The chemical properties of silica particle surface in relation to silica‐cell interactions

Xl, Shi; Ns, Dalal; Hu, Xin; Vallyathan,

doi:10.1080/15287398909531314

Cited by 49 publications

(21 citation statements)

References 71 publications

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“…This hypothesis is supported by the study showing that the silanol groups form hydrogen bonds with some sites on the cell membrane (Shi et al, 1989). Such hydrogen bonding could facilitate the process of phagocytosis.…”

Section: Discussionsupporting

confidence: 71%

Acute Pulmonary Toxicity Caused by Exposure to Colloidal Silica: Particle Size Dependent Pathological Changes in Mice

et al. 2005

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To compare the pulmonary toxicity between ultrafine colloidal silica particles (UFCSs) and fine colloidal silica particles (FCSs), mice were intratracheally instilled with 3 mg of 14 nm UFCSs and 230 nm FCSs and pathologically examined from 30 minutes to 24 hour postexposure. Histopathologically, lungs exposed to both sizes of particles showed bronchiolar degeneration and necrosis, neutrophilic inflammation in alveoli with alveolar type II cell swelling and particle-laden alveolar macrophage accumulation. UFCSs, however, induced extensive alveolar hemorrhage compared to FCSs from 30 minutes onwards. UFCSs also caused more severe bronchiolar epithelial cell necrosis and neutrophil influx in alveoli than FCSs at 12 and 24 hours postexposure. Laminin positive immunolabellings in basement membranes of bronchioles and alveoli of UFCSs treated animals was weaker than those of FCSs-treated animals in all observation times. Electron microscopy demonstrated UFCSs and FCSs on bronchiolar and alveolar wall surface as well as in the cytoplasm of alveolar epithelial cells, alveolar macrophages and neutrophils. Type I alveolar epithelial cell erosion with basement membrane damage in UFCSs treated animals was more severe than those in FCSs-treated animals. At 12 and 24 hours postexposure, bronchiolar epithelial cells in UFCSs-treated animals showed more intense vacuolation and necrosis compared to FCSs-treated animals. These findings suggest that UFCSs have greater ability to induce lung inflammation and tissue damages than FCSs.

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Section: Discussionsupporting

confidence: 71%

Acute Pulmonary Toxicity Caused by Exposure to Colloidal Silica: Particle Size Dependent Pathological Changes in Mice

et al. 2005

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“…SOD, catalase, and the *OH scavenger sodium benzoate all efficiently inhibit lipid peroxidation, supporting the role of oxygen radicals in silicainduced lipid peroxidation. This finding is particularly interesting since membrane damage via silica-induced lipid peroxidation is considered to be a primary step in the pathogenesis of silicosis (4).…”

Section: Discussionmentioning

confidence: 99%

“…Based on the results reported here and those in the literature (4,11) H202 is thought to be generated by reaction of H20 with silicon-based radicals (5,19) and/or by Op-related reactions involving surface metal oxidation (11,23 …”

Section: Discussionmentioning

confidence: 99%

“…Thus, consider-able effort is currently devoted to understanding the mechanism whereby silica particles disrupt the cell membrane. Earlier studies (4)(5)(6)(7) have suggested that the silicon-based free radicals (Si, SO, and SiOO ) on the surface of freshly fractured silica and the associated generation of H202 and hydroxyl radicals ("OH) might be directly or indirectly involved in the mechanism of lipid peroxidation, leading to the loss of membrane integrity and eventual pulmonary fibrosis.…”

Section: Introductionmentioning

confidence: 99%

“…Indeed it is not known whether damage to DNA plays a role in the carcinogenesis process. It is thought that one event of primary importance is the perturbation of cell membranes due to silica particle interactions (2,4). This cell membrane damage releases certain lytic enzymes that cause additional cell injury and eventual fibrosis (2).…”

Section: Introductionmentioning

confidence: 99%

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Silica Radical-Induced DNA Damage and Lipid Peroxidation

Shi¹,

Mao²,

Daniel³

et al. 1994

Environmental Health Perspectives

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In recent years, more attention has been given to the mechanism of disease induction caused by the surface properties of minerals. In this respect, specific research needs to be focused on the biologic interactions of oxygen radicals generated by mineral particles resulting in cell injury and DNA damage leading to fibrogenesis and carcinogenesis. In this investigation, we used electron spin resonance (ESR) and spin trapping to study oxygen radical generation from aqueous suspensions of freshly fractured crystalline silica. Hydroxyl radical (0OH), superoxide radical (02-) and singlet oxygen (102) were all detected. Superoxide dismutase (SOD) partially inhibited *OH yield, whereas catalase abolished 0OH generation. H202 enhanced 0OH generation while deferoxamine inhibited it, indicating that OH is generated via a Haber-Weiss type reaction. These spin trapping measurements provide the first evidence that aqueous suspensions of silica particles generate O-and 10 Oxygen consumption measurements indicate that freshly fractured silica uses molecular oxygen to generate 02-and 10 . Electrophoretic assays of in vitro DNA strand breakages showed that freshly fractured silica induced DNA strand breakage, which was inhibited by catalase and enhanced by H202. In an argon atmosphere, DNA damage was suppressed, showing that molecular oxygen is required for the silica-induced DNA damage. Incubation of freshly fractured silica with linoleic acid generated linoleic acid-derived free radicals and caused dose-dependent lipid peroxidation as measured by ESR spin trapping and malondialdehyde formation. SOD, catalase, and sodium benzoate inhibited lipid peroxidation by 49, 52, and 75%, respectively, again showing the role of oxygen radicals in silica-induced lipid peroxidation. These results show that in addition to -OH, 0°and 102 may play an important role in the mechanism of silica-induced cellular injury. -Environ Health Perspect 102(Suppl 10):149-154 (1994)

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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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The chemical properties of silica particle surface in relation to silica‐cell interactions

Cited by 49 publications

References 71 publications

Acute Pulmonary Toxicity Caused by Exposure to Colloidal Silica: Particle Size Dependent Pathological Changes in Mice

Acute Pulmonary Toxicity Caused by Exposure to Colloidal Silica: Particle Size Dependent Pathological Changes in Mice

Silica Radical-Induced DNA Damage and Lipid Peroxidation

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

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