nitric oxide (NO, endothelium derived relaxation factor {EDRF})
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Function
- a colorless gas & a free radical
- nitric oxide reacts rapidly with oxygen to form nitrogen oxides, which ultimately convert to nitrite (NO2-) & nitrate (NO3-)
NO + O2 -> NO2 + N2O3 + N2O2 -> NO2- + NO3-
- nitric oxide is a gaseous mediator of cell to cell communication & a potent vasodilator
- insufficient NO may contribute to hypertension
- nitric oxide activates soluble guanylate cyclase
- it mediates penile erection.
- in the immune system, macrophages use nitric oxide as a cytotoxic agent.
- free nitric oxide in the circulation is rapidly reduced by Fe+2 of hemoglobin
- nitric oxide covalently binds to Cyst of proteins resulting in S-nitrosylated derivatives[2][3]
- S-nitrosylation is reversible
- targets of S-nitrosylation include:
- Na+ pump
- Na+ K+ ATPase
- alpha tubulin
- NMDA receptor
- GAPDH*
* S-nitrosylation of GAPDH triggers nuclear translocation via binding to Siah1. Nitrosylated GAPDH stabilizes Siah1, an E3-ubiquitin ligage that mediates proteolysis of nuclear proteins leading to apoptosis
Expression
nitric oxide is formed from L-arginine by:
- a constitutuve NO synthase (NO synthase-1 or NO synthase-3) in
- an inducible NO synthase (NO synthase-2) in
Laboratory
More general terms
Additional terms
Component of
References
- ↑ Stedman's Medical Dictionary 27th ed, Williams & Wilkins, Baltimore, 1999
- ↑ 2.0 2.1 Tidball J, 9th Annual UCLA Research Conference on Aging, June 17, 2004 (conference speaker)
- ↑ 3.0 3.1 Sedlak TW, Snyder SH. Messenger molecules and cell death: therapeutic implications. JAMA. 2006 Jan 4;295(1):81-9. PMID: https://www.ncbi.nlm.nih.gov/pubmed/16391220