Title

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

Creators

James R. Roede, Colorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus
Ramakrishna Podila, Clemson Nanomaterials Center and Comset, Clemson University
Valerie C. Minarchick, Colorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus
Achyut J. Raghavendra, Clemson Nanomaterials Center and Comset, Clemson University
Archini Paruthi, Materials Science and Engineering, Indian Institute of Technology
Jared M. Brown, Colorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus
Indushekhar Persaud, Colorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus
Nasser B. Alsaleh, Colorado Center for Nanomedicine and Nanosafety, Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus

Description

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.

Publication Date

1-1-2019

Publisher

figshare Academic Research System

DOI

10.6084/m9.figshare.9902369.v1

Document Type

Data Set

Recommended Citation

Roede, James R.; Podila, Ramakrishna; Minarchick, Valerie C.; Raghavendra, Achyut J.; Paruthi, Archini; Brown, Jared M.; Persaud, Indushekhar; Alsaleh, Nasser B. (2019), "Defect-induced electronic states amplify the cellular toxicity of ZnO nanoparticles", figshare Academic Research System, doi: 10.6084/m9.figshare.9902369.v1

https://doi.org/10.6084/m9.figshare.9902369.v1

Identifier

10.6084/m9.figshare.9902369.v1

Related Content

10.1080/17435390.2019.1668067

Embargo Date

1-1-2019