Evidence map›Paper›PMID 31553248›Full record

ArticleNanotoxicology2020

Defect-induced electronic states amplify the cellular toxicity of ZnO nanoparticles.

Indushekhar Persaud, Achyut J Raghavendra, Archini Paruthi, Nasser B Alsaleh, Valerie C Minarchick, James R Roede, Ramakrishna Podila, Jared M Brown

Abstract read
In one paragraph

Article in Nanotoxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
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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.

Indushekhar PersaudColorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Achyut J RaghavendraDepartment of Physics and Astronomy, Clemson University, Clemson, SC, USA.
Archini ParuthiColorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Nasser B AlsalehColorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Valerie C MinarchickColorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
James R RoedeColorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Ramakrishna PodilaDepartment of Physics and Astronomy, Clemson University, Clemson, SC, USA.
Jared M BrownColorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Funding

Mechanisms of non-IgE Mast Cell Activation by Environmental ParticulatesR01ES019311 · NIEHS · UNIVERSITY OF COLORADO DENVER · PI BROWN, JARED MICHAEL · 2010 to 2024
$7.0M
NIEHS NIH HHS R01 ES019311
6 · The paper itself

Abstract

Zinc oxide nanoparticles (ZnO NPs) are used in numerous applications, including sunscreens, cosmetics, textiles, and electrical devices. Increased consumer and occupational exposure to ZnO NPs potentially poses a risk for toxicity. While many studies have examined the toxicity of ZnO NPs, little is known regarding the toxicological impact of inherent defects arising from batch-to-batch variations. It was hypothesized that the presence of varying chemical defects in ZnO NPs will contribute to cellular toxicity in rat aortic endothelial cells (RAECs). Pristine and defected ZnO NPs (oxidized, reduced, and annealed) were prepared and assessed three major cellular outcomes; cytotoxicity/apoptosis, reactive oxygen species production and oxidative stress, and endoplasmic reticulum (ER) stress. ZnO NPs chemical defects were confirmed by X-ray photoelectron spectroscopy and photoluminescence. Increased toxicity was observed in defected ZnO NPs compared to the pristine NPs as measured by cell viability, ER stress, and glutathione redox potential. It was determined that ZnO NPs induced ER stress through the PERK pathway. Taken together, these results demonstrate a previously unrecognized contribution of chemical defects to the toxicity of ZnO NPs, which should be considered in the risk assessment of engineered nanomaterials.

Indexed as

ApoptosisCell LineCell SurvivalEndoplasmic Reticulum StressEndothelial CellsNanoparticlesOxidative StressReactive Oxygen SpeciesSolubilitySurface PropertiesZinc OxideReactive Oxygen SpeciesZinc Oxidedefectselectronic statesendothelial cellNanotoxicityzinc oxide

Identifiers

PMID31553248
PMCPMC7036006

What OpenQuestion holds

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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.