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Chemical Compound Review:

D-NONOate N-diethylamino-N-oxido-nitrous amide

Synonyms: Dea-No, CCRIS 8432, KST-1B9312, LS-76731, AR-1B4615, ...

Gordge, M.P. et al., Hardy, P. et al., Wink, D.A. et al., Mullick, A.E. et al., Strecker, T. et al., et al.

Lawler, Song,

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High impact information on N-diethylamino-N-oxido-nitrous amide

BAY 41-2272 and the NO-donor, diethylamine-NONOate, reduced leukocyte rolling and adhesion in eNOS(-/-) mice to levels observed in WT animals [1].
The NO donors sodium nitroprusside (SNP) and diethylamine-NONOate caused comparable concentration-dependent relaxation that was partially (approximately 40%) attenuated by the guanylate cyclase inhibitors methylene blue and LY83583 and reduced to a lesser extent (approximately 25%) by the inhibitor of cGMP-dependent kinase, KT 5823 [2].
However, treatment of endothelium-denuded rings with the NO donor, diethylamine-NONOate (0.1 mum), restored LPS-induced relaxation (61.6 +/- 6.6%) and iNOS expression to levels comparable with arteries with intact endothelium [3].
The nitric oxide (NO) donors S-nitroso-N-acetylpenicillamine, spermine-NONOate, and diethylamine-NONOate produced less death in SOD1-Tg neurons than in wild-type neurons (p < 0.01) [4].
Modification of AR by the non-thiol NO donor diethylamine NONOate (DEANO) increased enzyme activity and resulted in the formation of AR-NO [5].

Biological context of N-diethylamino-N-oxido-nitrous amide

We report that NO generated by 1,1-diethyl-2-hydroxy-2-nitrosohydrazine (DEA/NO, Et2NN(O)NO-Na+), a compound known to release NO in a predictable manner, caused irreversible damage at physiological concentrations to the zinc finger-containing DNA repair enzyme formamidopyrimidine-DNA glycolyase (Fpg protein) [6].
4. Comparison of the dose-response curves obtained with GSNO, DEANO and 8-bromo cyclic GMP showed DEANO to be the most potent stimulator of intraplatelet cyclic GMP accumulation (P < 0.001 vs both GSNO and 8-bromo cyclic GMP), but GSNO to be the most potent inhibitor of platelet aggregation (P < 0.01 vs DEANO, and P < 0.001 vs 8-bromo cyclic GMP) [7].

Anatomical context of N-diethylamino-N-oxido-nitrous amide

Local application of the NO donator diethylamine-NONOate (NONOate) to the exposed dura mater encephali of the rat caused dose-dependent increases in meningeal blood flow recorded by laser Doppler flowmetry [8].
Conduction in rat peripheral nerve has been monitored following the stimulated release of nitric oxide (NO) from diethylamine-NONOate (DEA-NONOate) [9].
Laser confocal microscopy reveals protein expression of BK(Ca) channels on clitoral smooth muscle cells; these cells exhibit BK(Ca) channel activity that is activated by both DEANO and sildenafil [10].

Associations of N-diethylamino-N-oxido-nitrous amide with other chemical compounds

To demonstrate a specific effect of NO, we used a novel compound named diethylamine dinitric oxide (DEA/NO; 1,1-diethyl-2-hydroxy-2-nitrosohydrazine, sodium salt; [Et2NN(O)NO]Na), which releases NO in aqueous solution at neutral pH [11].
Two nitric oxide donors, 1-hexanamine, 6-(2hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-nitroso- hydrazine (MMNN) and 1,1-diethyl-2-hydroxy-2-nitrosohydrazine, modulated prostaglandin I2 synthase activity in a bidirectional manner [12].
Compared with preincubation values, X/XO and dl-homocysteine increased (P < 0.05) permeability by 66 +/- 11% and 123 +/- 8%, respectively. dl-Homocysteine-induced increases in dextran accumulation were blunted (P < 0.05) by simultaneous incubation with DEANO or tiron [13].

Gene context of N-diethylamino-N-oxido-nitrous amide

DEANO resulted in a 50% reduction in CAT, GPX, and a dose-dependent inhibition of Cu, Zn-SOD [14].
In the present study, preincubation of purified rat liver microsomal GST with S-nitrosoglutathione (GSNO) or the nitric oxide (NO) donor, 1,1-diethyl-2-hydroxy-2-nitrosohydrazine (DEA/NO), resulted in a 2-fold increase in enzyme activity [15].
In contrast, BCS had no effect on either the rate of NO release, or the anti-platelet action of the non-nitrosothiol compound DEANO [7].
Hemisected skulls with adhering dura mater were filled with synthetic interstitial fluid and stimulated with the NO donor diethylamine-NONOate (10(-5)-10(-3) M) or with NO gas (1,000 ppm), which caused concentration-dependent increases in CGRP release up to 166.8% [16].

References

Antiinflammatory activity of soluble guanylate cyclase: cGMP-dependent down-regulation of P-selectin expression and leukocyte recruitment. Ahluwalia, A., Foster, P., Scotland, R.S., McLean, P.G., Mathur, A., Perretti, M., Moncada, S., Hobbs, A.J. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
A major role for prostacyclin in nitric oxide-induced ocular vasorelaxation in the piglet. Hardy, P., Abran, D., Hou, X., Lahaie, I., Peri, K.G., Asselin, P., Varma, D.R., Chemtob, S. Circ. Res. (1998) [Pubmed]
autoregulatory role of endothelium-derived nitric oxide (NO) on Lipopolysaccharide-induced vascular inducible NO synthase expression and function. Vo, P.A., Lad, B., Tomlinson, J.A., Francis, S., Ahluwalia, A. J. Biol. Chem. (2005) [Pubmed]
Differing effects of copper,zinc superoxide dismutase overexpression on neurotoxicity elicited by nitric oxide, reactive oxygen species, and excitotoxins. Ying, W., Anderson, C.M., Chen, Y., Stein, B.A., Fahlman, C.S., Copin, J.C., Chan, P.H., Swanson, R.A. J. Cereb. Blood Flow Metab. (2000) [Pubmed]
Structural and kinetic modifications of aldose reductase by S-nitrosothiols. Srivastava, S., Dixit, B.L., Ramana, K.V., Chandra, A., Chandra, D., Zacarias, A., Petrash, J.M., Bhatnagar, A., Srivastava, S.K. Biochem. J. (2001) [Pubmed]
The Fpg protein, a DNA repair enzyme, is inhibited by the biomediator nitric oxide in vitro and in vivo. Wink, D.A., Laval, J. Carcinogenesis (1994) [Pubmed]
Evidence for a cyclic GMP-independent mechanism in the anti-platelet action of S-nitrosoglutathione. Gordge, M.P., Hothersall, J.S., Noronha-Dutra, A.A. Br. J. Pharmacol. (1998) [Pubmed]
Increase in meningeal blood flow by nitric oxide--interaction with calcitonin gene-related peptide receptor and prostaglandin synthesis inhibition. Strecker, T., Dux, M., Messlinger, K. Cephalalgia : an international journal of headache. (2002) [Pubmed]
Nerve conduction block by nitric oxide that is mediated by the axonal environment. Shrager, P., Custer, A.W., Kazarinova, K., Rasband, M.N., Mattson, D. J. Neurophysiol. (1998) [Pubmed]
The neurovascular mechanism of clitoral erection: nitric oxide and cGMP-stimulated activation of BKCa channels. Gragasin, F.S., Michelakis, E.D., Hogan, A., Moudgil, R., Hashimoto, K., Wu, X., Bonnet, S., Haromy, A., Archer, S.L. FASEB J. (2004) [Pubmed]
Characterization of nitric oxide-stimulated ADP-ribosylation of various proteins from the mouse macrophage cell line ANA-1 using sodium nitroprusside and the novel nitric oxide-donating compound diethylamine dinitric oxide. Sheffler, L.A., Wink, D.A., Melillo, G., Cox, G.W. J. Leukoc. Biol. (1995) [Pubmed]
Nitric oxide modulates the activity of the hemoproteins prostaglandin I2 synthase and thromboxane A2 synthase. Wade, M.L., Fitzpatrick, F.A. Arch. Biochem. Biophys. (1997) [Pubmed]
Hyperhomocysteinemia increases arterial permeability and stiffness in mice. Mullick, A.E., Zaid, U.B., Athanassious, C.N., Lentz, S.R., Rutledge, J.C., Symons, J.D. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2006) [Pubmed]
Specificity of antioxidant enzyme inhibition in skeletal muscle to reactive nitrogen species donors. Lawler, J.M., Song, W. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
Regulation of microsomal and cytosolic glutathione S-transferase activities by S-nitrosylation. Ji, Y., Toader, V., Bennett, B.M. Biochem. Pharmacol. (2002) [Pubmed]
Nitric oxide releases calcitonin-gene-related peptide from rat dura mater encephali promoting increases in meningeal blood flow. Strecker, T., Dux, M., Messlinger, K. J. Vasc. Res. (2002) [Pubmed]

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