Cultured airway epithelium responses to mineral particles: role of the oxidative stress

Guilianelli, Catherine

doi:10.1016/0378-4274(96)82677-4

Cited by 6 publications

(5 citation statements)

References 22 publications

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“…12 Hematite in micrometric size exhibits a very low toxicity in cellular and cell-free tests, if any: it does not produce free radical species in cell-free systems, 10 is not cytotoxic, and does not induce neoplastic transformation in mouse embryo cells, 21 or reactive oxygen species (ROS) generation in rabbit tracheal epithelial cells. 22,23 Moreover, intrapulmonary instillation in humans produces only transient inflammation. 24 A decrease in size, however, might cause toxicity because crystalline dust usually increases the amount of structural defects and may consequently induce modifications of some properties responsible for toxicological effects.…”

Section: ■ Introductionmentioning

confidence: 99%

“…Hematite in micrometric size exhibits a very low toxicity in cellular and cell-free tests, if any: it does not produce free radical species in cell-free systems, is not cytotoxic, and does not induce neoplastic transformation in mouse embryo cells, or reactive oxygen species (ROS) generation in rabbit tracheal epithelial cells. , Moreover, intrapulmonary instillation in humans produces only transient inflammation …”

Section: Introductionmentioning

confidence: 99%

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Hematite Nanoparticles Larger than 90 nm Show No Sign of Toxicity in Terms of Lactate Dehydrogenase Release, Nitric Oxide Generation, Apoptosis, and Comet Assay in Murine Alveolar Macrophages and Human Lung Epithelial Cells

Freyria

Bonelli

Tomatis

et al. 2012

Chem. Res. Toxicol.

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Three hematite samples were synthesized by precipitation from a FeCl₃ solution under controlled pH and temperature conditions in different morphology and dimensions: (i) microsized (average diameter 1.2 μm); (ii) submicrosized (250 nm); and (iii) nanosized (90 nm). To gain insight into reactions potentially occurring in vivo at the particle-lung interface following dust inhalation, several physicochemical features relevant to pathogenicity were measured (free radical generation in cell-free tests, metal release, and antioxidant depletion), and cellular toxicity assays on human lung epithelial cells (A549) and murine alveolar macrophages (MH-S) were carried out (LDH release, apoptosis detection, DNA damage, and nitric oxide synthesis). The decrease in particles size, from 1.2 μm to 90 nm, only caused a slight increase in structural defects (disorder of the hematite phase and the presence of surface ferrous ions) without enhancing surface reactivity or cellular responses in the concentration range between 20 and 100 μg cm⁻².

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Section: ■ Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hematite Nanoparticles Larger than 90 nm Show No Sign of Toxicity in Terms of Lactate Dehydrogenase Release, Nitric Oxide Generation, Apoptosis, and Comet Assay in Murine Alveolar Macrophages and Human Lung Epithelial Cells

Freyria

Bonelli

Tomatis

et al. 2012

Chem. Res. Toxicol.

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“…In an experiment to investigate the potential for minerals to induce lipid peroxidation in rabbit tracheal epithelial cells via the generation of reactive oxygen species, chrysotile, nemalite, and hematite (Fe 2 O 3 ) were incubated with the cells for 1 h at a concentration of 100 μg/cm 2 . 20 Chrysotile and nemalite caused lipid peroxidation, whereas Fe 2 O 3 did not. In a previous study, Guilianelli et al saw a 12% inhibition of rabbit tracheal epithelial culture growth at the concentration of 50 μg/cm 2 (Fe 2 O 3 particles of 1 μm); no inhibition of cell growth was seen at a dose of 10 μg/cm 2 , and dose−responses indicate that these observed effects on cell growth in vitro are at the threshold.…”

Section: ■ Introductionmentioning

confidence: 87%

“…To further explore the potential for iron oxides to generate ROS, there have been a number of studies investigating varying forms, both “bulk” and “nano” in cells. Guilianelli et al investigated the potential for chrysotile, nemalite, and hematite (10 μg/cm 2 ) to induce oxidative stress and the activity of superoxide dismutase and catalase in rabbit tracheal epithelial cells . While chrysotile and nemalite fibers increased the activity of superoxide dismutase, and chrysotile also increased catalase activity, hematite particulates had no effect on these antioxidant enzyme activities, indicating that Fe 2 O 3 did not induce oxidative stress.…”

Section: Potential Modes Of Action For Tumorigenicity In Ratsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Review of the Evidence from Epidemiology, Toxicology, and Lung Bioavailability on the Carcinogenicity of Inhaled Iron Oxide Particulates

Pease

Rucker

Birk

2016

Chem. Res. Toxicol.

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Since the iron-age and throughout the industrial age, humans have been exposed to iron oxides. Here, we review the evidence from epidemiology, toxicology, and lung bioavailability as to whether iron oxides are likely to act as human lung carcinogens. Current evidence suggests that observed lung tumors in rats result from a generic particle overload effect and local inflammation that is rat-specific under the dosing conditions of intratracheal instillation. This mode of action therefore, is not relevant to human exposure. However, there are emerging differences seen in vitro, in cell uptake and cell bioavailability between "bulk" iron oxides and "nano" iron oxides. "Bulk" particulates, as defined here, are those where greater than 70% are >100 nm in diameter. Similarly, "nano" iron oxides are defined in this context as particulates where the majority, usually >95% for pure engineered forms of primary particulates (not agglomerates), fall in the range 1-100 nm in diameter. From the weight of scientific evidence, "bulk" iron oxides are not genotoxic/mutagenic. Recent evidence for "nano" iron oxide is conflicting regarding genotoxic potential, albeit genotoxicity was not observed in an in vivo acute oral dose study, and "nano" iron oxides are considered safe and are being investigated for biomedical uses; there is no specific in vivo genotoxicity study on "nano" iron oxides via inhalation. Some evidence is available that suggests, hypothetically due to the larger surface area of "nano" iron oxide particulates, that toxicity could be exerted via the generation of reactive oxygen species (ROS) in the cell. However, the potential for ROS generation as a basis for explaining rodent tumorigenicity is only apparent if free iron from intracellular "nano" scale iron oxide becomes bioavailable at significant levels inside the cell. This would not be expected from "bulk" iron oxide particulates. Furthermore, human epidemiological evidence from a number of studies suggests that iron oxide is not a human carcinogen, and therefore, based upon the complete weight of evidence, we conclude that "bulk" iron oxides are not human carcinogens.

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Different cellular responses evoked by natural and stoichiometric synthetic chrysotile asbestos

Gazzano

Foresti

Lesci

et al. 2005

Toxicology and Applied Pharmacology

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Cultured airway epithelium responses to mineral particles: role of the oxidative stress

Cited by 6 publications

References 22 publications

Hematite Nanoparticles Larger than 90 nm Show No Sign of Toxicity in Terms of Lactate Dehydrogenase Release, Nitric Oxide Generation, Apoptosis, and Comet Assay in Murine Alveolar Macrophages and Human Lung Epithelial Cells

Hematite Nanoparticles Larger than 90 nm Show No Sign of Toxicity in Terms of Lactate Dehydrogenase Release, Nitric Oxide Generation, Apoptosis, and Comet Assay in Murine Alveolar Macrophages and Human Lung Epithelial Cells

Review of the Evidence from Epidemiology, Toxicology, and Lung Bioavailability on the Carcinogenicity of Inhaled Iron Oxide Particulates

Different cellular responses evoked by natural and stoichiometric synthetic chrysotile asbestos

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