Defect-induced electronic states amplify the cellular toxicity of ZnO nanoparticles
| Autor: | Archini Paruthi, Achyut J. Raghavendra, Ramakrishna Podila, Indushekhar Persaud, Valerie C. Minarchick, Nasser B. Alsaleh, Jared M. Brown, James R. Roede |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
inorganic chemicals
Cell Survival Surface Properties Biomedical Engineering Nanoparticle Apoptosis 02 engineering and technology 010501 environmental sciences Toxicology medicine.disease_cause 01 natural sciences Redox Article Cell Line mental disorders medicine Nanotoxicity Viability assay defects health care economics and organizations 0105 earth and related environmental sciences chemistry.chemical_classification Reactive oxygen species technology industry and agriculture Endothelial Cells respiratory system 021001 nanoscience & nanotechnology Endoplasmic Reticulum Stress Oxidative Stress chemistry Solubility Nanotoxicology Toxicity Unfolded protein response Biophysics endothelial cell Nanoparticles Zinc Oxide 0210 nano-technology electronic states Reactive Oxygen Species Oxidative stress |
| Zdroj: | Nanotoxicology |
| ISSN: | 1743-5404 |
| Popis: | 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. by Indushekhar Persaud, Achyut J. Raghavendra, Archini Paruthi, Nasser B. Alsaleh, Valerie C. Minarchick, James R. Roede, Ramakrishna Podila and Jared M. Brown |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|