| Autor: |
Chen F; Department of Pathology, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, USA., Kuhn DC, Gaydos LJ, Demers LM |
| Jazyk: |
angličtina |
| Zdroj: |
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica [APMIS] 1996 Mar; Vol. 104 (3), pp. 176-82. |
| DOI: |
10.1111/j.1699-0463.1996.tb00705.x |
| Abstrakt: |
Nitric oxide (NO), a nitrogen-free radical, plays an important role in mediating inflammatory reaction and cytotoxicity of tissue. To determine whether NO was involved in silica-induced pulmonary tissue damage, we studied the effects of silica on nitric oxide (NO) production and inducible NO synthase (iNOS) mRNA expression by THP-1 cells, a monocyte-like cell line with properties of the pulmonary alveolar macrophage. Experimental results showed that silica elicited a marked stimulation of nitric oxide production in a time-dependent manner by THP-1 cells in vitro following the priming of these cells with the phorbol ester PMA. Both nitric oxide synthase inhibitor N-monomethyl-L-arginine (NMMA) and xanthine oxidase inhibitor allopurinol can partially suppress silica-induced NO production in PMA-primed THP-1 cells. Northern blot analysis indicated that, after 2 h of silica exposure, PMA-primed THP-1 cells began to express iNOS mRNA, which reached peak expression at 8 h. Endotoxin treatment of these cells produced a similar effect. These results indicated that silica is a potent inducer of NO production in macrophages and its ability to induce tissue damage may partially be attributed to its ability to initiate excessive production of nitric oxide from macrophages. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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