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S-Nitrosoglutathione Antibody, Anti-GSNO
[N1125]
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PRODUCT: S-Nitrosoglutathione Antibody, Anti-GSNO Antibody
DESCRIPTION: New Polyclonal antibody for the detection of S-Nitrosoglutathione (GSNO). Useful as a tool to investigate the level of GSNO in human plasma proteins. Suitable for a variety of applications.
QUANTITY: 100 ul
IMMUNOGEN: NO-Glutathione-Glutaraldehyde-BSA
ISOTYPE: Polyclonal
HOST: Rat
APPLICATIONS:Immunoblotting, Immunoprecipitation, ELISA, Immunohistochemistry, Immunocytochemistry, Recommended dilution:1/2,000 -1/5,000. The minimum level of GSNO that the antibody can detect is about 8-10M. It can be used in mouse tissue and plasma.
STORAGE & HANDLING: Long term storage -20C
BACKGROUND INFORMATION:
Nitric Oxide (NO) acts as a neuronal and vascular messenger implying diffusion through intracellular environments containing glutathione. Nitric oxide reacts with glutathione (1) under aerobic conditions generating S-Nitrosoglutathione (GSNO). A novel reaction mechanism for the formation of GSNO suggests that under physiological conditions NO reacts directly with GSH to form GSNO in the presence of an electron acceptor (2).
Formation of S-Nitrosoglutathione
S-nitrosoglutathione (3) (GSNO) can be formed through nitrosation of the cysteine residue of the tripeptide, glutathione (GSH) by higher oxides of nitrogen and peroxynitrite in vivo (4).
Peroxynitrite (ONOO-), a potent oxidant formed by reaction of nitric oxide (NO) with superoxide anion, reacts with glutathione (5) to proceed through formation of a S-nitroglutathione (GSNO2) intermediate and yields S-Nitrosoglutathione (GSNO), both of which are theoretical sources of NO.
Physiological roles of S-Nitrosoglutathione
S-Nitrosothiols like GSNO have generated considerable interest due to their ability to act as NO donors and due to their possible involvement in bioregulatory systems as NO transfer reactions. Many of the biological functions that have been described for S-Nitrosothiols have clinical correlates:
Generation of GSNO might act as a means of detoxifying harmful nitrogen containing species to form an intracellular store of NO (6) that has been implicated as an intermediate in a new pathway for NO: guanylate cyclase signaling (7).
Exogenous GSNO has been shown to have several potentially beneficial cardiovascular effects: Firstly, its powerful inhibitory effect on platelet activation (8) has been shown to be of benefit following balloon angioplasty (9) and in patients with acute myocardial infarction and unstable angina (10). Furthermore, GSNO has been shown to reduce the rate of embolization in humans (11).
The platelet activity of GSNO is complemented by arterioselective vasodilator properties (12), which together present an attractive proposition in a range of cardiovascular diseases, particularly in view of the non-toxic by-products generated after NO delivery.
Besides the cardiovascular system, GSNO has been shown to be a powerful bronchodilator agent (13,14,15).
Recent research has shown that endogenous GSNO levels are elevated in the airway of patients with pneumonia and reduced in those with severe asthma (16).
Literature References:
1. N. Hoog et al. FEBS Lett. (1996) 382, 223
2. A.J. Gow et al. J. Biol Chem. (1997) 272, 2841.
3. J.S. Scharfstein et al. J. Clin. Invest. (1994) 94, 1432.
4. M.A. Mora et al. Br. J. Pharmacol. (1995) 116, 1999.
5. A Van Der vliet et al. J. Biol. Chem. (1998) 273, 30255.
6. I. Lizasoain et al. Biochem. J. (1996) 314, 877.
7. B. Mayer et al. J. Biol. Chem. (1998) 273 3264.
8. M.W. Radomski et al. Br. J. Pharmacol. (1992) 107, 745.
9. E.J. Langford et al. Lancet (1994) 344, 1458.
10. E.J. Langford et al. Arterioscler. Thromb Vasc. Biol. (1996) 16, 51.
11. J. Molloy et al. Circulation (1998) 98, 1372.
12. A.J. De Belder et al. Cardiovasc. Res. (1994) 28, 691.
13. B. Gaston et al. Proc. Natl. Acad Sci. USA (1993) 90, 10957.
14. B. Gaston et al. J.Pharmacol. Exp. Ther (1994) 268, 978.
15. G.Bannenberg et al. J. Pharmacol. Exp. Ther (1995) 272, 1238.
16. B. Gaston et al. Lancet (1998) 351, 1317.
17. ALENCAR J.L., GEFFARD M., STOCLET J.C. and MULLER B. Evidence for the formation of vasoactive nitric oxide stores by S-nitrosation of cysteine residues in isolated blood vessels exposed to S-nitrosoglutathione. Br. J. Pharmacol. (Proceedings of the winter Meeting, London), in press (2003).
18. ALENCAR J.L., LOBYSHEVA I., CHALUPSKY K., GEFFARD M., NEPVEU F., STOCLET J.C. and MULLER B. Differential ability among NO donors to induce S-nitrosation-mediated long-lasting inhibition of contraction in isolated arteries. J. Pharmacol. Exp. Ther., submitted (2003).
Product intended for research purposes only. Not for Human or Clinical use.
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$450.00
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Note: All products sold by A.G. Scientific are for Laboratory or Manufacturing purposes only. They are not intended for Human Drug, Food Additive, Clinical or Household use.
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