H2S

Hydrogen sulfide (H2S)

• Overproduced in the gut
• Can cause some pretty unpleasant symptoms.
• Irritable bowel syndrome (IBS),
• Inflammatory bowel disease (IBD),
• Colorectal cancer, and more.

• Breath testing and stool testing for hydrogen sulfide
• The four major sources of sulfur in the gut for hydrogen sulfide producers
• Evidence-based strategies for addressing hydrogen sulfide overgrowth

Lucy Mailing is a microbiome researcher, educator, and passionate scholar of integrative, evidence-based gut health

PhD in Nutritional Sciences from the University of Illinois

impact of diet and exercise on the gut microbiota

www.lucymailing.com

Authored numerous peer-reviewed journal articles, regularly presents at national and international conferences, and was named an Emerging Leader in Nutritional Sciences by the American Society for Nutrition in 2017

H2S

• Sulphurous thermal water inhalation has
• Mucolitic,
• Antioxidant
• Antielastase activity
• May help to control airway inflammation at the upper alveolar or lower bronchial level
• Benefit of thermal sulphurous water inhalation could be attributed to the presence of hydrogen sulphide (H2S)
• H2S produced at significant amounts (50?microM) in most tissues
• Exerts many physiological effects
• Role as a regulatory mediator
• Working hypothesis of antioxidant effect of thermal water was not confirmed

www.hindawi.com/journals/isrn/2012/534290/

H2S is closely related to respiratory activities and can affect the outcome of various respiratory diseases. For example, several studies have indicated that serum levels of H2S in patients with chronic obstructive pulmonary disease (COPD) are low. This event is correlated with reduced chronic inflammation of the airway and vascular remodeling. Such activity shows the curative effects on pulmonary hypertension and asthma [35,36,37,38]. H2S in the respiratory tract induces anti-apoptosis and anti-inflammatory effects and regulates vascular permeability. According to recent reports, patients with acute exacerbation of COPD have significantly low serum H2S, while serum levels of H2S in smokers are much lower than in non-smokers [39].Several pathways describe the damage of H2S in respiratory diseases. However, some mechanisms are still not fully clarified. H2S inhibits respiratory rhythm in neonates through the medulla [40]. H2S can reduce other substances and is oxidized via circulating oxidants. H2S, together with NO, CO and cyanide, are highly toxic, and micromolar concentrations can ultimately inhibit mitochondrial respiration [7]. H2S is found in combination with sulfate and sulfur species. The compounds have variable forms ranging from persulfide and polysulfide to elemental sulfur. The compounds are reactive [41]. A species of sulfane-sulfur acts as a store of H2S, which maintains toxicity and allows H2S to react with biological signals through sulfhydration [42,43]. Similarly, the sulfur compounds act through S-sulfhydration and are involved in most activities of H2S [44]. Altered biosynthesis of H2S is also linked with sulfate-sulfur levels based on pathophysiology, suggesting a close relationship.The defective production of H2S initiates several systemic disorders, and such a situation reveals the advance of effective pharmacological mediators that increase H2S levels. H2S modulation in pharmacy is a recent dynamic field that is well-reported and examined for specific significance [45,46,47]. Currently, a considerable number of natural and artificial compounds have been documented as potent H2S donors [48], and many of them are in clinical trials for the treatment of cardiovascular disease (SG-1002 for heart failure) [48] and cancer (sulforaphane) [49]. In this review, the production and metabolism of H2S in the lung are highlighted. Besides, the mechanisms and roles associated with the effects of H2S in respiratory diseases are further explored.
H2S forms from homocysteine and cysteine via CBS and CSE. 3-MSPT forms 3-MST-cysteine persulfide (MST-SSH) using mercapto pyruvate, which is formed from cysteine via CAT. H2S is formed from MST-SSH via a non-enzymatic reaction. H2S is oxidized via sulfide oxidation to form thiosulfate and sulfate. H2S is produced from thiosulfate through a non-enzymatic reaction through reductants via the catalytic activity of thiosulfate sulfurtransferase or 3-MST. H2S: hydrogen sulfide; SQR: sulfide-quinone reductase; CBS: cystathionine beta-synthase; CSE: cystathionine ?-lyase; 3-MPST: 3-mercaptopyravute sulfurtransferase; TST: thiosulfate sulfurtransferase; CAT: cysteine aminotransferase; GSSH: glutathione.