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Iron-bearing nanoparticles trigger human umbilical vein endothelial cells ferroptotic responses by promoting intracellular iron level.

Authors
  • Liu, Zixuan1
  • Xia, Xiaomin1
  • Lv, Xuying1
  • Song, Erqun1
  • Song, Yang2
  • 1 Key Laboratory of Luminescence Analysis and Molecular Sensing, Ministry of Education, College of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, China. , (China)
  • 2 Key Laboratory of Luminescence Analysis and Molecular Sensing, Ministry of Education, College of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, China; State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, 100085, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Environmental pollution (Barking, Essex : 1987)
Publication Date
Oct 15, 2021
Volume
287
Pages
117345–117345
Identifiers
DOI: 10.1016/j.envpol.2021.117345
PMID: 34004477
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Iron-bearing nanoparticles (IBNPs) were abundant in particulate matter (PM). Due to their high reactivity, IBNPs were considered hazardous to human health, however, their toxic mode-of-action(s) are highly unclear. Ferroptosis is a novel programmed cell death (PCD) that highly associated with intracellular iron. However, the pro-ferroptotic effect of IBNPs has not been characterized. To this end, we ought to investigate whether and how IBNPs (synthetic γ-Fe2O3 and Fe3O4 NPs were selected as the model compounds) are involved in ferroptosis. We found that human umbilical vein endothelial cells (HUVECs) phagocytized large qualities of γ-Fe2O3 and Fe3O4 NPs, resulting in increased intracellular iron level. We further observed the disrupted cystine/glutamate reverse transporter (System Xc-) and glutathione peroxidase 4 (GPX4) signaling in γ-Fe2O3 and Fe3O4 NPs-challenged HUVECs. γ-Fe2O3 and Fe3O4 NPs could also cause mitochondrial fusion and fission dysregulation, activate lipid peroxidation and iron metabolism-related genes in a P53-dependent manner. Together, the ferroptotic activity of IBNPs should be acknowledged for the risk assessment of PM associated health effects. Copyright © 2021 Elsevier Ltd. All rights reserved.

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