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Stöger, T. ; Takenaka, S. ; Frankenberger, B. ; Ritter, B. ; Karg, E.W. ; Maier, K.L. ; Schulz, S. ; Schmid, O.

Deducing in vivo toxicity of combustion-derived nanoparticles from a cell-free oxidative potency assay and metabolic activation of organic compounds.

Environ. Health Perspect. 117, 54-60 (2009)
Verlagsversion Volltext DOI PMC
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BACKGROUND: The inhalation of combustion-derived nanoparticles (CDNPs) is believed to cause an oxidative stress response, which in turn may lead to pulmonary or even systemic inflammation. OBJECTIVE AND METHODS: In this study we assessed whether the in vivo inflammatory response-which is generally referred to as particle toxicity-of mice to CDNPs can be predicted in vitro by a cell-free ascorbate test for the surface reactivity or, more precisely, oxidative potency (Ox(Pot),) of particles. RESULTS: For six types of CDNPs with widely varying particle diameter (10-50 nm), organic content (OC; 1-20%), and specific Brunauer, Emmett, and Teller (BET) surface area (43-800 m(2)/g), Ox(Pot) correlated strongly with the in vivo inflammatory response (pulmonary polymorphonuclear neutrophil influx 24 hr after intratracheal particle instillation). However, for CDNPs with high organic content, Ox(Pot) could not explain the observed inflammatory response, possibly due to shielding of the Ox(Pot) of the carbon core of CDNPs by an organic coating. On the other hand, a pathway-specific gene expression screen indicated that, for particles rich in polycyclic aromatic hydrocarbon (PAHs), cytochrome P450 1A1 (CYP1A1) enzyme-mediated biotransformation of bioavailable organics may generate oxidative stress and thus enhance the in vivo inflammatory response. CONCLUSION: The compensatory nature of both effects (shielding of carbon core and biotransformation of PAHs) results in a good correlation between inflammatory response and BET surface area for all CDNPs. Hence, the in vivo inflammatory response can either be predicted by BET surface area or by a simple quantitative model, based on in vitro Ox(Pot) and Cyp1a1 induction.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter air pollution; BET; biotransformation; carbonaceous particles; Cyp1a1; dose response; nanoparticles; nanotoxicity; organic compounds; oxidative stress; particle toxicity; soot particles; specific surface area; surface toxicity; ultrafine particles; diesel exhaust particles; airway epithelial-cells; ultrafine particles; surface-area; inflammatory response; aromatic-hydrocarbons; cytochrome-p450 1a1; gene-expression; stress; exposure; DIESEL EXHAUST PARTICLES; AIRWAY EPITHELIAL-CELLS; ULTRAFINE PARTICLES; SURFACE-AREA; INFLAMMATORY RESPONSE; AROMATIC-HYDROCARBONS; CYTOCHROME-P450 1A1; GENE-EXPRESSION; STRESS; EXPOSURE
Sprache englisch
Veröffentlichungsjahr 2009
HGF-Berichtsjahr 2009
ISSN (print) / ISBN 0091-6765
e-ISSN 1552-9924
Zeitschrift Environmental Health Perspectives
Quellenangaben Band: 117, Heft: 1, Seiten: 54-60 Artikelnummer: , Supplement: ,
Verlag Research Triangle Park
Verlagsort NC [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Lung Health and Immunity (LHI)
POF Topic(s) 30202 - Environmental Health
Forschungsfeld(er) Lung Research
PSP-Element(e) G-505000-001
G-505000-002
G-505000-004
DOI 10.1289/ehp.11370
WOS ID 000262483900029
Scopus ID 60749103918
PubMed ID 19165387
Erfassungsdatum 2009-07-09
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