2. Academic Validation
  3. Realistic Nanoplastics Induced Pulmonary Damage via the Crosstalk of Ferritinophagy and Mitochondrial Dysfunction

Realistic Nanoplastics Induced Pulmonary Damage via the Crosstalk of Ferritinophagy and Mitochondrial Dysfunction

  • ACS Nano. 2024 Jul 2;18(26):16790-16807. doi: 10.1021/acsnano.4c02335.
Yunxia Ji 1 2,  Libang Chen 1,  Yunqing Wang 3,  Jinjin Zhang 2,  Yue Yu 1,  Meirong Wang 1,  Xiaoyan Wang 1,  Weili Liu 2,  Bing Yan 4,  Liang Xiao 5,  Xiaodong Song 1,  Changjun Lv 2,  Lingxin Chen 1 3 6
Affiliations

Affiliations

  • 1 Department of Cellular and Genetic Medicine, School of Pharmaceutical Sciences, Binzhou Medical University, Yantai 264003, China.
  • 2 Department of Respiratory and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou Medical University, Binzhou 256603, China.
  • 3 Key Laboratory of Coastal Environmental Processes and Ecological Remediation, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, Yantai 264003, China.
  • 4 Institute of Environmental Research at the Greater Bay Area, Key Laboratory for Water Quality and Conservation of the Pearl River Delta, Ministry of Education, Guangzhou University, Guangzhou 510006, China.
  • 5 Faculty of Naval Medicine, Naval Medical University (Second Military Medical University), Shanghai 200433, China.
  • 6 Laboratory for Marine Biology and Biotechnology, Qingdao Marine Science and Technology Center, Qingdao 266237, China.
PMID: 38869479 DOI: 10.1021/acsnano.4c02335
Abstract

The smaller size fraction of plastics may be more substantially existing and detrimental than larger-sized particles. However, reports on nanoplastics (NPs), especially their airborne occurrences and potential health hazards to the respiratory system, are scarce. Previous studies limit the understanding of their real respiratory effects, since sphere-type polystyrene (PS) nanoparticles differ from NPs occurring in nature with respect to their physicochemical properties. Here, we employ a mechanical breakdown method, producing NPs directly from bulk plastic, preserving NP properties in nature. We report that among four relatively high abundance NP Materials PS, polyethylene terephthalate (PET), polyvinyl chloride (PVC), and polyethylene (PE) with a size of 100 nm, PVC induced slightly more severe lung toxicity profiles compared to the other plastics. The lung cytotoxicity of NPs is higher than that of commercial PS NPs and comparable to natural particles silicon dioxide (SiO2) and anatase titanium dioxide (TiO2). Mechanistically, BH3-interacting domain death agonist (Bid) transactivation-mediated mitochondrial dysfunction and nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy or Ferroptosis are likely common mechanisms of NPs regardless of their chemical composition. This study provides relatively comprehensive data for evaluating the risk of atmospheric NPs to lung health.

Keywords

ferritinophagy; ferroptosis; mitochondrial damage; nanoplastic; pulmonary toxicity.

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