Air Pollution Particulate SRM 1648 Causes Oxidative Stress in RAW 264.7 Macrophages Leading to Production of Prostaglandin E2, a Potential Th2 Mediator

Particulates in air pollution have been strongly associated with asthma symptoms. These particulates are a conglomeration of many components, including metals, polyaromatic hydrocarbons, and lipopolysaccharide, that may cause oxidative stress upon uptake by alveolar macrophages. The objective of thi...

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Bibliographic Details
Published in:Inhalation toxicology 2005-12, Vol.17 (14), p.871-877
Main Authors: Schneider, Jordan C., Card, George L., Pfau, Jean C., Holian, Andrij
Format: Article
Language:English
Subjects:
Air Pollutants
Air Pollution
Animals
Cell Line
Dinoprostone - metabolism
Glutathione - metabolism
Humans
Macrophages, Alveolar - cytology
Macrophages, Alveolar - metabolism
Mice
Mice, Inbred BALB C
Oxidative Stress
Th2 Cells - metabolism
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Summary:Particulates in air pollution have been strongly associated with asthma symptoms. These particulates are a conglomeration of many components, including metals, polyaromatic hydrocarbons, and lipopolysaccharide, that may cause oxidative stress upon uptake by alveolar macrophages. The objective of this study was to assess whether uptake of a model air particulate (SRM 1648) causes oxidative stress in macrophages resulting in the production of the eicosanoid mediator prostaglandin E2 (PGE2) that might exacerbate asthma. SRM 1648 suspended in phosphate-buffered saline (PBS) was introduced into wells with plated RAW 264.7 monocyte/macrophages. Following incubation of SRM 1648 with RAW 264.7 macrophages, prostaglandin E2 was measured by enzyme immunosorbent assay (EIA), and oxidative stress was assessed by the levels of intracellular reduced glutathione (GSH) as well as by the oxidation of dihydrodichlorofluorescein (H2DCFDA) to the fluorescent dichlorofluoresecein (DCF). The results indicated that SRM 1648 caused oxidative stress in RAW 264.7 macrophages, as shown by a compensatory increase in GSH levels in comparison to the controls of titanium dioxide and media alone. Prostaglandin E2 levels significantly increased at the 3-, 6-, and 12-h time points. Introduction of GSH ester to buffer against oxidative stress was able to block the elevation of PGE2. The data show that SRM 1648 causes oxidative stress in RAW 264.7 macrophages resulting in formation of the potential Th2 mediator prostaglandin E2.
ISSN:0895-8378
1091-7691
DOI:10.1080/08958370500244498