S-nitrosoglutathione

S-Nitrosoglutathione

Names
Systematic IUPAC name (2S)-2-Amino-5-[[(2R)-1-(carboxymethylamino)-3-nitrososulfanyl-1-oxopropan-2-yl]amino]-5-oxopentanoic acid
Other names L-γ-Glutamyl-S-nitroso-L-cysteinylglycine; Glutathione thionitrite; S-Nitroso-L-glutathione
Identifiers
CAS Number	57564-91-7 Y
3D model (Jmol)	Interactive image
Beilstein Reference	3566211
ChEBI	CHEBI:50091 Y
ChemSpider	94647 Y
ECHA InfoCard	100.165.055
MeSH	S-Nitrosoglutathione
PubChem CID	104858
RTECS number	MC0558000
InChI InChI=1S/C10H16N4O7S/c11-5(10(19)20)1-2-7(15)13-6(4-22-14-21)9(18)12-3-8(16)17/h5-6H,1-4,11H2,(H,12,18)(H,13,15)(H,16,17)(H,19,20)/t5-,6-/m0/s1 Y Key: HYHSBSXUHZOYLX-WDSKDSINSA-N Y
SMILES C(CC(=O)N[C@@H](CSN=O)C(=O)NCC(=O)O)[C@@H](C(=O)O)N
Properties
Chemical formula	C10H16N4O7S
Molar mass	336.32 g·mol−1
log P	−2.116
Acidity (pKa)	2.212
Basicity (pKb)	11.785
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

S-Nitrosoglutathione (GSNO) is an endogenous S-nitrosothiol (SNO) that plays a critical role in nitric oxide (NO) signaling and is a source of bioavailable NO. NO coexists in cells with SNOs that serve as endogenous NO carriers and donors. SNOs spontaneously release NO at different rates and can be powerful terminators of free radical chain propagation reactions, by reacting directly with ROO• radicals, yielding nitro derivatives as end products. NO is generated intracellularly by the nitric oxide synthase (NOS) family of enzymes: nNOS, eNOS and iNOS while the in vivo source of many of the SNOs is unknown. In oxygenated buffers, however, formation of SNOs is due to oxidation of NO to dinitrogen trioxide (N₂O₃). Some evidence suggests that both exogenous NO and endogenously derived NO from nitric oxide synthases can react with glutathione to form GSNO.

The enzyme GSNO reductase (GSNOR) reduces S-nitrosoglutathione (GSNO) to an unstable intermediate, S-hydroxylaminoglutathione, which then rearranges to form glutathione sulfonamide, or in the presence of GSH, forms oxidized glutathione (GSSG) and hydroxylamine. Through this catabolic process, GSNOR regulates the cellular concentrations of GSNO and plays a central role in regulating the levels of endogenous S-nitrosothiols and controlling protein S-nitrosylation-based signaling.

The generation of GSNO can serve as a stable and mobile NO pool which can effectively transduce NO signaling. Unlike other low molecular weight messengers that bind to and activate target cellular receptors, NO signaling is mediated by a coordinating complex between NO and transition metals or target cellular proteins, often via S-nitrosylation of cysteine residues. Studies suggest that NO metabolism has a significant role in human cardiovascular and respiratory diseases as well as in immune tolerance during organ transplantation.

GSNO and NO concentrations regulate respiratory function by modulating airway tone and pro- and anti-inflammatory responses in the respiratory tract. Because NO is a labile gas and endogenous levels are difficult to manipulate, it has been proposed that exogenous GSNO could be used to regulate circulating levels of NO and NO-derived species, and GSNO could have value in patients with pulmonary diseases such as cystic fibrosis. Consistent with this therapeutic goal, a recent study showed that acute treatment with aerosolized GSNO was well tolerated by cystic fibrosis patients.