Vacancies on 2D transition metal dichalcogenides elicit ferroptotic cell death

Shujuan Xu, Huizhen Zheng, Ronglin Ma, Di Wu, Yanxia Pan, Chunyang Yin, Meng Gao, Weili Wang, Wei Li, Sijin Liu, Zhifang Chai and Ruibin Li ()
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Shujuan Xu: Soochow University
Huizhen Zheng: Soochow University
Ronglin Ma: Soochow University
Di Wu: Soochow University
Yanxia Pan: Soochow University
Chunyang Yin: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences
Meng Gao: Soochow University
Weili Wang: Soochow University
Wei Li: Soochow University
Sijin Liu: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences
Zhifang Chai: Soochow University
Ruibin Li: Soochow University

Nature Communications, 2020, vol. 11, issue 1, 1-14

Abstract: Abstract Sustainable developments of nanotechnology necessitate the exploration of structure-activity relationships (SARs) at nano-bio interfaces. While ferroptosis may contribute in the developments of some severe diseases (e.g., Parkinson’s disease, stroke and tumors), the cellular pathways and nano-SARs are rarely explored in diseases elicited by nano-sized ferroptosis inducers. Here we find that WS2 and MoS2 nanosheets induce an iron-dependent cell death, ferroptosis in epithelial (BEAS-2B) and macrophage (THP-1) cells, evidenced by the suppression of glutathione peroxidase 4 (GPX4), oxygen radical generation and lipid peroxidation. Notably, nano-SAR analysis of 20 transition metal dichalcogenides (TMDs) disclosures the decisive role of surface vacancy in ferroptosis. We therefore develop methanol and sulfide passivation as safe design approaches for TMD nanosheets. These findings are validated in animal lungs by oropharyngeal aspiration of TMD nanosheets. Overall, our study highlights the key cellular events as well as nano-SARs in TMD-induced ferroptosis, which may facilitate the safe design of nanoproducts.

Date: 2020
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DOI: 10.1038/s41467-020-17300-7

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