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Peroxyni trite

Calcium antagonists are able to affect nitric oxide production and suppress the peroxyni-trite-induced damage. Thus, nifedipine enhanced the bioavailability of endothelial NO in porcine endothelial cell cultures supposedly through an antioxidative mechanism [288], Pretreatment with nisoldipine, a vascular-selective calcium blocker of dihydropyridine-type, of confluent bovine aortic endothelial cells suppressed the peroxynitrite-induced GSH loss and increased cell survival [289]. [Pg.884]

Chang, T., Wang, R., and Wu, L. (2005). Methylglyoxal-induced nitric oxide and peroxyni-trite production in vascular smooth muscle cells. Free Radic. Biol. Med. 38, 286-293. [Pg.137]

Amyotrophic lateral sclerosis (ALS), peroxyni-trite implicated, 46 402 Anabaena, heterocyst ferredoxin, 38 229 Anabaena sphaeria, ferredoxins, 38 228-229 Anaerobic controlled potential electrolysis, Azotobacter, 38 129... [Pg.11]

Yermilov V, Rubio J, Ohshima H (1995) Formation of 8-nitroguanine in DNA treated with peroxyni-trite in vitro and its rapid removal from DNA by depurination. FEBS Lett 376 207-210 Yermilov V, Yoshie Y, Rubio J, Oshima H (1996) Effects of carbon dioxide/bicarbonate on induction of DNA single-strand breaks and formation of 8-nitroguanine, 8-oxoguanine and base-propenal mediated by peroxynitrite. FEBS Lett 399 67-70... [Pg.47]

The -N02 radical (and also the C03 radical) are of some biological interest (Augusto et al. 2002) because they play some role in the reactions of peroxyni-trite (Chap. 2.4). For example, "N02 oxidizes tyrosine to nitrotyrosine (Prutz et al. 1985b), and the latter has been considered a promoter of free-radical damage in DNA model systems (Prutz 1986). In this context, it may be of interest that CCV reacts with a self-complementary ODN (k = 1.9 x 107 dm3 mol-1 s 1) exclusively at G (by ET) (Chap. 11.2). [Pg.95]

The several SODs in mammalian cells constitute a major form of protection against ROS. Since superoxide dismutase generates H2O2, its detoxifying effect primarily results from preventing the accumulation of free Fe + and the production of peroxyni-trite. [Pg.1357]

Recently, molsidomine (31) and SIN-1 (32) have been extensively utilized as a probe to elucidate the biomedical mechanisms of NO and/or peroxyni-trite. Molsidomine has a high bio availability, and the long-lasting duration of its action possibly stimulates the permeability through the blood-brain barrier. Molsidomine does not display any side effects at doses displaying an... [Pg.142]

Beckman JS, Beckman TW, Chen J, Marshall PA, Freeman BA. 1990. Apparent hydroxyl radical production by peroxyni-trite implication for endothelial injury from nitric oxide and superoxide. Proc. Natl. Acad. Sci. USA 87 1620-24... [Pg.93]

It has been hypothesized that the same elevated nitric oxide/peroxyni-trite mechanism described for MCS (Section 26.5), 23 also applies to CFS. 45-51 In this hypothesis, CFS symptoms are ascribed to nitric oxide, peroxynitrite, and related hypoxia as follows 461... [Pg.443]

Peroxyni trite Biological samples Dialysis (for sampling) CL 1 x 1CU11 and 1 x 1CT10 mol L 1 for systems without and with dialysis Flow injection system permselective cellulose acetate membrane sampler [544]... [Pg.386]

Pannala, A. S., Rice-Evans, C. S., and Halliwell, B. 1997. Inhibition of peroxyni-trite-mediated nitrition by catechin polyphenols. Biochem. Biophys. Res. Commun. 232 164-68. [Pg.158]

Mohr, S., Stamler, J. S., and BrUne, G. (1994). Mechanism of covalent modification of glyceraldehyde-3-phosphate dehydrogenase at its active site thiol by nitric oxide, peroxyni-trite and related nitrosating agents. FEES Lett. 348, 213-117. [Pg.359]

The photolysis of nitrate and nitrite in sea water produces nitrogen dioxide (NO2) and nitric oxide (NO), respectively (eqns [I] and [II]). Previous work indicated that the photolysis of nitrite could act as a small net source of NO to the marine atmosphere under some conditions. However, this conclusion seems to be at odds with estimates of the steady-state concentrations of superoxide and the now known rate constant for the reaction of superoxide with nitric oxide (6.7 x 10 M s ) to form peroxyni-trite in aqueous phases (eqn [V]). [Pg.94]

Beharka, A.A., Wu, D., Serafini, M., and Meydani, S.N. (2002) Mechanism of Vitamin E Inhibition of Cyclooxygenase Activity in Macrophages from Old Mice Role of Peroxyni-trite,Eree Radio. Biol. Med. 32,503-511. [Pg.238]

Nitric oxide ( NO) and its derivative peroxyni-trite (ONOO ) inhibit mitochondrial respiration by distinct mechanisms. Nanomolar concentrations of NO specifically inhibit cytochrome oxidase in competition with oxygen, and this inhibition is fully reversible when NO is removed. The NO inhibition of cytochrome oxidase may be involved in the cytotoxicity of NO, and may cause increased oxygen radical production by mitochondria, with may in turn lead to the generation of peroxynitrite. Mitochondrial damage by peroxynitrite may mediate the cytotoxicity of NO, and may be involved in a variety of pathologies (for review see Brown 1999). Under turnover conditions, depending on the cytochrome concentration, either the cytochrome aj -NO or the nitrite bound enzyme is formed (Sarti et al. 2000). The predominance of one of the two inhibitory pathways depends on the occupancy of the turnover intermediates. In the dark, the respiration recovers at the rate of NO dis-... [Pg.84]

Human matrix metalloproteinases may be processed from their proenzyme forms to their active forms by two new and unique mechanisms (Maeda et al. 1998) Firstly, by bacterial proteases such as Pseudomonas elastase and Vibrio cholerae protease, which cleave off the N-terminal autoinhibitory domain (so-called cysteine switch) from pro-matrix metalloproteinases. The second mechanism depends on free radical generation by activated polymorphonuclear leucocytes. In this case, peroxyni-trite (ONOO") or nitrogen dioxide radical ("NOj) are the key reagents. [Pg.271]

Mice of the nonobese diabetic strain develop a progressive insulinitis resulting in P-cell destruction and autoimmune-type diabetes mellitus with features mimicking the disease in humans (Making et al. 1980, Atkinson and Feiter 1999). Superoxide radicals are abundantly formed by leucocytes and other mechanisms in inflammatory reactions. The overexpression of extracellular-superoxide dis-mutase presumably by the P-cells in the pancreata of transgenic non-obese diabetic mice (Sandstrom et al. 2002) should reduce formation of peroxyni-trite from O2 " and NO present in the islet intersti-tium. [Pg.576]

Cui L, Ye WJ, Prestwich EG, Wishnok JS, Taghizadeh K, Dedon PC, Tannenbaum SR (2013) Comparative analysis of four oxidized guanine lesions from reaetions of DNA with peroxyni-trite, singlet oxygen, and gamma-radiation. Chem Res Toxieol 26 195-202... [Pg.87]

Brannan, R.G., Conolly, B.J., Decker, E.A. Peroxyni-trite a potential initiator of lipid oxidation in food. Trends Food Sci. Technol. 72,164 (2001)... [Pg.245]

It has been proposed that the presence of comorbid illness among patients with MCS, CFS, and FM supports a single syndrome hypothesis, i.e., that all are variants of a single functional disorder [79]. This is supported by the nitric oxide/peroxyni-trite hypothesis that has been previously discussed [26, 49-52] and by the shared symptoms in Gulf War veterans [73, 74]. It is argued here, however, that though these illnesses have overlapping symptoms, this hypothesis is yet to be definitively proven. Each of the illnesses has distinct differences from the others and at least one, MCS, demonstrates a resolution of symptoms when exposures to the causative chemicals are eliminated. [Pg.379]


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See also in sourсe #XX -- [ Pg.1069 ]




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