Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/140313
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dc.contributor.authorWu, Zhuoranen_US
dc.contributor.authorYang, Haiboen_US
dc.contributor.authorArchana, Gautamen_US
dc.contributor.authorRakshit, Moumitaen_US
dc.contributor.authorNg, Kee Woeien_US
dc.contributor.authorTay, Chor Yongen_US
dc.date.accessioned2020-05-28T02:42:57Z-
dc.date.available2020-05-28T02:42:57Z-
dc.date.issued2018-
dc.identifier.citationWu, Z., Yang, H., Archana, G., Rakshit, M., Ng, K. W., & Tay, C. Y. (2018). Human keratinocytes adapt to ZnO nanoparticles induced toxicity via complex paracrine crosstalk and Nrf2-proteasomal signal transduction. Nanotoxicology, 12(10), 1215-1229. doi:10.1080/17435390.2018.1537409en_US
dc.identifier.issn1743-5390en_US
dc.identifier.urihttps://hdl.handle.net/10356/140313-
dc.description.abstractZinc oxide nanoparticles (Nano-ZnO) is currently one of the most extensively used inorganic particles in a wide range of skin care and consumable products. Therefore, examining the biological effects of Nano-ZnO, especially in the non-cytotoxic levels, thus holds important contemporary practical implications. Herein, our study demonstrates that long-term conditioning of human keratinocytes (HaCaTs) to non-cytoxic dose of Nano-ZnO (∼100 nm) can induce an adaptive response, leading to an enhancement of the cells tolerance against cytotoxic level of Nano-ZnO. It was found that the Nano-ZnO induced adaptive alteration is mediated by a strong synergism between the generation of reactive oxygen species (ROS) flares by a sub-population of cells that are loaded with Nano-ZnO and upregulation of several pro-inflammatory transcripts. Further studies revealed activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf-2) stress response pathway and the associated downstream sustained augmented level of chymotrypsin-like 20 s proteasome activity to be the major mechanism underpinning this phenomenon. Interestingly, these cytoprotective responses can further aid the Nano-ZnO conditioned HaCaT cells to cross-adapt to harmful effects of ultraviolet-A (UVA) by reducing radiation-induced DNA damage. Our findings have unveiled a range of previously undocumented potent and exploitable bioeffects of Nano-ZnO induced ROS mediated signaling within the framework of nano-adaptation.en_US
dc.description.sponsorshipMOE (Min. of Education, S’pore)en_US
dc.language.isoenen_US
dc.relation.ispartofNanotoxicologyen_US
dc.rights@ 2018 Informa UK Limited, trading as Taylor & Francis Group. All rights reserved.en_US
dc.subjectEngineering::Materialsen_US
dc.titleHuman keratinocytes adapt to ZnO nanoparticles induced toxicity via complex paracrine crosstalk and Nrf2-proteasomal signal transductionen_US
dc.typeJournal Articleen
dc.contributor.schoolSchool of Materials Science & Engineeringen_US
dc.contributor.schoolSchool of Biological Sciencesen_US
dc.identifier.doi10.1080/17435390.2018.1537409-
dc.identifier.pmid30428752-
dc.identifier.scopus2-s2.0-85057533336-
dc.identifier.issue10en_US
dc.identifier.volume12en_US
dc.identifier.spage1215en_US
dc.identifier.epage1229en_US
dc.subject.keywordsZinc Oxide Nanoparticlesen_US
dc.subject.keywordsReactive Oxygen Speciesen_US
item.fulltextNo Fulltext-
item.grantfulltextnone-
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