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. 2015 May 19;20(5):9099–9123. doi: 10.3390/molecules20059099

Table 1.

Nitric oxide and hydrogen sulfide biochemistry and physiology.

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Physiological concentrations
serum 1 nM [132] 30–100 μM
brain/tissue 100–250 nM [133] 50–160 μM [106]
toxic 0.5 µM [134] 250 μM
Biochemical properties
Half-life Seconds—minutes [135] Seconds [135]
Physiological forms NO exists as a free radical [136] 20% exist as H2S, 80% as HS−, trace amounts of S2− [137]
Crosstalk interaction on catalyzing enzymes
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NO donor increases the expression and activity of CSE in cultured aortic smooth muscle cells (SMCs) [97] NaHS inhibits iNOS expression and NO production in macrophage cells (RAW264.7) [138]
NO cooperates with H2S via activation of guanylyl cyclase and increase of cGMP [139] NaHS treatment reduces eNOS activity and expression but not nNOS and iNOS in isolated rat aortas [140]
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NO does not increase the expression of H2S-generating enzymes and the H2S level in endothelial cells. [141] NaHS/Na2S profoundly increases the expression or/and the activity of eNOS [141,142,143,144]
H2S interacts with NO synthase to transform NO to nitroxyl (HNO) ↓ NO → ↑HNO [145] Na2S augmented NO production in chronically ischemic tissues, by influencing iNOS and nNOS expression and stimulating nitrite reduction to NO via xanthine oxidase (XO) under hypoxic condition [146]
Potent mechanisms of gastroprotection
I/R injury ↑ gastric blood flow ↓ lipid peroxidation ↓ free radicals [147] ↓ plasma level of IL-1β and TNF-α mRNA expression [114]
WRS injury ↓ lipid peroxidation ↑ SOD activity ↑ GSH concentration [58] ↓ acid output, ↑ gastric juice pH and mucin concentration, ↑GSH, CAT and SOD enzymes activities [148]
↓ lipid peroxidation products [110]
Ethanol injury ↓ free radicals ↑prostaglandins production [149] Involvement of KATP channels, capsaicin-sensitive nerve fibers and TRPV1 receptors [2]
Gastric ulcers healing
NO inhibits oxidative stress leading to acceleration of chronic gastric ulcers healing [150] Beneficial effect is not dependent on NO synthesis and do not occur through activation of ATP-sensitive K+ channels [90]
HHS Vulnerability Disclosure