Cytotoxic effects of quartz and chrysotile asbestos: In vitro interspecies comparison with alveolar macrophages

Schimmelpfeng, Jutta; Seidel, A.

doi:10.1080/15287399109531513

Cited by 19 publications

(14 citation statements)

References 13 publications

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“…Several studies showed that fibers with a high aspect ratio generate reactive oxygen species (ROS), stimulate tumor necrosis factor (TNF) α release, and stimulate inflammatory transcription factor NF-κB activation (Brown et al, 2007;Dogra & Donaldson, 1995;Hill et al, 1995). MWCNT were also found to resemble asbestos fibers in that MWCNT fibers interfered with the ability of macrophages to produce phagocytosis (Soto et al, 2004;Manning et al, 2002;Schimmelpfeng & Seidel, 1991).…”

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confidence: 97%

Determination of Cytotoxicity Attributed to Multiwall Carbon Nanotubes (MWCNT) in Normal Human Embryonic Lung Cell (WI-38) Line

Kim

Song

Joo

et al. 2010

Journal of Toxicology and Environmental Health, Part A

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Carbon nanotubes (CNT) possess beneficial physicochemical and mechanical properties; however, despite these advantages there are concerns regarding the adverse effects of CNT on lung and development of diseases, such as lung cancer and mesothelioma. According to fiber characteristics of length and diameter (aspect ratio), fibers with high aspect ratio (10-15 nm diameter and containing two different length distributions of 545 ± 230 and 10451 ± 8422 nm length) are more toxic to lung than low-aspect-ratio fibers (10-15 nm diameter and length of 192 nm). It was thus of interest to investigate the effects of multiwall carbon nanotubes (MWCNT) on the viability of normal human embryonic lung cells (WI-38) using trypan blue dye exclusion, the tetrazolium salt WST-1 (4-[3-(4-iodophenyl)-2-(4-nitrophenyl)-2H-5-tetrazolio]-1,3-benzene disulfonate) assay, and lactate dehydrogenase (LDH) activity assay. MWCNT produced cell growth inhibition and death at 12.5-200 μg/ml after 24-72 h of incubation. In addition, high-aspect-ratio MWCNT were found to produce higher incidence of cytotoxicity than low-aspect-ratio fibers at 50-200 μg/ml concentration. In the presence of less than 10% trace element content such as iron in MWCNT, the trace element exerted no marked effect on cellular viability. Data indicate that MWCNT inhibited cell proliferation and triggered cell death, and it would appear that the MWCNT fiber characteristics rather than impurities play a predominant role in the observed the cytotoxicity attributed to MWCNT.

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confidence: 97%

Determination of Cytotoxicity Attributed to Multiwall Carbon Nanotubes (MWCNT) in Normal Human Embryonic Lung Cell (WI-38) Line

Kim

Song

Joo

et al. 2010

Journal of Toxicology and Environmental Health, Part A

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“…Silica-induced lung injury is an established murine model of pulmonary fibrosis [7,33]. A single dose of the highly toxic DQ12 silica [7,34,35] induced a severe and persistent alveolitis characterized by significant increases in lactate dehydrogenase (LDH) and total protein content in BAL fluid. Concomitantly, a rapid and significant recruitment of monocytes/macrophages and neutrophils was also noted in response to silica (table 2).…”

Section: Discussionmentioning

confidence: 99%

Expression of plasminogen activator inhibitors type-1 and type-2 in the mouse lung after administration of crystalline silica

Lardot

Heusterpreute²,

Mertens³

et al. 1998

Eur Respir J

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Altered expression of plasminogen activator inhibitors (PAIs) is of potential relevance to the process of lung fibrosis. To clarify the involvement of PAIs in interstitial lung diseases, we examined whether alterations in PAI-1 and PAI-2 were induced in response to a single intratracheal administration of a fibrosing dose of crystalline silica in mice (5 mg x animal(-1)). The time course of changes in PAI activity and PAI-1 protein were characterized in bronchoalveolar lavage fluid (BALF) and changes in PAI-1 and PAI-2 messenger ribonucleic acid (mRNAs) were monitored by reverse transcriptase polymerase chain reaction (RT-PCR) in BALF cells and lung tissue up to the fibrotic stage of the disease. Substantial levels of PAI activity were found in BALF of control animals, whereas no PAI-1 protein was detected. In response to silica treatment, we observed an acute increase of PAI activity and PAI-1 protein levels in BALF (day 1), associated with an induction of PAI-1 and PAI-2 mRNA levels in lung tissue. In alveolar macrophages, silica treatment induced a persistent upregulation of PAI-2 mRNA only. One month after silica treatment, PAI activity was undetectable in BALF while substantial PAI activity was still present in controls. At the same time point, sustained upregulation of PAI-1 and PAI- 2 mRNAs was, however, noted in lung tissue of animals treated with silica. These findings support the possible implication of PAIs in the remodelling process induced by silica in the lung.

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“…The NE cell hyperplasia in the rat-the species of choice for silica carcinogenesis-and its possible role in stimulating cell proliferation in the adjacent epithelia represents a further hypothetical mechanism. These species differences may be related to other differences in the inflammatory cell response to silica (Driscoll et al, 1996;Schimmelpfeng and Seidel, 1991) and to the role of growth factors such as TGF-␤ and TNF-␣ (Saffiotti, 1993;Williams et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Hyperplasia of Alveolar Neuroendocrine Cells in Rat Lung Carcinogenesis by Silica with Selective Expression of Proadrenomedullin-Derived Peptides and Amidating Enzymes

Elizegi

Pino

Vicent

et al. 2001

Laboratory Investigation

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SUMMARY:Pulmonary neuroendocrine (NE) cells are found as clusters called neuroepithelial bodies (NEBs) or as single cells scattered in the respiratory epithelium. They express a variety of bioactive peptides, and they are thought to be the origin of NE lung tumors. Proadrenomedullin N-terminal 20 peptide (PAMP) is a peptide derived from the same precursor as adrenomedullin (AM). AM and PAMP are C-terminally amidated during their processing by a well-characterized amidating enzyme, peptidylglycine alpha-amidating monooxygenase (PAM). We explored AM, PAMP, and PAM expression as markers for NE hyperplasia in three rodent species (Fischer 344 rats, Syrian golden hamsters, and A/J mice) after a single intratracheal instillation of crystalline silica (quartz), which was previously found to induce different reactions in the three species. Rats developed a marked silicosis, with alveolar and bronchiolar hyperplasia and formation of peripheral lung epithelial tumors. Mice developed a moderate degree of silicosis, but not epithelial hyperplasia or tumors. Hamsters showed dust-storage lesions, but not silicosis or tumors. NE cells were immunolabeled for calcitonin gene-related peptide (CGRP), AM, PAMP, and PAM in serial sections of each lung. The numbers of positive NEBs per lung area and positive cells per NEB were quantified. A marked hyperplastic reaction in the NEBs of silica treated rats occurred only in alveolar NEBs, but not in bronchiolar NEBs. From Month 11 onwards, there were marked differences in the number of alveolar NEBs per section and in the number of cells per alveolar NEB immunoreactive for CGRP. No hyperplastic NE cell reaction was observed in silica-treated mice and hamsters. Significant PAMP and PAM expression was seen only in rat hyperplastic alveolar and in bronchiolar NEBs from Month 11 onwards. In E18, rat fetal lung NEBs were found to be strongly positive for PAMP and PAM. (Lab Invest 2001, 81:1627-1638.

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Cytotoxic effects of quartz and chrysotile asbestos: In vitro interspecies comparison with alveolar macrophages

Cited by 19 publications

References 13 publications

Determination of Cytotoxicity Attributed to Multiwall Carbon Nanotubes (MWCNT) in Normal Human Embryonic Lung Cell (WI-38) Line

Determination of Cytotoxicity Attributed to Multiwall Carbon Nanotubes (MWCNT) in Normal Human Embryonic Lung Cell (WI-38) Line

Expression of plasminogen activator inhibitors type-1 and type-2 in the mouse lung after administration of crystalline silica

Hyperplasia of Alveolar Neuroendocrine Cells in Rat Lung Carcinogenesis by Silica with Selective Expression of Proadrenomedullin-Derived Peptides and Amidating Enzymes

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