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. 2020 Jan 31;10:1617. doi: 10.1038/s41598-020-58526-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic of the uptake and the general toxicity mechanism of ZnO NPs. The NPs may be taken up by the cells by active internalization or endocytosis-free mechanisms (the uptake may also dependent on the cell type involved). NP uptake by energy-dependent processes are confined in vesicular structures, endosomes, and finally in lysosomes. The acidic lysosomal pH may trigger enhanced release of the relatively toxic ions, which may subsequently result in elevated ROS levels thereby inducing apoptosis, DNA and membrane damage, and other toxic responses. The limited uptake and ion release by endocytosis-free mechanisms may be responsible for the manifestation of only a small part of the overall toxic responses (modified from Sabella et al., 2014, Published by The Royal Society of Chemistry⁷⁶).