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

Show simple item record

dc.contributor.author Persaud, Indushekhar
dc.contributor.author Raghavendra, Achyut J.
dc.contributor.author Paruthi, Archini
dc.contributor.author Alsaleh, Nasser B.
dc.contributor.author Minarchick, Valerie C.
dc.contributor.author Roede, James R.
dc.contributor.author Podila, Ramakrishna
dc.contributor.author Brown, Jared M.,
dc.date.accessioned 2019-10-11T07:26:59Z
dc.date.available 2019-10-11T07:26:59Z
dc.date.issued 2019-09
dc.identifier.citation Persaud, Indushekhar; Raghavendra, Achyut J.; Paruthi, Archini; Alsaleh, Nasser B.; Minarchick, Valerie C.; Roede, James R.; Podila, Ramakrishna and Brown, Jared M.,"Defect-induced electronic states amplify the cellular toxicity of ZnO nanoparticles", Nanotoxicology, DOI: 10.1080/17435390.2019.1668067, pp. 1-17, Sep. 2019. en_US
dc.identifier.issn 1743-5390
dc.identifier.issn 1743-5404
dc.identifier.uri http://dx.doi.org/10.1080/17435390.2019.1668067
dc.identifier.uri https://repository.iitgn.ac.in/handle/123456789/4876
dc.description.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.
dc.description.statementofresponsibility by Indushekhar Persaud, Achyut J. Raghavendra, Archini Paruthi, Nasser B. Alsaleh, Valerie C. Minarchick, James R. Roede, Ramakrishna Podila and Jared M. Brown
dc.language.iso en_US en_US
dc.publisher Taylor & Francis en_US
dc.subject Nanotoxicity en_US
dc.subject defects en_US
dc.subject electronic states en_US
dc.subject zinc oxide en_US
dc.subject endothelial cell en_US
dc.title Defect-induced electronic states amplify the cellular toxicity of ZnO nanoparticles en_US
dc.type Article en_US
dc.relation.journal Nanotoxicology


Files in this item

Files Size Format View

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record

Search Digital Repository


Browse

My Account