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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Antioxidant treatment attenuates cytokine and chemokine levels in murine macrophages following silica exposure.

Authors: Barrett, E G; Johnston, C; Oberdorster, G; Finkelstein, J N

Published In Toxicol Appl Pharmacol, (1999 Aug 1)

Abstract: Alveolar macrophages play a key role in the development of silicosis by releasing a host of mediators, such as, cytokines and chemokines, which contribute to a complex network of interactions that result in the onset of lung injury, inflammation, and potentially fibrosis. Using a murine macrophage cell line, RAW 264.7, we exposed the cells to cristobalite-silica (35 micrograms/cm(2)) in the presence or absence of antioxidants and various modifiers of cellular antioxidant status. Treatment with dimethyl sulfoxide, extracellular glutathione, or N-acetyl-L-cysteine (NAC) decreased cristobalite-induced tumor necrosis factor (TNF)-alpha mRNA levels by 40%, 20%, and 42%, respectively. TNF-alpha protein levels were decreased by 90%, 32%, and 53%, respectively. Cristobalite-induced macrophage inflammatory protein (MIP)-2 mRNA levels were reduced by 52%, 38%, and 57%, with DMSO, GSH, and NAC treatment, respectively. Both MIP-1alpha and MIP-1beta mRNA levels were reduced at a magnitude similar to the reduction in TNF-alpha mRNA levels, whereas monocyte chemotactic protein (MCP)-1 mRNA levels were reduced at a magnitude similar to the reduction in MIP-2 mRNA levels following antioxidant treatment. These results suggests that the macrophage response to cristobalite exposure is mediated at least in part by oxidant stress.

PubMed ID: 10438654 Exiting the NIEHS site

MeSH Terms: Acetylcysteine/pharmacology; Animals; Antidotes/pharmacology; Antioxidants/pharmacology*; Cell Death/drug effects; Cells, Cultured; Chemokines/biosynthesis*; Cytokines/biosynthesis*; Dimethyl Sulfoxide/pharmacology; Enzyme-Linked Immunosorbent Assay; Free Radical Scavengers/pharmacology; Glutathione/pharmacology; L-Lactate Dehydrogenase/metabolism; Macrophages/drug effects; Macrophages/enzymology; Macrophages/metabolism*; Male; Mice; Oxidative Stress/drug effects; Research Support, U.S. Gov't, P.H.S.; Ribonucleases/metabolism; Silicon Dioxide/toxicity*; Tumor Necrosis Factor-alpha/biosynthesis

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