Document Detail

Apoptotic and inflammatory effects induced by different particles in human alveolar macrophages.
MedLine Citation:
PMID:  15764474     Owner:  NLM     Status:  MEDLINE    
Pollutant particles induce apoptosis and inflammation, but the relationship between these two biological processes is not entirely clear. In this study, we compared the proapoptotic and proinflammatory effects of four particles: residual oil fly ash (ROFA), St. Louis particles SRM 1648 (SL), Chapel Hill PM10 (CHP), and Mount St. Helens dust (MSH). Human alveolar macrophages (AM) were incubated with these particles at 100 microg/ml. Cell death was assessed by annexin V (AV) expression, histone release, nuclear morphology, caspase 3-like activity and release of caspase 1 for apoptosis, and propidium iodide (PI) for necrosis, and inflammation was measured by interleukin (IL)-1beta and IL-6. We found that particle effects on these cell death measurements varied, and ROFA affected most (four out of five) endpoints, including nuclear morphological changes. CHP and SL also caused necrosis. For cytokine release, the potency was CHP > SL > ROFA > MSH. The proapoptotic and proinflammatory effects induced by the whole particles were unaltered after the particles were washed with water. The water-soluble fraction was relatively inactive, as were individual soluble metals (V, Ni, Fe). ROFA-induced nuclear fragmentation was associated with upregulation and mitochondrial release of apoptosis-inducing factor (AIF), a caspase-independent chromatin condensation factor, and upregulation of DNase II, a lysosomal acid endonuclease. These results indicate that the potential for particles to induce apoptosis does not correlate with their proinflammatory properties, although active components for both processes reside in the water-insoluble core. Both apoptosis and inflammatory endpoints should be included when the toxicity of different pollutant particles is assessed.
Yuh-Chin T Huang; Zhuowei Li; Shirley D Harder; Joleen M Soukup
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Inhalation toxicology     Volume:  16     ISSN:  0895-8378     ISO Abbreviation:  Inhal Toxicol     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2005-03-14     Completed Date:  2005-03-29     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8910739     Medline TA:  Inhal Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  863-78     Citation Subset:  IM    
National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, Chapel Hill, North Carolina, USA.
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MeSH Terms
Air Pollutants / toxicity*
Annexin A5 / metabolism
Apoptosis / drug effects*
Carbon / toxicity
Caspase 1 / metabolism
Caspase 3
Caspases / metabolism
Cell Nucleus / drug effects,  pathology
Histones / metabolism
Industrial Waste / adverse effects
Interleukin-1 / biosynthesis*
Interleukin-6 / biosynthesis*
Macrophages, Alveolar / drug effects*,  metabolism,  pathology
Particle Size
Particulate Matter
Volcanic Eruptions / adverse effects
Reg. No./Substance:
0/Air Pollutants; 0/Annexin A5; 0/Histones; 0/Industrial Waste; 0/Interleukin-1; 0/Interleukin-6; 0/Particulate Matter; 68131-74-8/fly ash; 7440-44-0/Carbon; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases; EC 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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