Peroxynitrite Anion Stimulates Arginine Release from Cultured Rat Astrocytes
| Autor: | Vega-Agapito, Angeles Almeida, S. J. R. Heales, J M Medina, Juan P. Bolaños |
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| Rok vydání: | 2002 |
| Předmět: |
inorganic chemicals
Arginine Glutamic Acid Biology Biochemistry Nitric oxide Cellular and Molecular Neuroscience chemistry.chemical_compound Serine medicine Citrulline Animals Nitric Oxide Donors Rats Wistar Cells Cultured Nitrates Arginine transport Superoxide Lysine Hydrogen Peroxide Oxidants Rats Nitric oxide synthase Kinetics Animals Newborn chemistry Astrocytes cardiovascular system biology.protein Sodium nitroprusside Peroxynitrite medicine.drug |
| Zdroj: | Journal of Neurochemistry. 73:1446-1452 |
| ISSN: | 0022-3042 |
| DOI: | 10.1046/j.1471-4159.1999.0731446.x |
| Popis: | The biosynthesis of the physiological messenger nitric oxide (*NO) in neuronal cells is thought to depend on a glial-derived supply of the *NO synthase substrate arginine. To expand our knowledge of the mechanism responsible for this glial-neuronal interaction, we studied the possible roles of peroxynitrite anion (ONOO-), superoxide anion (O2*-), *NO, and H2O2 in L-[3H]arginine release in cultured rat astrocytes. After 5 min of incubation at 37 degrees C, initial concentrations of 0.05-2 mM ONOO- stimulated the release of arginine from astrocytes in a concentration-dependent way; this effect was maximum from 1 mM ONOO- and proved to be approximately 400% as compared with control cells. ONOO(-)-mediated arginine release was prevented by arginine transport inhibitors, such as L-lysine and N(G)-monomethyl-L-arginine, suggesting an involvement of the arginine transporter in the effect of ONOO-. In situ xanthine/xanthine oxidase-generated O2*- (20 nmol/min) stimulated arginine release to a similar extent to that found with 0.1 mM ONOO-, but this effect was not prevented by arginine transport inhibitors. *NO donors, such as sodium nitroprusside, S-nitroso-N-acetylpenicillamine, or 1-[2-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium+ ++-1,2-diolate, and H2O2 did not significantly modify arginine release. As limited arginine availability for neuronal *NO synthase activity may be neurotoxic due to ONOO- formation, our results suggest that ONOO(-)-mediated arginine release from astrocytes may contribute to replenishing neuronal arginine, hence avoiding further generation of ONOO- within these cells. |
| Databáze: | OpenAIRE |
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