Oxidized Carbon Black Nanoparticles Induce Endothelial Damage Through C-X-C Chemokine Receptor 3-Mediated Pathway

Details

• Personal Author:
  Amedro J ; Bitounis D ; Demokritou P ; Erdely A ; Hasan Mazumder MH ; Hussain S ; Kelley EE ; Khramtsov VV ; Kodali VK ; Majumder N ; Nurkiewicz T ; Velayutham M
• Description:
  Oxidation of engineered nanomaterials during application in various industrial sectors can alter their toxicity. Oxidized nanomaterials also have widespread industrial and biomedical applications. In this study, we evaluated the cardiopulmonary hazard posed by these nanomaterials using oxidized carbon black (CB) nanoparticles (CBox) as a model particle. Particle surface chemistry was characterized by X-ray photo electron spectroscopy (XPS) and Fourier-transform infrared spectroscopy (FTIR). Colloidal characterization and in vitro dosimetry modeling (particle kinetics, fate and transport modeling) were performed. Lung inflammation was assessed following oropharyngeal aspiration of CB or oxidized CBox particles (20 µg per mouse) in C57BL/6J mice. Toxicity and functional assays were also performed on murine macrophage (RAW 264.7) and endothelial cell lines (C166) with and without pharmacological inhibitors. Oxidant generation was assessed by electron paramagnetic resonance spectroscopy (EPR) and via flow cytometry. Endothelial toxicity was evaluated by quantifying pro-inflammatory mRNA expression, monolayer permeability, and wound closure. XPS and FTIR spectra indicated surface modifications, the appearance of new functionalities, and greater oxidative potential (both acellular and in vitro) of CBox particles. Treatment with CBox demonstrated greater in vivo inflammatory potentials (lavage neutrophil counts, secreted cytokine, and lung tissue mRNA expression) and air-blood barrier disruption (lavage proteins). Oxidant-dependent pro-inflammatory signaling in macrophages led to the production of CXCR3 ligands (CXCL9,10,11). Conditioned medium from CBox-treated macrophages induced significant elevation in endothelial cell pro-inflammatory mRNA expression, enhanced monolayer permeability and impairment of scratch healing in CXCR3 dependent manner. In summary, this study mechanistically demonstrated an increased biological potency of CBox particles and established the role of macrophage-released chemical mediators in endothelial damage. [Description provided by NIOSH]
• Subjects:
  Blood Laboratories Lung Macrophages Occupational Health Ozone Respiratory System Safety Spectrum Analysis
• Keywords:
  Author Keywords: Nanoparticle Carbon Black Carbon Black Electron Paramagnetic Spectroscopy Endothelial Cells Infrared Spectroscopy Laboratory Animals Lung Function Macrophage Nanomaterials Nanoparticles Oxidation Oxidized Carbon Black Spectrographic Analysis

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• ISSN:
  2213-2317
• Document Type:
  Text
• Genre:
  Journal Article
• Place as Subject:
  Massachusetts ; OSHA Region 1 ; OSHA Region 3 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  47
• NIOSHTIC Number:
  nn:20063751
• Citation:
  Redox Biol 2021 Nov; 47:102161
• Contact Point Address:
  Salik Hussain, Department of Physiology and Pharmacology, School of Medicine, 64 Medical Center Drive. Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26506-9229, USA
• Email:
  salik.hussain@hsc.wvu.edu
• CAS Registry Number:
  Carbon black (CAS RN 1333-86-4)
• Federal Fiscal Year:
  2022
• NORA Priority Area:
  Construction ; Manufacturing
• Peer Reviewed:
  True
• Source Full Name:
  Redox Biology
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:99f577e6525342a6342b52fd58e176d650796bc940c1cedbf94753cf28d2691299e702f30e2ab45c260c19c3c05f6838a543bde316a1dd99694ccd0295befa23
• Download URL:
  https://stacks.cdc.gov/view/cdc/222307/cdc_222307_DS1.pdf
• File Type:
  [PDF - 7.85 MB ]