In vitro assays to predict the pathogenicity of mineral fibers

Mossman, Brooke T.; Sesko, Ann

doi:10.1016/0300-483x(90)90162-a

Cited by 38 publications

(11 citation statements)

References 9 publications

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“…Both apoptosis and necrosis were observed in lung epithelial cells in culture (Buder-Hoffmann et al, 2009; Liu et al, 2010; Mossman & Sesko, 1990; Panduri et al, 2006; Shukla et al, 2009; Yuan et al, 2004), but whether these phenomena occur after exposures to asbestos fibers by inhalation is unclear. However, these in vitro models using amphibole types of asbestos (crocidolite, amosite) showed that the duration of cell signaling pathways, specifically extracellular signal-regulated kinases (ERK), regulates whether cell proliferation or death occurs.…”

Section: Mechanisms Of Action Of Asbestos In Vitromentioning

confidence: 99%

Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos

Mossman

Lippmann

Hesterberg

et al. 2011

Journal of Toxicology and Environmental Health, Part B

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164

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Lung carcinomas and pulmonary fibrosis (asbestosis) occur in asbestos workers. Understanding the pathogenesis of these diseases is complicated because of potential confounding factors, such as smoking, which is not a risk factor in mesothelioma. The modes of action (MOA) of various types of asbestos in the development of lung cancers, asbestosis, and mesotheliomas appear to be different. Moreover, asbestos fibers may act differentially at various stages of these diseases, and have different potencies as compared to other naturally occurring and synthetic fibers. This literature review describes patterns of deposition and retention of various types of asbestos and other fibers after inhalation, methods of translocation within the lung, and dissolution of various fiber types in lung compartments and cells in vitro. Comprehensive dose-response studies at fiber concentrations inhaled by humans as well as bivariate size distributions (lengths and widths), types, and sources of fibers are rarely defined in published studies and are needed. Species-specific responses may occur. Mechanistic studies have some of these limitations, but have suggested that changes in gene expression (either fiber-catalyzed directly or by cell elaboration of oxidants), epigenetic changes, and receptor-mediated or other intracellular signaling cascades may play roles in various stages of the development of lung cancers or asbestosis.

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Section: Mechanisms Of Action Of Asbestos In Vitromentioning

confidence: 99%

Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos

Mossman

Lippmann

Hesterberg

et al. 2011

Journal of Toxicology and Environmental Health, Part B

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190

164

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“…The molecular events that precede the development of mesothelioma by asbestos are unclear, but the activation of cell-signaling cascades at the plasma membrane may lead to alterations in gene expression, contributing to chronic inflammation and unregulated mesothelial cell proliferation (24,25). It is thought that a number of crucial changes are required in a population of mesothelial cells in order for them to become transformed (21).…”

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confidence: 98%

Activation of p38 MAP kinase by asbestos in rat mesothelial cells is mediated by oxidative stress

Swain

O’Byrne²,

Faux³

2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Asbestos fibers are biopersistent particles that are capable of stimulating chronic inflammatory responses in the pleura of exposed individuals. Exposure of pleural mesothelial cells, the progenitor cell of malignant mesothelioma, to asbestos induces an array of cellular responses. The present studies investigated whether the p38 mitogen-activated protein kinase cascade was induced under asbestos-exposed conditions. p38 plays a vital role in the response to stressful stimuli and enables the cell to enter an inflammatory state characterized by cytokine production. Western blot and in vitro kinase assays showed increases in dual phosphorylation and actual activity of p38 after exposure to fibrous and nonfibrous (milled) crocidolite; in contrast, polystyrene beads and iron (III) oxide had no such effects. In common with other asbestos-induced events, this was shown to be an oxidative stress-sensitive effect, inasmuch as preincubation with N-acetyl-L-cysteine or -tocopherol (vitamin E) ameliorated the effect. The present studies show that p38 activity is important for crocidolite-induced activator protein-1 DNA binding, inasmuch as an inhibitor of p38, SB-203580, reduced this activity. Crocidolite-induced cytotoxicity was also reduced with SB-203580, indicating a role for p38 in asbestos-mediated cell death. Our studies suggest that p38 activity could be a crucial factor in the chronic immune response elicited by asbestos and may represent a target for future pharmacological intervention.

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“…There are several reasons we chose to examine zeolites as model systems. Even though the exposure of zeolites to the general population is quite limited, with possibly the exception of detergents, there is a particular zeolite called erionite that is highly toxic and causes mesothelioma (13,14). Several other zeolites have also been examined for their toxicity, but none so far has paralleled the effects of erionite.…”

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Analysis of the biological and chemical reactivity of zeolite-based aluminosilicate fibers and particulates.

Fach

Waldman

Williams

et al. 2002

Environ Health Perspect

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Environmental and/or occupational exposure to minerals, metals, and fibers can cause lung diseases that may develop years after exposure to the agents. The presence of toxic fibers such as asbestos in the environment plus the continuing development of new mineral or vitreous fibers requires a better understanding of the specific physical and chemical features of fibers/particles responsible for bioactivity. Toward that goal, we have tested aluminosilicate zeolites to establish biological and chemical structure-function correlations. Zeolites have known crystal structure, are subject to experimental manipulation, and can be synthesized and controlled to produce particles of selected size and shape. Naturally occurring zeolites include forms whose biological activity is reported to range from highly pathogenic (erionite) to essentially benign (mordenite). Thus, we used naturally occurring erionite and mordenite as well as an extensively studied synthetic zeolite based on faujasite (zeolite Y). Bioactivity was evaluated using lung macrophages of rat origin (cell line NR8383). Our objective was to quantitatively determine the biological response upon interaction of the test particulates/fibers with lung macrophages and to evaluate the efficacy of surface iron on the zeolites to promote the Fenton reaction. The biological assessment included measurement of the reactive oxygen species by flow cytometry and chemiluminescence techniques upon phagocytosis of the minerals. The chemical assessment included measuring the hydroxyl radicals generated from hydrogen peroxide by iron bound to the zeolite particles and fibers (Fenton reaction). Chromatography as well as absorption spectroscopy were used to quantitate the hydroxyl radicals. We found that upon exposure to the same mass of a specific type of particulate, the oxidative burst increased with decreasing particle size, but remained relatively independent of zeolite composition. On the other hand, the Fenton reaction depended on the type of zeolite, suggesting that the surface structure of the zeolite plays an important role.

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In vitro assays to predict the pathogenicity of mineral fibers

Cited by 38 publications

References 9 publications

Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos

Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos

Activation of p38 MAP kinase by asbestos in rat mesothelial cells is mediated by oxidative stress

Analysis of the biological and chemical reactivity of zeolite-based aluminosilicate fibers and particulates.

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