Gaseous mediator

Gaseous mediators are chemicals that are produced in small amounts by some cells of the mammalian body and have a number of biological signalling functions. There are three so-far-identified gaseous mediator molecules: nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO).[1]

## Clinical applications

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Endogenous gaseous mediators have shown anti-inflammatory and cytoprotective properties[2] Combination nonsteroidal anti-inflammatory drugs featuring both a cyclooxygenase inhibitor and gaseous mediator releasing component are being investigated as a safer alternative to current anti-inflammatory drugs[3] due to their potential reduction in risk for gastrointestinal ulcer formation.[4]

## Role of gaseous mediators during septic shock

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When septic shock occurs in the human body due to bacterial toxins, nitric oxide is released by a variety of cells through the expression of inducible nitric oxide synthase in order to induce vasodilation as part of the inflammatory response.[5] The released nitric oxide can be crucial to the body by reducing instances of platelet and leukocyte adhesion while also counteracting apoptosis.[6] However, prolonged septic shock could lead to the overproduction of nitric oxide, which could lead to cell damage due to nitric oxide radical formation and peroxynitrite (ONOO−) formation after interacting with oxygen in the body.[5] In order to alleviate the toxic effects caused by overproduction of nitric oxide during septic shock, a single high dose (5g IV) of Vitamin B12 has shown the potential to inhibit nitric oxide synthase while acting as a radical scavenger that assists in the elimination of excess nitric oxide produced during prolonged septic shock.[6]

## References

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1. ^ Leffler, C. W.; Parfenova, H; Jaggar, J. H.; Wang, R (March 2006). "Carbon monoxide and hydrogen sulfide: gaseous messengers in cerebrovascular circulation". J. Appl. Physiol. 100 (3): 1065–76\. doi:10.1152/japplphysiol.00793.2005. PMC 1363746. PMID 16467393.1065-76&rft.date=2006-03&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1363746#id-name=PMC&rft_id=info:pmid/16467393&rft_id=info:doi/10.1152/japplphysiol.00793.2005&rft.aulast=Leffler&rft.aufirst=C.+W.&rft.au=Parfenova,+H&rft.au=Jaggar,+J.+H.&rft.au=Wang,+R&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1363746&rfr_id=info:sid/en.wikipedia.org:Gaseous+mediator" class="Z3988">
2. ^ Rodrigues, L.; Ekundi-Valentim, E.; Florenzano, J.; Cerqueira, A. R. A.; Soares, A. G.; Schmidt, T. P.; Santos, K. T.; Teixeira, S. A.; Ribela, M. T. C. P.; Rodrigues, S. F.; de Carvalho, M. H. (2017-01-01). "Protective effects of exogenous and endogenous hydrogen sulfide in mast cell-mediated pruritus and cutaneous acute inflammation in mice". Pharmacological Research. 115: 255–266\. doi:10.1016/j.phrs.2016.11.006. hdl:10871/24576. ISSN 1043-6618. PMID 27840098. S2CID 1165855.255-266&rft.date=2017-01-01&rft_id=info:hdl/10871/24576&rft_id=https://api.semanticscholar.org/CorpusID:1165855#id-name=S2CID&rft_id=info:doi/10.1016/j.phrs.2016.11.006&rft.issn=1043-6618&rft_id=info:pmid/27840098&rft.aulast=Rodrigues&rft.aufirst=L.&rft.au=Ekundi-Valentim,+E.&rft.au=Florenzano,+J.&rft.au=Cerqueira,+A.+R.+A.&rft.au=Soares,+A.+G.&rft.au=Schmidt,+T.+P.&rft.au=Santos,+K.+T.&rft.au=Teixeira,+S.+A.&rft.au=Ribela,+M.+T.+C.+P.&rft.au=Rodrigues,+S.+F.&rft.au=de+Carvalho,+M.+H.&rft_id=http://www.sciencedirect.com/science/article/pii/S1043661816305291&rfr_id=info:sid/en.wikipedia.org:Gaseous+mediator" class="Z3988">
3. ^ Sulaieva, Oksana; Wallace, John L (2015-12-01). "Gaseous mediator-based anti-inflammatory drugs". Current Opinion in Pharmacology. Gastrointestinal • Endocrine and metabolic diseases. 25: 1–6\. doi:10.1016/j.coph.2015.08.005. ISSN 1471-4892. PMID 26319186.1-6&rft.date=2015-12-01&rft.issn=1471-4892&rft_id=info:pmid/26319186&rft_id=info:doi/10.1016/j.coph.2015.08.005&rft.aulast=Sulaieva&rft.aufirst=Oksana&rft.au=Wallace,+John+L&rft_id=http://www.sciencedirect.com/science/article/pii/S1471489215000983&rfr_id=info:sid/en.wikipedia.org:Gaseous+mediator" class="Z3988">
4. ^ Sulaieva, O. N.; Wallace, J. L. (2016). "New strategy for gastrointestinal protection based on gaseous mediators application". Russian Journal of Gastroenterology, Hepatology, Coloproctology. 26 (3): 17–23\. doi:10.22416/1382-4376-2016-26-3-17-23. Retrieved 2020-04-27.17-23&rft.date=2016&rft_id=info:doi/10.22416/1382-4376-2016-26-3-17-23&rft.aulast=Sulaieva&rft.aufirst=O.+N.&rft.au=Wallace,+J.+L.&rft_id=https://www.gastro-j.ru/jour/article/view/56&rfr_id=info:sid/en.wikipedia.org:Gaseous+mediator" class="Z3988">
5. ^ a b Hermann, Anton; Sitdikova, Guzel F.; Weiger, Thomas M., eds. (2012). Gasotransmitters: Physiology and Pathophysiology. Berlin, Heidelberg: Springer Berlin Heidelberg. pp. 18–19\. doi:10.1007/978-3-642-30338-8. ISBN 978-3-642-30337-1.18-19&rft.pub=Springer+Berlin+Heidelberg&rft.date=2012&rft_id=info:doi/10.1007/978-3-642-30338-8&rft.isbn=978-3-642-30337-1&rft_id=https://link.springer.com/10.1007/978-3-642-30338-8&rfr_id=info:sid/en.wikipedia.org:Gaseous+mediator" class="Z3988">
6. ^ a b Diaz Soto, Juan C.; Nabzdyk, Christoph G.S. (2023). "Running on (Too Many) Fumes? Gaseous Mediators in Septic Shock". Chest Journal. 163 (2): 262–263\. doi:10.1016/j.chest.2022.10.012. PMID 36759109.262-263&rft.date=2023&rft_id=info:doi/10.1016/j.chest.2022.10.012&rft_id=info:pmid/36759109&rft.aulast=Diaz+Soto&rft.aufirst=Juan+C.&rft.au=Nabzdyk,+Christoph+G.S.&rft_id=https://linkinghub.elsevier.com/retrieve/pii/S0012369222040028&rfr_id=info:sid/en.wikipedia.org:Gaseous+mediator" class="Z3988">