Cited by 415Occupational and environmental lung diseasesInterstitial Lung Diseases and Idiopathic Pulmonary FibrosisSarcoidosis and Beryllium Toxicity Research

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Silica binding and toxicity in alveolar macrophages

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Hamilton, Raymond F., Thakur, Sheetal A., Holian, Andrij·2008·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2007.12.027PMC PMC2680955

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Abstract

Inhalation of the crystalline form of silica is associated with a variety of pathologies, from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer. Basic science investigators looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage interacts with the inhaled silica particle and the consequences of silica-induced toxicity on the cellular level. Based on experimental results, several rationales have been developed for exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle. For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica), triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, by which silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis are described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

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Retracted
Association Analysis Identifies New Risk Loci for Coal Workers’ Pneumoconiosis in Han Chinese Men
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Authors: Hamilton, R. F., Thakur, S. A., & Holian, A.
Affiliations: University of Montana (US)
Corresponding author: Holian, Andrij
ORCID: Hamilton, Raymond F.
Holian, Andrij
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 2008-04
Volume: 44
Issue: 7
Pages: 1246-1258
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/j.freeradbiomed.2007.12.027
PMC: PMC2680955
OpenAlex: W2044353844
Cited by: 415
References: 124
Citations by year: 2026: 19 · 2025: 16 · 2024: 25 · 2023: 33 · 2022: 32 · 2021: 33 · 2020: 23 · 2019: 21 · 2018: 24 · 2017: 22 · 2016: 23 · 2015: 16 · 2014: 19 · 2013: 23 · 2012: 18
FWCI: 2.11
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of General Medical Sciences (P30GM103338)
National Institute of Environmental Health Sciences (R01ES015294, ES-015294)
National Center for Research Resources (P20RR017670)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Occupational and environmental lung diseases
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Sarcoidosis and Beryllium Toxicity Research
Keywords: crystalline silica, silica toxicity, alveolar macrophages, reactive oxygen species, reactive nitrogen species, respiratory burst, cytokine production, apoptosis, scavenger receptors, silicosis, particle clearance
MeSH terms: Animals, Free Radicals, Humans, Lung, Lysosomes, Macrophages, Models, Biological, Protein Binding, Silicon Dioxide, Surface-Active Agents, Signal Transduction, Macrophages, Alveolar, Apoptosis, Reactive Nitrogen Species, Mice

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Silica binding and toxicity in alveolar macrophages

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