Hydrogen sulfide {90000132}

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Parent:[  ]
Definition:
Hydrogen sulfide
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Details


Initialisation date:[  ]
Specification:

H2S

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Structural Type:[  ]
Functional Type:[  ]
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Shared Reference Notes


  • [1.1
    - In the cardiovascular system, H2S plays important roles in the regulation of blood pressure, angiogenesis, smooth muscle cell proliferation and apoptosis, anti-oxidative stress, cardiac functions.
  • [1.2] [#Alzheimer’s disease
    - H2S > important signaling molecule in organisms > improve the progression of AD by enhancing Nrf2 > reduce the production of Aβ by inhibiting β secretase 1 (BACE1) > and protect neurons by maintaining mitochondrial function
  • [#Colorectal cancer, #Thyroid carcinoma] - H2S at a safe and nontoxic concentration can protect not only healthy cells, such as neurons, but also cancerous cells from apoptosis. - In a variety of cancers, including #Ovarian cancer, #Oral cancer, thyroid cancer, colon cancer, #Breast cancer, etc., the upregulation of H2S-producing enzyme CBS > can enhance the proliferation ability of cancer cells and make cancer cells more sensitive to it
  • [1.3] [#Colorectal cancer
    - H2S increased the in vitro proliferation of human cells obtained from mucosal biopsies. - Interestingly, this effect was inhibited by #Butyrate.
  • [#Colorectal cancer] - #Fusobacterium nucleatum, a Gram negative, anaerobic bacterium over-represented in CRC tissues, is a H2S-producer. - F. nucleatum also produces the metabolite #Formate, which triggers AhR and increases cancer cell stemness and invasiveness.
  • [#Colorectal cancer] - Fecal H2S concentrations are elevated in CRC patients. - Increased levels of H2S can decrease tissue integrity by reducing disulfide bonds in mucosal tissues. - H2S can also directly cause DNA damage.
  • [1.4] [#Alpha-synuclein
    - gut inflammation reduces the capacity of H2S inactivation system, which allows #Desulfovibrio -produced H2S to accumulate and enhance alpha-syn aggregation.
  • [#Parkinson’s Disease] [#Alpha-synuclein] - H2S has been reported to facilitate the release of cytochrome c from mitochondria to the cytoplasm in human cells. - cytochrome c potentially triggers alpha-syn aggregation in the presence of reactive oxygen species
  • [#Parkinson’s Disease] - increased amounts of H2S producing bacteria such as #Desulfovibrio bacteria play a role in the pathogenesis of PD
  • [1.5] [#Parkinson’s Disease
    - hydrogen sulfide produced by several #Enterobacteriaceae and #Desulfovibrionaceae can enter host cells, cause the release of cytochrome c protein from mitochondria into the cytoplasm, mediate the accumulation of cytosolic iron and #Reactive Oxygen Species, thus boosting α-synuclein synthesis
  • [1.6] [#Alpha-synuclein
    - #Desulfovibrio is a hydrogen sulfide (H2S) and #Lipopolysaccharide (LPS)-producing bacteria. - LPS-treated mice would present intestinal hyperpermeability and a higher level of pathological α-syn accumulation
  • [#Parkinson’s Disease] [#Alpha-synuclein] - The production of H2S also had a potential of inducing α-syn oligomerization, an initial step of α-synucleinopathy, and inhibiting gastrointestinal motility.
  • [1.7
    - Some oral #Bacteria (e.g., #Porphyromonas gingivalis, #Prevotella intermedia, #Aggregatibacter actinomycetemcomitans, and #Fusobacterium nucleatum) produce volatile #Sulfur compounds (VSCs), such as hydrogen #Sulfide (H2S), methyl mercaptan (CH3SH), dimethyl #Sulfide ((CH3)2S), and dimethyl disulfide (CH3SSCH3).
  • [1.8] [#Treponema medium
    - Complete utilization of #Taurine as electron acceptor in modified #Desulfovibrio liquid medium with electron donors #Lactate and #Pyruvate in excess resulted in production of nearly quantitative amounts of H2S and excess #Acetate
  • - Hydrogen sulfide may suppress the #Oxygen-dependent metabolism of some pathogens - #Taurinivorans muris has a protective role against #Klebsiella and #Salmonella, two important gut pathogens.
  • - #Taurinivorans muris feeds exclusively on #Taurine > Hydrogen sulfide
  • [1.9
    - H2S can inhibit mitochondrial cytochrome C oxidase, decrease #Butyrate oxidation, and act on disulfide bonds in mucin to facilitate mucin degradation
  • - Hydrogen sulfide (H2S) and methanethiol are produced during the decomposition of #Sulfur-containing amino acids, and have been linked to the progression of #Chronic kidney disease (CKD), cardiovascular disease, and bone metabolic disorders
  • - #Butyrate is a major energy source in colonocytes, and H2S is known to inhibit beta-oxidation of #Butyrate
  • - increased #Sulfate-reducing bacteria, thereby increasing bacterially derived H2S levels, increased Th17- and T regulatory-cell-type cytokine production and activation profiles in mesenteric lymph nodes in experimental #Colitis
  • [#Crohn’s disease, #Inflamatory bowel disease] - pathological relevance between mitochondrial H2S detoxification and IBD was reported: impaired H2S detoxification pathways were observed in colon biopsy samples obtained from CD patients.
  • [#Crohn’s disease] - the relative abundance of H2S-producing bacteria was increased in stool samples from CD patients
  • [1.11] [#Crohn’s disease, #Inflamatory bowel disease
    - microbiome of IBD patients is particularly deficient in secreting metabolites containing sulfur - H2S consumer species are disproportionately lost in CD.
  • [#Crohn’s disease] - CD patients lack microbial community members to support a healthy H2S balance. - This gas is expected to have a protective effect in the gut when present in small amounts, but it disrupts the mucus layer and may cause inflammation when present in larger quantities
  • [1.12
    - In #Cancer patients, endogenous synthesis of #Methanethiol may substantially increase due to elevated levels of metabolites, such as #Methionine (Met), #Glucose (Glc), H2S, and SAM, in tumor cells.
  • [1.13] [#Colitis
    - #Desulfovibrio are #Sulfate-reducing bacteria have the ability to reduce #Sulfate to hydrogen sulfide, which, when accumulated, can lead to damage to the intestinal epithelium, causing chronic inflammation and disrupting the balance between cellular proliferation and apoptosis

References Notes


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Common References


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