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Nitric oxide cell culture

Haburcak M, Wei L, Viana F, Prenen J, Droogmans G and Nilius B, Calcium-activated potassium channels in cultured human endothelial cells are not directly modulated by nitric oxide. Cell Calcium 21(4) 291-300, 1997. [Pg.129]

D Apuzzo M, Relink A, Loetscher M, Hoxie JA, Clark-Lewis I, Melchers F, Baggiolini M, Moser B (1997) The chemokine SDF-1, stromal cell-derived factor 1, attracts early stage B cell precursors via the chemokine receptor CXCR4. Eur J Immunol 27 1788-1793 Dawson VL, Dawson TM, Uhl GR, Snyder SH (1993) Human immunodeficiency virus type 1 coat protein neurotoxicity mediated by nitric oxide in primary cortical cultures. Proc Natl Acad Sci USA 90 3256-3259... [Pg.137]

Schaefer U, Schneider A, Rixen D, Neugebauer E (1998) Neutrophil adhesion to histamine stimulated cultured endothelial cells is primarily mediated via activation of phospholipase C and nitric oxide synthase isozymes. Inflamm Res 47(6) 256-264 Schaefer U, Schmitz V, Schneider A, Neugebauer E (1999) Histamine induced homologous and heterologous regulation of histamine receptor subtype mRNA expression in cultured endothelial ceUs. Shock 12(4) 309-315... [Pg.351]

Hong CH, Sun KH, Jin O, Sun SK, Kyung AN, Sang KL. Evaluation of natural products on inhibition of inducible cyclooxygenase (COX-2) and nitric oxide synthase (iNOS) in cultured mouse macrophage cells. J Ethnopharmacol 2002 83 153-159. [Pg.63]

Taylor, M.J., Cross, H.F., Mohammed, A.A., Trees, A.J. and Bianco, A.E. (1996) Susceptibility of Brugia malayi and Onchocerca lienalis microfilariae to nitric oxide and hydrogen peroxide in cell-free culture and from IFN gamma-activated macrophages. Parasitology 112, 315-322. [Pg.404]

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]

Marczin N, Jilling T, Papapetropoulos A, Go C, Catravas JD 1996 Cytoskeleton-dependent activation of the inducible nitric oxide synthase in cultured aortic smooth muscle cells. Br J Pharmacol 118 1085—1094... [Pg.253]

Effect of a nitric oxide synthase inhibitor, S-ethylisothiourea, on cultured cells and cardiovascular functions of normal and lipopolysaccharide-treated rabbits, J. Biochem. (Tokyo) 119 (1996), p. 553-558... [Pg.277]

Klemm, P., Hecker, M., Stockhausen, H., Wu, C. C., Thiemermann, C., Inhibition by N-acetyl-5-hydroxytryptamine of nitric oxide synthase expression in cultured cells and in the anaesthetized rat, Br. [Pg.280]

Figure 25.3 Presentation of estradiol to A. endothelial cells affects signaling. (A) Physiological levels of estradiol (E2) complexed with albumin do not elicit the production of nitric oxide when presented to cultured endothelial cells although E2-albumin binds to caveolar SR-B1. (B) Physiological levels of estradiol complexed with HDL elicit the production of nitric oxide by activating AMPK and then eNOS. Although it is depicted in this figure that AMPK is activated by binding of estradiol to the estrogen receptor, B. this mechanism has not been experimentally demonstrated. Other mechanisms of E2-HDL activation of AMPK and eNOS are thus possible (See also color insert). Figure 25.3 Presentation of estradiol to A. endothelial cells affects signaling. (A) Physiological levels of estradiol (E2) complexed with albumin do not elicit the production of nitric oxide when presented to cultured endothelial cells although E2-albumin binds to caveolar SR-B1. (B) Physiological levels of estradiol complexed with HDL elicit the production of nitric oxide by activating AMPK and then eNOS. Although it is depicted in this figure that AMPK is activated by binding of estradiol to the estrogen receptor, B. this mechanism has not been experimentally demonstrated. Other mechanisms of E2-HDL activation of AMPK and eNOS are thus possible (See also color insert).
Grenier M, Sun P, Drobitch R. Effect of St. John s wort preparations on cell viability, induction of nitric oxide and ethoxyresomfin O-deethylase activity in glial cell culture. Proceedings of the 5th Annual S5Tnposium on Pharmaceutical Sciences. J Pharm Pharmaceut Sci 2002 5 106. [Pg.67]

In the process, the iron is reduced to the ferrous form. Ferric cytochrome c is reduced by nitric oxide through a nitrosyl intermediate to produce ferrous cytochrome c and nitrite (Orii and Shimada, 1978). The nitrosyl cytochrome c absorbs at 560 nm, which is slightly higher than the 550-nm peak observed for reduced cytochrome c. Nitric oxide may be an interference in the assay of superoxide from cultured cells by the cytochrome c method. When nitric oxide reacts with cytochrome c, there is an initial decrease in absorbance at 550 nm as the nitrosyl complex is formed followed by a rise in absorbance as the complex decomposes to nitrite and reduced cytochrome c. This is a potential artifact in studies measuring the release of superoxide from cultured endothelial cells or other cells that make nitric oxide. [Pg.26]

Kooy and Royall (1994) have shown that cultured endothelial cells produce peroxynitrite when stimulated by bradykinen. They used an ultrasensitive chemiluminescent assay based on luminol developed by Radi et al. (1993). Peroxynitrite is a potent toxin to trypanosomes, attacking both sulfhydryl dependent enzymes and respiratory enzymes (Rubbo et al., 1994). Radi et al. (1994) have also shown that it is far more damaging to mitochondria than nitric oxide. [Pg.68]

Mulsch, A., and Busse, R. (1991). Nitric oxide synthase in native and cultured endothelial cells Calcium/calmodulin and tetrahydrobiopterin are cofactors. J. Cardiovasc. Pharmacol. 17, S52-S56. [Pg.135]

Drapier, J. C., Pellat, C., and Henry, Y. (1992). Characterization of the nitrosyl-iron complexes generated in tumour cells after co-culture with activated macrophages. In The Biology of Nitric Oxide. 2. Enzymology, Biochemistry and Immunology. (S. Moncada, M. A. Marietta, J. B. Hibbs, Jr., and E. A. Higgs, eds.), pp. 72-76, Portland Press, London. [Pg.166]

Kelm, M., Feelisch, M., Spahr, R., Piper, H. M., Noack, E., and Schrader, J. (1988). Quantitative and kinetic characterization of nitric oxide and EDRF released from cultured endothelial cells. Biochem. Biophys. Res. Commun. 154, 236-244. [Pg.169]

We believe that the /3 cell is a source of nitric oxide production by human islets because (1) IL-1 and IFN-induced nitric oxide production by human macrophages has not been clearly demonstrated (2) the cytokine combination of IL-1, IFN, and TNF induces the formation of nitric oxide by human islets either freshly isolated or cultured for 7 days at 25°C (a procedure which removes 80-90% of nonendocrine cells from the islet) and also by islets cryoperserved and (3) NADPH—diaphorase staining reveals that approximately 60-70% of human islet cells treated with cytokines stain for NADPH-diaphorase (J. A. Corbett and M. L. McDaniel, unpublished data). TTiis staining procedure has been shown to colocalize with nitric oxide synthase in a number of cells including rat islets (Corbett et al., 1993c), and nitric oxide synthase has been demonstrated to contain NADPH-diaphorase enzymatic activity (Dawson et al., 1991 Hope et... [Pg.203]

Garg, U. C., and Hassid, A. (1989). Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells. J. Clin. Invest. 83, 1774-1777. [Pg.254]

A study has been undertaken to clarify whether glucocorticoid excess affects endothelium-dependent vascular relaxation in glucocorticoid treated patients and whether dexamethasone alters the production of hydrogen peroxide and the formation of peroxynitrite, a reactive molecule between nitric oxide and superoxide, in cultured human umbilical endothelial cells (7). Glucocorticoid excess impaired endothelium-dependent vascular relaxation in vivo and enhanced the production of reactive oxygen species to cause increased production of peroxynitrite in vitro. Glucocorticoid-induced reduction in nitric oxide availability may cause vascular endothelial dysfunction, leading to hypertension and atherosclerosis. [Pg.4]


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