygenic photosynthesis. It was found that these thylakoids have the capacity to catalyze electron transfer, from sulfide to externally added quinones, in the dark. Assay conditions were developed to measure the reaction either as quinone-dependent sulfide oxidation (colorimetrically) or as sulfide-dependent quinone reduction (by UV dual-wavelength spectrophotometry). The main features of this reaction are as follows. (i) It is exclusively catalyzed by thylakoids of sulfide-induced cells. Noninduced thylakoids lack this reaction. (ii) Plastoquinone-1 or -2 are equally good substrates. Ubiquinone-1 and duroquinone yield somewhat slower rates. (iii) The apparent Km for plastoquinone-1 was 32 microM and for sulfide about 4 microM. Maximal rates (at 25 degrees C) were about 75 mumol of quinone reduced per mg of chlorophyll.h. (iv) The reaction was not affected by extensive washes of the membranes. (v) Unlike sulfide-dependent NADP photoreduction activity of these thylakoids, which is sensitive to all the specific inhibitors of the cytochrome b6f complex, the new dark reaction exhibited differential sensitivity to these inhibitors. 2-n-Nonyl-4-hydroxyquinoline-N-oxide was the most potent inhibitor of both light and dark reactions, working at submicromolar concentrations. 5-n-Undecyl-6-hydroxy-4,7-dioxobenzothiazole also inhibited the two reactions to a similar extent, but at 10 times higher concentrations than 2-n-nonyl-4-hydroxyquinoline-N-oxide. 2,5-Dibromo-3-methyl-6-isopropyl-p-benzoquinone, 2-iodo-6-isopropyl-3-methyl-2',4,4'-trinitrodiphenyl ether, and stigmatellin had no effect on the dark reaction at concentrations sufficient to fully inhibit the light reaction from sulfide. We propose that the sulfide-induced factor which enables the use of sulfide as the electron donor for anoxygenic photosynthesis in Oscillatria limnetica is a membrane-bound sulfide-quinone reductase. Its site of interaction is suggested to be either the cytochrome b6 (at the Qc quinone binding site or the bH site) or the plastoquinone pool. The analogy to other anoxygenic photosynthetic systems is discussed.

Chloramphenicol↗
PubMed2005

Nickel sulfide and copper sulfide nanocrystal synthesis and polymorphism.

Nickel sulfide and copper sulfide nanocrystals were synthesized by adding elemental sulfur to either dichlorobenzene-solvated (copper sulfide) or oleylamine-solvated metal(II) precursors (nickel sulfide) at relatively high temperature to produce the metal sulfide. Nickel sulfide nanocrystals are cubic Ni(3)S(4) (polydymite) with irregular prismatic shapes, forming by a two-step reduction-sulfidation mechanism where Ni(II) reduces to Ni metal before sulfidation to Ni(3)S(4). Despite extensive efforts to optimize the Ni(3)S(4) nanocrystal size and shape distributions, polydisperse nanocrystals are produced. In contrast, copper sulfide nanocrystals can be obtained with narrow size and shape distributions. The copper sulfide stoichiometry depended on the Cu:S mole ratio used in the reaction: Cu:S mole ratios of 1:2 and 2:1 gave CuS (covellite) and Cu(1.8)S (digenite), respectively. CuS nanocrystals formed as hexagonal disks that assemble into stacked ribbons when cast from solution onto a substrate. CuS, Cu(1.8)S, and Ni(3)S(4) differ from the Cu(2)S and NiS nanocrystals obtained by solventless decomposition of metal thiolate single source precursors, in terms of stoichiometry for copper sulfide, and both stoichiometry and morphology for nickel sulfide [Ghezelbash, A.; Sigman, M. B., Jr.; Korgel, B. A. Nano Lett. 2004, 4, 537-542. Sigman, M. B. Ghezelbash, A.; Hanrath, T.; Saunders, A. E.; Lee, F.; Korgel, B. A. J. Am. Chem. Soc. 2003, 125, 16050-16057].

Journal Article↗
PubMedDate not supplied

High-performance liquid chromatography detection of sulfide in tissues from sulfide-treated mice.

The biological and forensic use of ion-interaction reversed-phase high-performance liquid chromatography for the determination of hydrogen sulfide-derived methylene blue is evaluated by measuring the sulfide content in tissues from sulfide-treated mice. Various preparative conditions were examined. The determinations of background levels of sulfide from brain, liver and kidney were compared to sulfide levels from mice exposed to 60 micrograms g-1 sodium hydrosulfide. At the time of death, significant increases above background sulfide levels were measured for all three biological tissues. To evaluate its forensic potential, we used this sulfide detection methodology to evaluate comparatively the sulfide levels from fresh and frozen samples of brain, liver and kidney. The stability of sulfide levels obtained from frozen brain makes this tissue the most reliable tissue for forensic evaluation. Samples of brain, liver and kidney obtained within 24 h of death by sulfide intoxication had demonstrable elevations in sulfide concentration.

Animals↗
PubMed2002

Cytochrome oxidase inhibition induced by acute hydrogen sulfide inhalation: correlation with tissue sulfide concentrations in the rat brain, liver, lung, and nasal epithelium.

Hydrogen sulfide (H2S) is an important brain, lung, and nose toxicant. Inhibition of cytochrome oxidase is the primary biochemical effect associated with lethal H2S exposure. The objective of this study was to evaluate the relationship between the concentration of sulfide and cytochrome oxidase activity in target tissues following acute exposure to sublethal concentrations of inhaled H2S. Hindbrain, lung, liver, and nasal (olfactory and respiratory epithelial) cytochrome oxidase activity and sulfide concentrations were determined in adult male CD rats immediately after a 3-h exposure to H2S (10, 30, 80, 200, and 400 ppm). We also determined lung sulfide and sulfide metabolite concentrations at 0, 1.5, 3, 3.25, 3.5, 4, 5, and 7 h after the start of a 3-h H2S exposure to 400 ppm. Lung sulfide concentrations increased during H2S exposure and rapidly returned to endogenous levels within 15 min after the cessation of the 400-ppm exposure. Lung sulfide metabolite concentrations were transiently increased immediately after the end of the 3-h H2S exposure. Decreased cytochrome oxidase activity was observed in the olfactory epithelium following exposure to > or = 30 ppm H2S. Increased olfactory epithelial sulfide concentrations were observed following exposure to 400 ppm H2S. Hindbrain and nasal respiratory epithelial sulfide concentrations were unaffected by acute H2S exposure. Nasal respiratory epithelial cytochrome oxidase activity was reduced following acute exposure to > or = 30 ppm H2S. Liver sulfide concentrations were increased following exposure to > or = 200 ppm H2S and cytochrome oxidase activity was increased following inhalation exposure to > or = 10 ppm H2S. Our results suggest that cytochrome oxidase inhibition is a sensitive biomarker of H2S exposure in target tissues, and sulfide concentrations are unlikely to increase postexposure in the brain, lung, or nose following a single 3-h exposure to < or = 30 ppm H2S.

Animals↗
PubMed2000

Diurnal changes in pore water sulfide concentrations in the seagrass Thalassia testudinum beds: the effects of seagrasses on sulfide dynamics.

The dynamics of the seagrass-sulfide interaction were examined in relation to diel changes in sediment pore water sulfide concentrations in Thalassia testudinum beds and adjacent bare areas in Corpus Christi Bay and lower Laguna Madre, Texas, USA, during July 1996. Pore water sulfide concentrations in seagrass beds were significantly higher than in adjacent bare areas and showed strong diurnal variations; levels significantly decreased during mid-day at shallow sediment depths (0-10 cm) containing high below-ground tissue biomass and surface area. In contrast, diurnal variations in sediment sulfide concentrations were absent in adjacent bare patches, and at deeper (>10 cm) sediment depths characterized by low below-ground plant biomass or when the grasses were experimentally shaded. These observations suggest that the mid-day depressions in sulfide levels are linked to the transport of photosynthetically produced oxygen to seagrass below-ground tissues that fuels sediment sulfide oxidation. Lower sulfide concentrations in bare areas are likely a result of low sulfate reduction rates due to low organic matter available for remineralization. Further, high reoxidation rates due to rapid exchange between anoxic pore water and oxic overlying water are probably stimulated in bare areas by higher current velocity on the sediment surface than in seagrass beds. The dynamics of pore water sulfides in seagrass beds suggest no toxic sulfide intrusion into below-ground tissues during photosynthetic periods and demonstrate that the sediment chemical environment is considerably modified by seagrasses. The reduced sediment sulfide levels in seagrass beds during photosynthetic periods will enhance seagrass production through reduced sulfide toxicity to seagrasses and sediment microorganisms related to the nutrient cycling.

Journal Article↗
PubMed1997

Competition for Dimethyl Sulfide and Hydrogen Sulfide by Methylophaga sulfidovorans and Thiobacillus thioparus T5 in Continuous Cultures.

Pure and mixed cultures of Methylophaga sulfidovorans and Thiobacillus thioparus T5 were grown in continuous cultures on either dimethyl sulfide, dimethyl sulfide and H(inf2)S, or H(inf2)S and methanol. In pure cultures, M. sulfidovorans showed a lower affinity for sulfide than T. thioparus T5. Mixed cultures, grown on dimethyl sulfide, showed coexistence of both species. M. sulfidovorans fully converted dimethyl sulfide to thiosulfate, which was subsequently further oxidized to sulfate by T. thioparus T5. Mixed cultures supplied with sulfide and methanol showed that nearly all the sulfide was used by T. thioparus T5, as expected on the basis of the affinities for sulfide. The sulfide in mixed cultures supplied with dimethyl sulfide and H(inf2)S, however, was used by both bacteria. This result may be explained by the fact that the H(inf2)S-oxidizing capacity of M. sulfidovorans remains fully induced by intracellular H(inf2)S originating from dimethyl sulfide metabolism.

Journal Article↗
PubMed2005

Stabilization of sulfide and sulfite and ion-pair chromatography of mixtures of sulfide, sulfite, sulfate and thiosulfate.

Ion chromatography of sulfide, sulfite, sulfate and thiosulfate in a mixture is often difficult because of instability of sulfide and sulfite, poor separation of sulfide from common anions such as bromide or nitrate and similar elution-times for sulfite and sulfate. An ion-pair chromatographic method for the determination of these sulfur anions has been established by stoichiometric conversion of sulfide and sulfite into stable thiocyanate and sulfate, respectively, prior to the chromatographic run. Sulfate, thiosulfate and thiocyanate were resolved on an octadecylsilica column with an acetonitrile-water mobile phase containing tetrapropylammonium salt (TPA) as an ion-paring reagent, and thiosulfate and thiocyanate in the effluent could be measured with a photometric detector (220 nm) and sulfate with a suppressed conductivity detector. When an acetonitrile-water (6:94, v/v) mobile phase (pH 5.0) containing 15 mM TPA and small amounts of acetic acid was used at a flow-rate of 0.6 ml min(-1), the three anions could be eluted within 32 min. Calibration plots of peak height versus concentration for sulfide (detected as thiocyanate) and thiosulfate gave straight lines up to 35 and 60 microM, respectively. The calibration plot for sulfide coincided with that obtained by using thiocyanate. A calibration plot for sulfite, measured as sulfate, was also linear up to 135 microM and was in accord with that of sulfate. Each calibration plot gave a correlation coefficient greater than 0.999. For six replicates obtained for a mixture of 30.0 microM sulfide, 50.0 microM sulfite, 50.0 microM sulfate and 20.0 microM thiosulfate, the proposed method gave a mean value of 30.1 microM with a standard deviation (SD) of 0.77 microM and a relative standard deviation (RSD) of 2.6% for sulfide, 101 microM (SD = 3.5 microM, RSD = 3.5%) for the total of sulfite and sulfate and 20.1 microM (SD = 0.44 microM, RSD = 2.2%) for thiosulfate. Recoveries for sulfide, sulfite plus sulfate, and thiosulfate in hot-spring water samples using the proposed method were found to be quantitative.

Anions↗
PubMed1976

[Single and complex effect of ammonia and hydrogen sulfide in the air on small laboratory animals (rats) under various environmental conditions 2. Effect of hydrogen sulfide alone and hydrogen sulfide with ammonia and dust].

The maximum tolerable concentrations per animal position of hydrogen sulphide alone (5 ppm) and with ammonia (5 ppm H2S; 30 ppm NH3) were established by model experiments under defined environmental conditions. The normal values of the contaminant gas combination were found to be acceptable even with additional dust load on the experimental animals. TGL 29084 should stipulate 5 ppm hydrogen sulphide as the new maximum concentration per animal position.

Ammonia↗
PubMed2004

Spectrophotometric determination of sulfide in the presence of sulfite and thiosulfate via the precipitation of bismuth(III) sulfide.

A photometric method has been developed for the determination of sulfide at 10(-5) mol dm(-3) levels, which is based on the reaction of sulfide with a given excess amount of bismuth(III) to form a precipitate of bismuth(III) sulfide and on the spectrophotometric measurement of the residual bismuth(III) at 335 nm after extracting with bismuthiol II reagent from an aqueous solution containing acetate buffer into benzene. The presence of sulfite and thiosulfate up to 0.002 mol dm(-3) did not cause any interference in the determination of sulfide, because both sulfite and thiosulfate do not produce any precipitate with bismuth(III). A linear calibration plot with a negative slope was obtained for sulfide over the range of 5.00 x 10(-7) - 3.00 x 10(-5) mol dm(-3) (16.0 - 960 ppb). An experimental calibration plot was in accord with the theoretical plot, taking into account the known excess of bismuth(III), showing that the reaction of sulfide with bismuth(III) proceeded to completion. The relative standard deviation of results from 10 replicate determinations of standard sulfide (2.00 x 10(-5) mol dm(-3)) was 0.44%. The proposed method was successfully applied to the determination of sulfide in hotspring water samples without any pretreatment.

Journal Article↗
PubMed2004

Variation in sulfide tolerance of photosystem II in phylogenetically diverse cyanobacteria from sulfidic habitats.

Physiological and molecular phylogenetic approaches were used to investigate variation among 12 cyanobacterial strains in their tolerance of sulfide, an inhibitor of oxygenic photosynthesis. Cyanobacteria from sulfidic habitats were found to be phylogenetically diverse and exhibited an approximately 50-fold variation in photosystem II performance in the presence of sulfide. Whereas the degree of tolerance was positively correlated with sulfide levels in the environment, a strain's phenotype could not be predicted from the tolerance of its closest relatives. These observations suggest that sulfide tolerance is a dynamic trait primarily shaped by environmental variation. Despite differences in absolute tolerance, similarities among strains in the effects of sulfide on chlorophyll fluorescence induction indicated a common mode of toxicity. Based on similarities with treatments known to disrupt the oxygen-evolving complex, it was concluded that sulfide toxicity resulted from inhibition of the donor side of photosystem II.

Cyanobacteria↗
PubMed1999

Sulfide oxidation by gene expressions of sulfide-quinone oxidoreductase and ubiquinone-8 biosynthase in Escherichia coli.

Sulfides (S2),SH-) such as hydrogen sulfide belong to a class of sulfur compounds with unpleasant odors. In order to confer sulfide-oxidizing ability on the intestine-inhabiting bacteria, the sulfide-quinone oxidoreductase gene (sqr) in Rhodobacter capsulatus DSM-155 and genes for quinone biosynthesis (ubiC, ubiA and ispB) in Escherichia coli XL1 Blue-MRF' were transduced into E. coli BL21(DE3). Plasmids pT7-7 and pSTV were used as vectors of sqr, and ubiCA and ispB, respectively. The recombinants sqr-BL21(DE3) and ubiCA,ispB-sqr-BL21(DE3) were successfully constructed. The maximal sulfide-removing activities of the whole cells and membrane fractions of sqr-BL21(DE3) attained at pH 8.0 and 7.8, were 267 nmol/mg cells (dry weight)/min and 1250 nmol/mg membrane fraction (protein)/min, respectively. The molecular ratio of sulfide (S2-) oxidized and oxygen (O2) consumed was 2:1. SQR activity in the recombinant cells was positively restricted under anaerobic conditions and also by the addition of electron transfer inhibitors. Ubiquinone-8 (UQ-8) biosynthesis in the cells of ubiCA,ispB-sqr-BL21(DE3) increased as much as 2.2-fold compared with that of (pSTV)-sqr-BL21(DE3) during the 12-16 h incubation period. The maximal sulfide removal in the quinone-raised E. coli was attained slightly earlier, however, SQR activities thereafter were lower than those in (pSTV)-sqr-BL21(DE3).

Journal Article↗
PubMed1978

Pulmonary excretion of hydrogen sulfide, methanethiol, dimethyl sulfide and dimethyl disulfide in mice.

Neither hydrogen sulfide nor any other volatile sulfur metabolites were found in the expired breath of mice given sodium sulfide intraperitoneally in doses up to the LD50. The detection system was sensitive to less than 0.1% of the sulfur in the given dose. The intraperitoneal administration of dimethyl disulfide resulted in its appearance in the expired breath of mice as well as much smaller amounts of both methanethiol and dimethyl sulfide. The intraperitoneal administration of methanethiol resulted in its pulmonary excretion as well as that of dimethyl sulfide. Administration of dimethyl sulfide led to its appearance alone in expired breath. Mice pretreated with ammonium acetate and then injected with dimethyl disulfide excreted the same three compounds via the lungs as above, but there were complex changes in the proportions and in the time sequence of their appearance. The absolute amounts of all three were increased, and the peak excretion for each was delayed. The amount excreted as dimethyl sulfide was particularly increased.

Animals↗
PubMed1986

Metabolism of S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine to hydrogen sulfide and the role of hydrogen sulfide in S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine-induced mitochondrial toxicity.

The nephrotoxic cysteine S-conjugate S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine (CTFC) is metabolized by kidney homogenates and subcellular fractions to pyruvate and a reactive thiol, which is cytotoxic and partially decomposes to yield hydrogen sulfide and thiosulfate. Although hydrogen sulfide is a potent mitochondrial poison, the mitochondrial toxicity of CTFC is not attributable to hydrogen sulfide formation, as shown by different sites of inhibition of mitochondrial respiration by CTFC and hydrogen sulfide. The efficient mitochondrial oxidation of hydrogen sulfide apparently serves to protect mitochondria against the toxic effects of hydrogen sulfide generated from CTFC.

Animals↗