These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Bicarbonate inhibits N-nitrosation in oxygenated nitric oxide solutions. Author: Caulfield JL, Singh SP, Wishnok JS, Deen WM, Tannenbaum SR. Journal: J Biol Chem; 1996 Oct 18; 271(42):25859-63. PubMed ID: 8824217. Abstract: N-Nitrosation in oxygenated nitric oxide (NO middle dot) solutions was previously shown to be significantly inhibited by phosphate and chloride presumably by anion scavenging of the nitrosating agent nitrous anhydride, N2O3 (Lewis, R. S., Tannenbaum, S. R., and Deen, W. M. (1995) J. Am. Chem. Soc. 117, 3933-3939). Here, bicarbonate is shown to exhibit this same inhibitory effect. Rate constants for reaction of morpholine, phosphate, and bicarbonate with N2O3 relative to N2O3 hydrolysis at pH 8.9 were determined to be (3.7 +/- 0.2) x 10(4) M-1, (4.0 +/- 0.9) x 10(2) M-1, and (9.3 +/- 1.5) x 10(2) M-1, respectively. The morpholine and phosphate rate constants at pH 8.9 are similar to those reported at pH 7.4 assuring that these results are relevant to physiological conditions. The rate constant for this previously unrecognized reaction of bicarbonate with N2O3 suggests the strong scavenging ability of bicarbonate; accordingly, bicarbonate may contribute to reducing deleterious effects of N2O3. This is biologically important due to substantial bicarbonate concentrations in vivo, approximately 30 mM. Bicarbonate was previously shown to alter peroxynitrite reactivity; however, carbon dioxide is the probable reactive species. Bicarbonate is therefore potentially important in determining the fate of two reactive species generated from nitric oxide, N2O3 and ONOO-, and may thus act as a regulator of NO middle dot-induced toxicity.[Abstract] [Full Text] [Related] [New Search]