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HERO ID
2811183
Reference Type
Journal Article
Subtype
Abstract
Title
Carbon black, and not Titanium dioxide nanoparticles cause mitochondrial dysfunction leading to cell death
Author(s)
Gupta, A; Powers, LS; Grassian, V; Monick, MM; Hunninghake, GW
Year
2010
Is Peer Reviewed?
Yes
Journal
American Journal of Respiratory and Critical Care Medicine
ISSN:
1073-449X
EISSN:
1535-4970
Volume
181
Page Numbers
A3094
Language
English
DOI
10.1164/ajrccm-conference.2010.181.1_MeetingAbstracts.A3094
Web of Science Id
WOS:000208771002205
Relationship(s)
is part of a larger document
3452678
Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Abstract
Rationale: Inhalation of ambient and manufactured nanoparticles has been implicated as a cause for respiratory and cardiovascular morbidity and mortality. Oxidative stress in macrophages contributes to lung injury and systemic inflammation. One source of intracellular oxidants is the mitochondria. We hypothesized that nanoparticle exposure causes mitochondrial dysfunction contributing to cell death.
Methods: We assessed the effect of exposure of two types of nanoparticles, i.e. carbon black and titanium dioxide, on mitochondrial function in a murine macrophage cell line (RAW 264.7). Carbon black (50 nm, Nanostructured and amorphous materials) and titanium dioxide (25 nm, Evonik) nanoparticles were characterized using a variety of techniques, including transmission electron microscopy and X-ray photoelectron spectroscopy. MTT assay (indicator of mitochondrial dehydrogenase activity, ATCC) and JC-1 staining (measure of mitochondrial membrane potential, Invitrogen) was performed in a dose and time dependent manner.
Results: Exposure to high doses (50-100 micrograms/ml) of carbon black, and not titanium dioxide caused a significant decrease in mitochondrial function within 4 hours. MTT assay showed a 50 percent decrease in number of metabolically active cells (indicating cell death) after four hours exposure to carbon black nanoparticles at 100 micrograms/ml. This was matched by a decrease in intensity of JC-1 staining at a similar dose and time point.
Conclusions: Mitochondrial dysfunction in macrophages exposed to carbon black nanoparticles contributes to cytotoxicity
Conference Name
American Thoracic Society 2010 International Conference
Conference Location
New Orleans, LA
Conference Dates
May 14-19, 2010
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