Evidence map›Paper›PMID 20639441›Full record

ArticleAmerican journal of respiratory and critical care medicine2010

Alveolar epithelial cell injury due to zinc oxide nanoparticle exposure.

Yong Ho Kim, Farnoosh Fazlollahi, Ian M Kennedy, Nazanin R Yacobi, Sarah F Hamm-Alvarez, Zea Borok, Kwang-Jin Kim, Edward D Crandall

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Zinc Toxicity: Understanding the Limits.Molecules (Basel, Switzerland) · 2024
    Review
  6. Review
  7. Article
  8. Review
  9. Journal of microbiology and biotechnology · 2023
    Article
  10. A multiplex inhalation platform to modelFrontiers in pharmacology · 2023
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Alveolar epithelial cell processing of nanoparticles activates autophagy and lysosomal exocytosis.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  19. Article
  20. Mitochondrial Dysfunction in Pulmonary Fibrosis.Annals of the American Thoracic Society · 2017
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Yong Ho KimWill Rogers Institute Pulmonary Research Center, University of Southern California, Los Angeles, California, USA.
Farnoosh Fazlollahi
Ian M Kennedy
Nazanin R Yacobi
Sarah F Hamm-Alvarez
Zea Borok
Kwang-Jin Kim
Edward D Crandall
University of Southern California · USUniversity of California, Davis · US

Funding

Research Supplements to Promote DiversityR01EY011386 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HAMM-ALVAREZ, SARAH F · 1996 to 2025
$9.3M
ABSORPTION MECHANISMS FOR PEPTIDE/PROTEIN DRUGS VIA LUNGR01HL064365 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CRANDALL, EDWARD DAVID · 1999 to 2008
$6.3M
Role of ATI cells in alveolar epithelial ion transportR01HL038621 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI CRANDALL, EDWARD DAVID · 1986 to 2010
$3.2M
Role of FoxP2 in AEC (trans)differentiationR01HL062569 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BOROK, ZEA · 2000 to 2008
$2.8M
Molecular programming of AEC differentiation: role of forkhead factorsR37HL062569 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BOROK, ZEA · 2010 to 2014
$2.2M
Nanoparticle properties and alveolar epithelial barrier/transport functionsR01ES017034 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CRANDALL, EDWARD DAVID · 2009 to 2013
$1.8M
REGULATION OF ALVEOLAR EPITHELIAL CELL DIFFERENTIATIONR01HL038578 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI BOROK, ZEA · 1986 to 2007
$1.7M
Alveolar epithelial-mesenchymal transition (EMT) in pulmonary fibrosisR01HL089445 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BOROK, ZEA · 2008 to 2011
$1.6M
Interactions of engineered nanomaterials with lung alveolar epitheliumRC2ES018782 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CRANDALL, EDWARD DAVID · 2009 to 2010
$800k
LUNG EPITHELIAL TRANSPORT PROPERTIES AND ALVEOLAR EDEMAR37HL038578 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI CRANDALL, EDWARD DAVID · 1987 to 1996
–
NEI NIH HHS EY011386NEI NIH HHS EY017923NHLBI NIH HHS HL038578NHLBI NIH HHS HL038621NHLBI NIH HHS HL062569NHLBI NIH HHS HL064365NHLBI NIH HHS HL089445NIEHS NIH HHS ES017034NIEHS NIH HHS ES018782NIEHS NIH HHS R01 ES017034
6 · The paper itself

Abstract

rationaleAlthough inhalation of zinc oxide (ZnO) nanoparticles (NPs) is known to cause systemic disease (i.e., metal fume fever), little is known about mechanisms underlying injury to alveolar epithelium.

objectivesInvestigate ZnO NP-induced injury to alveolar epithelium by exposing primary cultured rat alveolar epithelial cell monolayers (RAECMs) to ZnO NPs.

methodsRAECMs were exposed apically to ZnO NPs or, in some experiments, to culture fluid containing ZnCl₂ or free Zn released from ZnO NPs. Transepithelial electrical resistance (R(T)) and equivalent short-circuit current (I(EQ)) were assessed as functions of concentration and time. Morphologic changes, lactate dehydrogenase release, cell membrane integrity, intracellular reactive oxygen species (ROS), and mitochondrial activity were measured. MEASUREMENTS AND MAIN

resultsApical exposure to 176 μg/ml ZnO NPs decreased R(T) and I(EQ) of RAECMs by 100% over 24 hours, whereas exposure to 11 μg/ml ZnO NPs had little effect. Changes in R(T) and I(EQ) caused by 176 μg/ml ZnO NPs were irreversible. ZnO NP effects on R(T) yielded half-maximal concentrations of approximately 20 μg/ml. Apical exposure for 24 hours to 176 μg/ml ZnO NPs induced decreases in mitochondrial activity and increases in lactate dehydrogenase release, permeability to fluorescein sulfonic acid, increased intracellular ROS, and translocation of ZnO NPs from apical to basolateral fluid (most likely across injured cells and/or damaged paracellular pathways).

conclusionsZnO NPs cause severe injury to RAECMs in a dose- and time-dependent manner, mediated, at least in part, by free Zn released from ZnO NPs, mitochondrial dysfunction, and increased intracellular ROS.

Indexed as

AnimalsCell Culture TechniquesDisease Models, AnimalDose-Response Relationship, DrugElectric ImpedanceEpithelial CellsL-Lactate DehydrogenaseMaleMicroscopy, ConfocalMitochondriaNanoparticlesPulmonary AlveoliRatsRats, Sprague-DawleyReactive Oxygen SpeciesTime FactorsL-Lactate DehydrogenaseReactive Oxygen SpeciesZinc Oxide

Identifiers

PMID20639441
PMCPMC3029930
OpenAlexW2023244518

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.