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| hydrogen sulfide |
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| CHEBI:16136 |
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| A sulfur hydride consisting of a single sulfur atom bonded to two hydrogen atoms. A highly poisonous, flammable gas with a characteristic odour of rotten eggs, it is often produced by bacterial decomposition of organic matter in the absence of oxygen. |
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This entity has been manually annotated by the ChEBI Team.
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CHEBI:14414, CHEBI:45489, CHEBI:43058, CHEBI:5787, CHEBI:13356, CHEBI:24639
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| ChemicalBook:CB5853720, ChemicalBook:CB82551184, eMolecules:532436, Selleckchem:l-thyroxine, ZINC000003830993 |
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SDF
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more structures >>
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| Hydrogen sulfide is a chemical compound with the formula H2S. It is a colorless chalcogen-hydride gas, and is toxic, corrosive, and flammable, with trace amounts in ambient atmosphere having a characteristic foul odor of rotten eggs. Swedish chemist Carl Wilhelm Scheele is credited with having discovered the chemical composition of purified hydrogen sulfide in 1777.
Hydrogen sulfide is toxic to humans and most other animals by inhibiting cellular respiration in a manner similar to hydrogen cyanide. When it is inhaled or its salts are ingested in high amounts, damage to organs occurs rapidly with symptoms ranging from breathing difficulties to convulsions and death. Despite this, the human body produces small amounts of this sulfide and its mineral salts, and uses it as a signalling molecule.
Hydrogen sulfide is often produced from the microbial breakdown of organic matter in the absence of oxygen, such as in swamps and sewers; this process is commonly known as anaerobic digestion, which is done by sulfate-reducing microorganisms. It also occurs in volcanic gases, natural gas deposits, and sometimes in well-drawn water. |
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Read full article at Wikipedia
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| RWSOTUBLDIXVET-UHFFFAOYSA-N |
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Escherichia coli
(NCBI:txid562)
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See:
PubMed
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Bronsted acid
A molecular entity capable of donating a hydron to an acceptor (Bronsted base).
(via hydracid )
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Escherichia coli metabolite
Any bacterial metabolite produced during a metabolic reaction in Escherichia coli.
signalling molecule
A molecular messenger in which the molecule is specifically involved in transmitting information between cells. Such molecules are released from the cell sending the signal, cross over the gap between cells by diffusion, and interact with specific receptors in another cell, triggering a response in that cell by activating a series of enzyme controlled reactions which lead to changes inside the cell.
toxin
Poisonous substance produced by a biological organism such as a microbe, animal or plant.
metabolite
Any intermediate or product resulting from metabolism. The term 'metabolite' subsumes the classes commonly known as primary and secondary metabolites.
genotoxin
A role played by a chemical compound to induce direct or indirect DNA damage. Such damage can potentially lead to the formation of a malignant tumour, but DNA damage does not lead inevitably to the creation of cancerous cells.
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vasodilator agent
A drug used to cause dilation of the blood vessels.
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View more via ChEBI Ontology
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dihydridosulfur
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dihydrogen(sulfide)
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hydrogen sulfide
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sulfane
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[SH2]
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MolBase
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acide sulfhydrique
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ChemIDplus
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dihydrogen monosulfide
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NIST Chemistry WebBook
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dihydrogen sulfide
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NIST Chemistry WebBook
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H2S
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KEGG COMPOUND
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H2S
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IUPAC
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hydrogen monosulfide
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NIST Chemistry WebBook
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Hydrogen sulfide
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KEGG COMPOUND
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hydrogen sulphide
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ChemIDplus
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Hydrogen-sulfide
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KEGG COMPOUND
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hydrogène sulfuré
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ChemIDplus
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HYDROSULFURIC ACID
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PDBeChem
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Schwefelwasserstoff
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ChemIDplus
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Sulfide
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KEGG COMPOUND
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sulfure d'hydrogène
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ChEBI
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1709
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MolBase
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4260
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DrugCentral
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C00007266
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KNApSAcK
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C00283
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KEGG COMPOUND
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c0239
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UM-BBD
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H2S
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PDBeChem
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Hydrogen_sulfide
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Wikipedia
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| View more database links |
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303
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Gmelin Registry Number
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Gmelin
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3535004
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Beilstein Registry Number
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Beilstein
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7783-06-4
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CAS Registry Number
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ChemIDplus
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7783-06-4
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CAS Registry Number
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NIST Chemistry WebBook
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Montoya LA, Pluth MD (2012)
Selective turn-on fluorescent probes for imaging hydrogen sulfide in living cells.
Chemical communications (Cambridge, England) 48, 4767-4769 [PubMed:22473176]
[show Abstract]
Hydrogen sulfide (H(2)S) is an important biological messenger but few biologically-compatible methods are available for its detection. Here we report two bright fluorescent probes that are selective for H(2)S over cysteine, glutathione and other reactive sulfur, nitrogen, and oxygen species. Both probes are demonstrated to detect H(2)S in live cells. | Wang C, Pei Y (2012)
The removal of hydrogen sulfide in solution by ferric and alum water treatment residuals.
Chemosphere 88, 1178-1183 [PubMed:22520971]
[show Abstract]
This work investigated the characteristics and mechanisms of hydrogen sulfide adsorption by ferric and alum water treatment residuals (FARs) in solution. The results indicated that FARs had a high hydrogen sulfide adsorption capacity. pH 7 rather than higher pH (e.g. pH 8-10) was favorable for hydrogen sulfide removal. The Yan model fitted the breakthrough curves better than the Thomas model under varied pH values and concentrations. The Brunauer-Emmett-Teller surface area and the total pore volume of the FARs decreased after the adsorption of hydrogen sulfide. In particular, the volume of pores with a radius of 3-5 nm decreased, while the volume of pores with a radius of 2 nm increased. Therefore, it was inferred that new adsorption sites were generated during the adsorption process. The pH of the FARs increased greatly after adsorption. Moreover, differential scanning calorimetry analysis indicated that elemental sulfur was present in the FARs, while the derivative thermal gravimetry curves indicated the presence of sulfuric acid and sulfurous acid. These results indicated that both oxidization and ligand exchange contribute to the removal of hydrogen sulfide by FARs. Under anaerobic conditions, the maximum amount of hydrogen sulfide released was approximately 0.026 mg g(-1), which was less than 0.19% of the total amount adsorbed by the FARs. The hydrogen sulfide that was released may be re-adsorbed by the FARs and transformed into more stable mineral forms. Therefore, FARs are an excellent adsorbent for hydrogen sulfide. | Allan PK, Wheatley PS, Aldous D, Mohideen MI, Tang C, Hriljac JA, Megson IL, Chapman KW, De Weireld G, Vaesen S, Morris RE (2012)
Metal-organic frameworks for the storage and delivery of biologically active hydrogen sulfide.
Dalton transactions (Cambridge, England : 2003) 41, 4060-4066 [PubMed:22378060]
[show Abstract]
Hydrogen sulfide is an extremely toxic gas that is also of great interest for biological applications when delivered in the correct amount and at the desired rate. Here we show that the highly porous metal-organic frameworks with the CPO-27 structure can bind the hydrogen sulfide relatively strongly, allowing the storage of the gas for at least several months. Delivered gas is biologically active in preliminary vasodilation studies of porcine arteries, and the structure of the hydrogen sulfide molecules inside the framework has been elucidated using a combination of powder X-ray diffraction and pair distribution function analysis. | Rivers JR, Badiei A, Bhatia M (2012)
Hydrogen sulfide as a therapeutic target for inflammation.
Expert opinion on therapeutic targets 16, 439-449 [PubMed:22448627]
[show Abstract]
IntroductionThe view of hydrogen sulfide has changed from a toxic by-product to a crucial signaling molecule, with enormous potential as a pharmacological target for diseases ranging from heart disease to sepsis. Despite this progression of ideas, there is still a large amount that is unknown about this gaseous signaling molecule. Hydrogen sulfide has been implicated as a tissue protectant in many pathological conditions, the mechanisms of tissue protection is a point of controversy, particularly distinguishing the direct actions from the indirect downstream effects of hydrogen sulfide. This point of controversy is particularly pertinent in inflammation research.Areas coveredCurrent research into the pathways in which hydrogen sulfide can act as a pro-inflammatory molecule and as an anti-inflammatory molecule.Expert opinionHow controversies regarding hydrogen sulfide may have occurred is discussed. Addressed are the direct and indirect pathways of hydrogen sulfide on inflammation, the effects of different concentrations of hydrogen sulfide and how the effects of hydrogen sulfide on the immune system vary with different delivery mechanisms. Furthermore, there is a discussion on what key gaps exist in current knowledge and must be addressed before hydrogen sulfide can be considered a valid pharmacological target. | Liu C, Peng B, Li S, Park CM, Whorton AR, Xian M (2012)
Reaction based fluorescent probes for hydrogen sulfide.
Organic letters 14, 2184-2187 [PubMed:22486842]
[show Abstract]
A reaction based fluorescence turn-on strategy for hydrogen sulfide (H(2)S) was developed. This strategy was based on a H(2)S-specific Michael addition-cyclization sequence. Other biological thiols such as cysteine and glutathione did not pursue the reaction and therefore did not turn on the fluorescence/consume the substrates. The probes showed good selectivity and sensitivity for hydrogen sulfide. | Asif MJ, Exline MC (2012)
Utilization of hyperbaric oxygen therapy and induced hypothermia after hydrogen sulfide exposure.
Respiratory care 57, 307-310 [PubMed:22004989]
[show Abstract]
Hydrogen sulfide is a toxic gas produced as a by-product of organic waste and many industrial processes. Hydrogen sulfide exposure symptoms may vary from mild (dizziness, headaches, nausea) to severe lactic acidosis via its inhibition of oxidative phosphorylation, leading to cardiac arrhythmias and death. Treatment is generally supportive. We report the case of a patient presenting with cardiac arrest secondary to hydrogen sulfide exposure treated with both hyperbaric oxygen therapy and therapeutic hypothermia to achieve full neurologic recovery. | Dufton N, Natividad J, Verdu EF, Wallace JL (2012)
Hydrogen sulfide and resolution of acute inflammation: A comparative study utilizing a novel fluorescent probe.
Scientific reports 2, 499 [PubMed:22787557]
[show Abstract]
Hydrogen sulfide is an essential gasotransmitter associated with numerous pathologies. We assert that hydrogen sulfide plays an important role in regulating macrophage function in response to subsequent inflammatory stimuli, promoting clearance of leukocyte infiltrate and reducing TNF-α levels in vivo following zymosan-challenge. We describe two distinct methods of measuring leukocyte hydrogen sulfide synthesis; methylene blue formation following zinc acetate capture and a novel fluorescent sulfidefluor probe. Comparison of these methods, using pharmacological tools, revealed they were complimentary in vitro and in vivo. We demonstrate the application of sulfidefluor probe to spectrofluorimetry, flow cytometry and whole animal imaging, to monitor the regulation of hydrogen sulfide synthesis in vivo during dynamic inflammatory processes. Both methodologies revealed that granulocyte infiltration negatively affects hydrogen sulfide synthesis. Our report offers an insight into the profile of hydrogen sulfide synthesis during inflammation and highlight opportunities raised by the development of novel fluorescent hydrogen sulfide probes. | Samhan-Arias AK, Garcia-Bereguiain MA, Gutierrez-Merino C (2009)
Hydrogen sulfide is a reversible inhibitor of the NADH oxidase activity of synaptic plasma membranes.
Biochemical and biophysical research communications 388, 718-722 [PubMed:19695225]
[show Abstract]
Hydrogen sulfide is now accepted as a neuromodulator, which can be involved in neuronal defence against oxidative stress insults in the brain. In this work we show that concentrations of H(2)S within the physiological range reported in the brain produce a reversible inhibition of the NADH oxidase activity and coupled superoxide anion production by synaptic plasma membranes from rat brain. At physiological pH 7 the concentration of H(2)S needed for 50% inhibition of the NADH oxidase activity is 5+/-1 microM, which is within the low range of the reported physiological H(2)S concentrations. Thus, the NADH oxidase activity of the neuronal plasma membrane can act as a sensor of local H(2)S depletion in neurones. H(2)S inhibition of the NADH oxidase activity of the neuronal plasma membrane can be accounted for direct reduction by H(2)S of cytochrome b(5). However, H(2)S fails to afford a significant protection against the inhibition of this activity by peroxynitrite. In conclusion, our results point out that H(2)S is more potent as inhibitor of reactive oxygen species formation than as a sacrificial antioxidant. | Sun YG, Cao YX, Wang WW, Ma SF, Yao T, Zhu YC (2008)
Hydrogen sulphide is an inhibitor of L-type calcium channels and mechanical contraction in rat cardiomyocytes.
Cardiovascular research 79, 632-641 [PubMed:18524810]
[show Abstract]
AimsHydrogen sulphide (H(2)S) is an endogenously generated gaseous transmitter that has recently been suggested to regulate cardiovascular functions. To date, there is no direct evidence for a potential role of H(2)S in regulating calcium channels in the heart. The present study aims to examine the hypothesis that H(2)S is a novel inhibitor of the L-type calcium channel current (I(Ca,L)).Methods and resultsElectrophysiological measurements were performed in cardiomyocytes isolated from Wistar-Kyoto and spontaneously hypertensive rats. Bath application of 100 microM NaHS (a H(2)S donor) significantly reduced the time required for the repolarization of the action potential. Inhibition of the peak I(Ca,L) by NaHS was determined to be concentration-dependent (25, 50, 100, 200, and 400 microM). NaHS inhibited the recovery from depolarization-induced inactivation. Electric field-induced [Ca(2+)]i transients and contraction of single cardiomyocytes and isolated papillary muscles were reduced by NaHS treatment. In contrast, caffeine induced an increase in [Ca(2+)]i that was not altered by NaHS. NaHS had no effect on the K(ATP) current or on the levels of cAMP and cGMP in the current study.ConclusionH(2)S is a novel inhibitor of L-type calcium channels in cardiomyocytes. Moreover, H(2)S-induced inhibition of [Ca(2+)]i appears to be a secondary effect owing to its initial action towards I(Ca,L). The inhibitory effect of H(2)S on I(Ca,L) requires further investigation, particularly in the exploration of new pathways involved in cardiac calcium homeostasis and disease pathology. | Distrutti E, Mencarelli A, Santucci L, Renga B, Orlandi S, Donini A, Shah V, Fiorucci S (2008)
The methionine connection: homocysteine and hydrogen sulfide exert opposite effects on hepatic microcirculation in rats.
Hepatology (Baltimore, Md.) 47, 659-667 [PubMed:18098324]
[show Abstract]
UnlabelledIncreased intrahepatic resistance in cirrhotic livers is caused by endothelial dysfunction and impaired formation of two gaseous vasodilators, nitric oxide (NO) and hydrogen sulfide (H(2)S). Homocysteine, a sulfur-containing amino acid and H(2)S precursor, is formed from hepatic methionine metabolism. In the systemic circulation, hyperhomocystenemia impairs vasodilation and NO production from endothelial cells. Increased blood levels of homocysteine are common in patients with liver cirrhosis. In this study, we demonstrate that acute liver perfusion with homocysteine impairs NO formation and intrahepatic vascular relaxation induced by acetylcholine in methoxamine-precontracted normal livers (7.3% +/- 3.0% versus 26% +/- 2.7%; P < 0.0001). In rats with mild, diet-induced hyperhomocystenemia, the vasodilating activity of acetylcholine was markedly attenuated, and incremental increases in flow induced a greater percentage of increases in perfusion pressure than in control livers. Compared with normal rats, animals rendered cirrhotic by 12 weeks' administration of carbon tetrachloride exhibited a greater percentage of increments in perfusion pressure in response to shear stress (P < 0.05), and intrahepatic resistance to incremental increases in flow was further enhanced by homocysteine (P < 0.05). In normal hyperhomocysteinemic and cirrhotic rat livers, endothelial dysfunction caused by homocysteine was reversed by perfusion of the livers with sodium sulfide. Homocysteine reduced NO release from sinusoidal endothelial cells and also caused hepatic stellate cell contraction; this suggests a dual mechanism of action, with the latter effect being counteracted by H(2)S.ConclusionImpaired vasodilation and hepatic stellate cell contraction caused by homocysteine contribute to the dynamic component of portal hypertension. | Yang G, Wu L, Jiang B, Yang W, Qi J, Cao K, Meng Q, Mustafa AK, Mu W, Zhang S, Snyder SH, Wang R (2008)
H2S as a physiologic vasorelaxant: hypertension in mice with deletion of cystathionine gamma-lyase.
Science (New York, N.Y.) 322, 587-590 [PubMed:18948540]
[show Abstract]
Studies of nitric oxide over the past two decades have highlighted the fundamental importance of gaseous signaling molecules in biology and medicine. The physiological role of other gases such as carbon monoxide and hydrogen sulfide (H2S) is now receiving increasing attention. Here we show that H2S is physiologically generated by cystathionine gamma-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H2S levels in the serum, heart, aorta, and other tissues. Mutant mice lacking CSE display pronounced hypertension and diminished endothelium-dependent vasorelaxation. CSE is physiologically activated by calcium-calmodulin, which is a mechanism for H2S formation in response to vascular activation. These findings provide direct evidence that H2S is a physiologic vasodilator and regulator of blood pressure. | Attene-Ramos MS, Wagner ED, Plewa MJ, Gaskins HR (2006)
Evidence that hydrogen sulfide is a genotoxic agent.
Molecular cancer research : MCR 4, 9-14 [PubMed:16446402]
[show Abstract]
Hydrogen sulfide (H2S) produced by commensal sulfate-reducing bacteria, which are often members of normal colonic microbiota, represents an environmental insult to the intestinal epithelium potentially contributing to chronic intestinal disorders that are dependent on gene-environment interactions. For example, epidemiologic studies reveal either persistent sulfate-reducing bacteria colonization or H2S in the gut or feces of patients suffering from ulcerative colitis and colorectal cancer. However, a mechanistic model that explains the connection between H2S and ulcerative colitis or colorectal cancer development has not been completely formulated. In this study, we examined the chronic cytotoxicity of sulfide using a microplate assay and genotoxicity using the single-cell gel electrophoresis (SCGE; comet assay) in Chinese hamster ovary (CHO) and HT29-Cl.16E cells. Sulfide showed chronic cytotoxicity in CHO cells with a %C1/2 of 368.57 micromol/L. Sulfide was not genotoxic in the standard SCGE assay. However, in a modified SCGE assay in which DNA repair was inhibited, a marked genotoxic effect was observed. A sulfide concentration as low as 250 micromol/L (similar to that found in human colon) caused significant genomic DNA damage. The HT29-Cl.16E colonocyte cell line also exhibited increased genomic DNA damage as a function of Na2S concentration when DNA repair was inhibited, although these cells were less sensitive to sulfide than CHO cells. These data indicate that given a predisposing genetic background that compromises DNA repair, H2S may lead to genomic instability or the cumulative mutations found in adenomatous polyps leading to colorectal cancer. | Whiteman M, Cheung NS, Zhu YZ, Chu SH, Siau JL, Wong BS, Armstrong JS, Moore PK (2005)
Hydrogen sulphide: a novel inhibitor of hypochlorous acid-mediated oxidative damage in the brain?
Biochemical and biophysical research communications 326, 794-798 [PubMed:15607739]
[show Abstract]
Hydrogen sulphide (H(2)S) is a cytotoxic gas that has recently been proposed as a novel neuromodulator. Endogenous levels of H(2)S in the brain range between 50 and 160 microM, and considerably lower H(2)S levels are reported in the brains of Alzheimer's disease (AD) patients. Levels of myeloperoxidase (MPO), an enzyme that catalyses the formation of the oxidant hypochlorous acid (HOCl), are elevated in the prefrontal cortex, hippocampal microglia, and neurons of AD patients where MPO co-localised with beta-amyloid plaques. Recently 3-chlorotyrosine, a bio-marker for MPO activity (and HOCl production), was shown to be elevated threefold in hippocampal proteins from AD patients. Since H(2)S and HOCl are important mediators in brain function and disease, we investigated the effects of H(2)S on HOCl-mediated damage to bio-molecules and to cultured human SH-SY5Y cells. H(2)S significantly inhibited HOCl-mediated inactivation of alpha(1)-antiproteinase and protein oxidation to a comparable extent to reduced glutathione. H(2)S also inhibited HOCl-induced cytotoxicity, intracellular protein oxidation, and lipid peroxidation in SH-SY5Y cells. These data suggest that H(2)S has the potential to act as an inhibitor of HOCl-mediated processes in vivo and that the potential antioxidant action of H(2)S deserves further study, especially since extracellular GSH levels in the brain are very low. | Dombkowski RA, Russell MJ, Olson KR (2004)
Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout.
American journal of physiology. Regulatory, integrative and comparative physiology 286, R678-85 [PubMed:15003943]
[show Abstract]
Hydrogen sulfide (H(2)S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H(2)S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H(2)S concentration was measured colorimetrically (CM) and with ion-selective electrodes (ISE) in rainbow trout plasma. NaHS produced a triphasic response consisting of a relaxation (phase 1), constriction (phase 2), and relaxation (phase 3) in both unstimulated vessels and in stEBA precontracted with carbachol (Carb). Phase 1 and phase 3 in stEBA were decreased and phase 2 increased in unstimulated vessels by K(+)(ATP) channel inhibition (glibenclamide), or a cocktail of inhibitors of cyclooxygenase, lipoxygenase, and cytochrome P-450 (indomethacin, esculetin, and clotrimazole). Inhibition of soluble guanylate cyclase with ODQ o NS-2028 inhibited phase 3 in stEBA, although NaHS decreased cGMP production by tEBA. stEBA phase 2 contractions were partially inhibited by the myosin light chain kinase inhibitor, ML-9, but unaffected by L-type calcium channel inhibition (methoxyverapamil), whereas contraction in tEBA was partially inhibited by nifedipine or removal of extracellular calcium. Phase 3 relaxations were more pronounced in stEBA precontracted with Carb and no epinephrine (NE) than those cont acted by KCl or K(2)SO(4). stEBA phase 2 and phase 3 responses were dose dependent (EC(50) = 1.1 +/- 1.2 x 10(-3) M and 6.7 +/- 0.9 x 10(-5) M, respectively; n = 7). NaHS was also vasoactive in steelhead bulbus arteriosus, celiac mesenteric arteries, and anterior cardinal veins. Rainbow trout plasma sulfide concentration was 4.0 +/- 0.3 x 10(-5) M, n = 4 (CM) and 3.8 +/- 0.4 x 10(-5) M, n = 9 (ISE); similar to phase 3 EC(50). Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H(2)S, is a tonically active endogenous vasoregulator in trout. | Moore PK, Bhatia M, Moochhala S (2003)
Hydrogen sulfide: from the smell of the past to the mediator of the future?
Trends in pharmacological sciences 24, 609-611 [PubMed:14654297]
[show Abstract]
Gases such as nitric oxide and carbon monoxide play important roles both in normal physiology and in disease. In recent years, interest has been directed towards other naturally occurring gases, notably hydrogen sulfide (H(2)S), which is both a potent vasodilator and a mediator of long-term potentiation in the brain. This article focuses on recent work that suggests a role for H(2)S, and perhaps other gases, in the CNS and cardiovascular system. | Picton R, Eggo MC, Merrill GA, Langman MJ, Singh S (2002)
Mucosal protection against sulphide: importance of the enzyme rhodanese.
Gut 50, 201-205 [PubMed:11788560]
[show Abstract]
BackgroundHydrogen sulphide (H(2)S) is a potent toxin normally present in the colonic lumen which may play a role in ulcerative colitis (UC). Two enzymes, thiol methyltransferase (TMT) and rhodanese (RHOD), are thought to be responsible for sulphide removal but supportive evidence is lacking.AimsTo determine the distribution of TMT and RHOD in different sites throughout the gastrointestinal tract and their efficacy as detoxifiers of H(2)S.MethodsEnzyme activities were measured in normal tissue resected from patients with cancer. TMT and RHOD activities were determined using their conventional substrates, 2-mercaptoethanol and sodium thiosulphate, respectively. For measurement of H(2)S metabolism, sodium sulphide was used in the absence of dithiothreitol. Thiopurine methyltransferase (TPMT), which in common with TMT methylates sulphydryl groups but is not thought to act on H(2)S, was also examined.ResultsTMT, RHOD, and TPMT activities using their conventional substrates were found throughout the gastrointestinal tract with highest activity in the colonic mucosa. When H(2)S was given as substrate, no reaction product was found with TMT or TPMT but RHOD was extremely active (Km 8.8 mM, Vmax 14.6 nmol/mg/min). Incubation of colonic homogenates with a specific RHOD antibody prevented the metabolism of H(2)S, indicating that RHOD is responsible for detoxifying H(2)S. A purified preparation of RHOD also detoxified H(2)S.ConclusionsRHOD, located in the submucosa and crypts of the colon, is the principal enzyme involved in H(2)S detoxication. TMT does not participate in the detoxication of H(2)S. |
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2005-12-13
