Nitric-oxide synthases induction

Miyajima, T., Kotake, Y. (1997). Spin trap phenyl N-tert-butyl-nitrone (PBN) for the inhibition of nitric oxide synthase induction in mice. Free Radio. Biol. Med. 22 463-70. 

Kahl KG, Zielasek J, Uttenthal LO, Rodrigo J, Toyka KV, Schmidt HHHW (2003) Protective role of the cytokine-inducible isoform of nitric oxide synthase induction and nitrosative stress in experimental autoimmune encephalomyelitis of the DA rat. J Neurosci Res 73 198-205. 

Marczin, N., Papapetropoulos, A., Jilling, T., and Catravas, J. D. (1993b). Prevention of nitric oxide synthase induction in vascular smooth muscle cells by microtubule depolymerizing agents. Br. J. Pharmacol. 109, 603-605. 

Szabo, C., Mitchell, J. A., Thiemermann, C., and Vane, J. R. (1993a). Nitric oxide mediated hyporeactivity to norepinephrine precedes nitric oxide synthase induction in endotoxin shock. Br. J. Pharmacol. 108, 786-792. 

Besides, aT-cell response which essentially comprise of both CD4 and CDS" T-cells, production of interferon gamma, and nitric oxide synthase induction serves as an additional proof of evidence that the human-immune system is able to detect the parasite and hence responds accordingly ... 

Nitric oxide Synthase Induction as Influenced by Sydnonimines... 

Espey, M.G., Miranda, K.M., Pluta, R.M., Wink, D.A. (2000). Nitrosative capacity of macrophages is dependent on nitric-oxide synthase induction signals. J. Biol. Chem. 275, 11341-11347. 

Di Rosa, M., Radomski, M., Carnuccio, R. and Moncada, S. (1990). Glucocorticoids inhibit the induction of nitric oxide synthase in macrophages. Biochem. Biophys. Res. Commun. 173, 1246-1252. 

Boughton-Smith, N.K., Berry, S., Evans, S.M., Whittle, B.J.R, and Moncada, S. (1992c). Intestinal damage and the induction of nitric oxide synthase by endotoxin in the rat. Gastroenterology 102, A598. 

Dirsch, V. M. Kiemer, A. K. Wagner, H. Vollmar, A. M. The triterpenoid quinonemethide pristimerin inhibits induction of inducible nitric oxide synthase in murine macrophages. Eur. J. Pharm. 1997, 336, 211-217. 

Xie, Q., Kashiwabara, Y. Nathan, C. (1994). Role of transcription factor NF.kB/Rel in induction of nitric oxide synthase./. Biol. Chem. 269, 4705-8. 

FIGURE 34-5 Induction of endothelial nitric oxide synthase (eNOS) in medial thalamus of thiamine-deficient rats. (A) Increased eNOS mRNA. (B) Increased eNOS immunolabeling of vascular endothelial cells (magnification x200). 

The interaction of estrogen receptors with signaling systems of the cell membrane that respond to growth factors and mediate nongenomic, fast actions of estrogens will be reviewed as well. These mechanisms have a growing importance in the comprehension of phenomena like the induction of endothelial NOS (nitric oxide synthase) by estrogens (Rubanyi et al. 2002). 

Lin, Y.L. and Lin, J.K., (-)-Epigallocatechin-3-gallate blocks the induction of nitric oxide synthase by down-regulating lipopolysaccharide-induced activity of transcription factor nuclear factor-kappaB, Mol Pharmacol, 52, 465, 1997. 

Exposure to trichothecenes at levels that partially inhibit translation upregulates expression of many inflammatory and immune-related genes including macrophage, Thl and Th2 cytokines as well as chemokines, cyclooxygenase 2 and inducible nitric oxide synthase.1518 Contrastingly, suppressive effects of trichothecenes on leukocyte function are intimately linked with the induction of apoptosis as has been demonstrated in macrophages, T cells and B cells both in vivo and in vitro.19-20... 

Lowenstein CJ, Alley EW, Raval P, et al. Macrophage nitric-oxide synthase gene-2 upstream regions mediate induction by interferon-gamma and lipopoly-saccharide. Proc Natl Acad Sci USA 1993 90 9730-9734. 

To set up and validate the in vitro systems we initiated a study with rat Uver slices. Stimulation by Upopolysaccharide (LPS) in liver slices was used to evoke a pro-inflammatory response in the Uver. Lipopolysaccharide (LPS), a component of Gram-negative bacterial ceU walls (also called endotoxin), has been associated with tissue injury and sepsis. In the Uver LPS activates the resident macrophages, the Kupffer ceUs, which results in cytokine release [96]. Furthermore, LPS is cleared by the Uver, mainly by Kupffer ceUs [97]. One of the major features of endotoxic shock is the induction of nitric oxide S5mthase in the Uver [98]. Inducible nitric oxide synthase (iNOS), the expression of which is induced by LPS and cytokines, produces nitric oxide (NO) in large quantities [99]. 

Many pathological conditions, including ischemia/reperfusion, inflammation, and sepsis may induce tissues to simultaneously produce both superoxide and nitric oxide. For example, ischemia allows intracellular calcium to accumulate in endothelium (Fig. 20). If the tissue is reperfused, the readmission of oxygen will allow nitric oxide as well as superoxide to be produced (Beckman, 1990). For each 10-fold increase in the concentration of nitric oxide and superoxide, the rate of peroxynitrite formation will increase by 100-fold. Sepsis causes the induction of a second nitric oxide synthase in many tissues, which can produce a thousand times more nitric oxide than the normal levels of the constitutive enzyme (Moncada et al., 1991). Nitric oxide and indirectly peroxynitrite have been implicated in several important disease states. Blockade of nitric oxide synthesis with N-methyl or N-nitroarginine reduces glutamate-induced neuronal degeneration in primary cortical cultures (Dawson et al., 1991). Nitroarginine also decreases cortical infarct volume by 70% in mice subjected to middle cerebral artery occlusion (Nowicki et al., 1991). Myocardial injury from a combined hy-... 

Deng, W., Thiel, B., Tannenbaum, C. S., Hamilton, T. A., and Stuehr, D. J. (1993). Synergistic cooperation between T cell lymphokines for induction of the nitric oxide synthase gene in murine peritoneal macrophages. J. Immunol. 151, 322-329. 

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