Variability of Biological Responses to Silicas: Effect of Origin, Crystallinity, and State of Surface on Generation of Reactive Oxygen Species and Morphological Transformation of Mammalian Cells

Fubini, Bice; Fenoglio, Ivana; Elias, Z.; Poirot, O.

doi:10.1615/jenvironpatholtoxicoloncol.v20.isuppl.1.90

Cited by 52 publications

(59 citation statements)

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“…The Fenton process can be inhibited by the iron chelator desferrioxamineeral, and the ability of fractured silica to produce HO • decreases with time (20 hour half-life) [67]. It is believed that silica contaminated with iron is more cytotoxic than uncontaminated silica [78] because of the significant increase in hydroxyl radicals [79].…”

Section: Particle-derived Free Radicalsmentioning

confidence: 99%

“…In studies with artificial crystalline silica, the amount of exposed surface and size/shape of the particle also influenced cytotoxic potential [80]. Evidence strongly suggests that silica-derived ROS is directly responsible for in vitro DNA damage [81][82][83], various morphological changes including apoptosis in in vitro cell cultures [79,84,85], and acute lung damage in vivo [71]. The DNA damage is caused primarily by the hydroxyl radical, which is the by-product of iron contaminated silica [86].…”

Section: Particle-derived Free Radicalsmentioning

confidence: 99%

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Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

341

242

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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 researchers looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage (AM) interacts with the inhaled silica particle and the consequences of silicainduced toxicity on the cellular level. Based on experimental results, several rationales have been developed on 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 (RNS) are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, where 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 is 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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Section: Particle-derived Free Radicalsmentioning

confidence: 99%

Section: Particle-derived Free Radicalsmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

341

242

View full text Add to dashboard Cite

show abstract

“…15,20 EPR spectra were recorded at room temperature on a Miniscope 100 X band EPR spectrometer (Magnettech, Berlin, Germany) at a microwave power level of 10 mW, scan range of 120 G, and modulation amplitude of 1 G. The number of radicals 8 released is proportional to the intensity of the EPR signal after double integration. Kinetics of free radical yield was followed for at least one hour.…”

Section: Free Radical Detectionmentioning

confidence: 99%

Carbon in Intimate Contact with Quartz Reduces the Biological Activity of Crystalline Silica Dusts

Ghiazza

Tomatis

Doublier

et al. 2012

Chem. Res. Toxicol.

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In order to evaluate the effect of carbonaceous materials on the pathogenic activity of quartz dusts, mixtures of carbon soot (1% and 10%) and quartz (Min-U-Sil ) have been prepared, then milled so to attain an intimate association of carbon and the quartz surface. Both cellular and cell-free tests show that carbon associated to quartz completely inhibits the typical free radical generation of quartz dusts (through Fenton activity and homolytic cleavage of a C-H bond) and suppresses the oxidative stress and inflammation induced by quartz alone on MH-S murine macrophage cells (lipid peroxidation, nitric oxide release, tumour necrosis factor-α synthesis). Cytotoxic response to quartz is also largely reduced. An extremely pure quartz milled with 10% of soot showed inactivating effects on the adverse reactions to quartz similar to Min-U-Sil quartz. None of these effects takes place when the same experiments are carried out with mechanically mixed samples, which suggests that carbon acts not just as a radical quencher, but because of its association to the quartz surface.4

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“…Intratracheal instillation of α-quartz (Min-U-Sil 5) in rats induced apoptosis in both alveolar and granulomatous cells (Leigh et al, 1997). The ability of crystalline silica to induce pulmonary injury depends not only on length and amount of exposure but also from the type of quartz used (source, presence of metal impurity, particle size) and from the preparation modality (fresh or aged), which infl uences the biological activity (Donaldson and Borm 1998;Fubini et al, 2001;Schins et al, 2002;Seiler et al, 2004). The biological eff ects of crystalline silica are principally related to surface characteristics and reactivity, which determine the toxicological, oxidant and genotoxic properties of crystalline silica.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of cytotoxic concentration–time response in A549 cells exposed to respirable α‐quartz

Fanizza¹,

Fresegna

Maiello

et al. 2009

J of Applied Toxicology

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A causal pathway between quartz, silicosis and lung cancer has been postulated. The aim of our study was to assess cytotoxic effects induced in a human lung epithelial cell line (A549) by exposure to alpha-quartz. Cells were exposed to respirable alpha-quartz (SRM1878a, NIST) at 25, 50 or 100 microg ml(-1 )for 24 h and at 50 or 100 microg ml(-1) for 48 h. Cytotoxic effects were analyzed by scanning electron microscopy (SEM), apoptotic morphology analysis with Hoechst staining and lactate dehydrogenase (LDH) release assay. In cells exposed to alpha-quartz for 24 h, a concentration-dependent bleb development and in particular the localization of blebs at the cell edge at higher concentrations were observed. The blebbing phenomenon was more evident after 48 h of exposure to 50 or to 100 microg ml(-1) of alpha-quartz and large blebs were localized at the cell edge. At the same concentrations surface smoothing was also observed. Moreover the presence of holes and tears was detected at the highest concentration both at 24 and 48 h. Results of morphological analysis with Hoechst stain evidenced an increase concentration-time dependent of apoptotic cell percentage that was more marked after 48 h exposure to 100 microg ml(-1) and a prevalence of late apoptosis stage with the increase of exposure time and concentration. Cells exposed to 50 or 100 microg ml(-1) of alpha-quartz for 24 and 48 h produced a significant increase in LDH release. The concentration-time-dependent bleb induction evidenced by SEM correlates with the increase of apoptotic cells and LDH activity release, demonstrating the onset of cytotoxic effects in human lung cells exposed to alpha-quartz.

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Variability of Biological Responses to Silicas: Effect of Origin, Crystallinity, and State of Surface on Generation of Reactive Oxygen Species and Morphological Transformation of Mammalian Cells

Cited by 52 publications

References 0 publications

Silica binding and toxicity in alveolar macrophages

Silica binding and toxicity in alveolar macrophages

Carbon in Intimate Contact with Quartz Reduces the Biological Activity of Crystalline Silica Dusts

Evaluation of cytotoxic concentration–time response in A549 cells exposed to respirable α‐quartz

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