Mitochondrial oxidant production by a pollutant dust and NO-mediated apoptosis in human alveolar macrophage.

Published

Journal Article

Residual oil fly ash (ROFA) is a pollutant dust that stimulates production of reactive oxygen species (ROS) from mitochondria and apoptosis in alveolar macrophages (AM), but the relationship between these two processes is unclear. In this study, human AM were incubated with ROFA or vanadyl sulfate (VOSO(4)), the major metal constituent in ROFA, with or without nitro-L-arginine methyl ester (L-NAME), diphenyleneiodonium (DPI), and mitochondrial electron transport inhibitors. Interactions among production of ROS, nitric oxide (NO), and apoptosis of AM were determined. ROFA-stimulated ROS production was attenuated by DPI, rotenone, antimycin, and NaN(3), but not by L-NAME, a pattern mimicked by VOSO(4). ROFA-induced apoptosis was inhibited by L-NAME and a caspase-3-like protease inhibitor, but not by mitochondrial inhibitors. ROFA enhanced NO-mediated increase in caspase-3-like activity. VOSO(4) had minor effects on apoptosis. Thus ROFA-stimulated production of ROS from mitochondria was independent of apoptosis of AM, which was mediated by activation of caspase-3-like proteases and NO. The pro-oxidant effect but not the proapoptotic effect of ROFA was mediated by vanadium.

Full Text

Duke Authors

Cited Authors

  • Huang, Y-CT; Soukup, J; Harder, S; Becker, S

Published Date

  • January 2003

Published In

Volume / Issue

  • 284 / 1

Start / End Page

  • C24 - C32

PubMed ID

  • 12388087

Pubmed Central ID

  • 12388087

International Standard Serial Number (ISSN)

  • 0363-6143

Digital Object Identifier (DOI)

  • 10.1152/ajpcell.00139.2002

Language

  • eng

Conference Location

  • United States