l -Arginine Uptake and Metabolism by Lung Macrophages and Neutrophils Following Intratracheal Instillation of Silica In Vivo
| Autor: | Leif D. Nelin, John H. Wiessner, Ralph M. Schapira, Urias A. Almagro, James F Morrisey |
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| Rok vydání: | 1998 |
| Předmět: |
Pulmonary and Respiratory Medicine
Neutrophils Clinical Biochemistry Inflammation Arginine Nitric Oxide Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound In vivo Macrophages Alveolar medicine Animals Urea Lung Molecular Biology biology Pneumonia Cell Biology Metabolism respiratory system Silicon Dioxide Molecular biology Rats Trachea Nitric oxide synthase Arginase medicine.anatomical_structure chemistry Biochemistry biology.protein medicine.symptom |
| Zdroj: | American Journal of Respiratory Cell and Molecular Biology. 19:308-315 |
| ISSN: | 1535-4989 1044-1549 |
| DOI: | 10.1165/ajrcmb.19.2.2814 |
| Popis: | Nitric oxide (NO) has been associated with lung inflammation following exposure to silica. L-arginine can be converted to NO and L-citrulline by nitric oxide synthase (NOS), or into urea and L-ornithine by arginase. We tested the hypothesis that after instillation of silica into rat lungs in vivo, lung inflammatory cells increase L-arginine metabolism by both NOS and arginase, which is associated with an increase in L-arginine uptake. We isolated lung inflammatory cells 3 d after silica or saline (control) exposure. The uptake of [3H]L-arginine at 24 h by cells from silica-exposed lungs (73.9 +/- 4.8%) was significantly greater than uptake by control cells (24.7 +/- 2.2%; P0.05) and was a saturable process. The greater [3H]L-arginine uptake by cells from silica-exposed lungs was associated with greater NO and urea production than by control cells. The uptake of [3H]L-arginine by cells from control or silica-exposed lungs was blocked in a dose-dependent manner by L-ornithine (an inhibitor of L-arginine transport) and by Nomega-nitro-L-arginine methyl ester (L-NAME) (an NOS inhibitor), but not by L-valine (an arginase inhibitor). The production of NO by cells from silica-exposed lungs was completely blocked by L-NAME. The addition of L-arginine to media resulted in dose-dependent production of NO and urea. The results show that lung inflammatory cells increase L-arginine uptake and metabolism by both NOS and arginase following in vivo silica exposure. The increase in L-arginine uptake may represent a mechanism to maintain an intracellular supply of this amino acid. NO can react to generate peroxynitrite, a potential mediator of lung injury following silica exposure. |
| Databáze: | OpenAIRE |
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