Effects of asbestos on initiation of DNA damage, induction of DNA-strand breaks, P53-expression and apoptosis in primary, SV40-transformed and malignant human mesothelial cells

Burmeister, Bryan; Schwerdtle, Tanja; Poser, Ina; Hoffmann, Eik; Hartwig, Andrea; Müller, W.-U.; Rettenmeier, Albert W.; Seemayer, N.H.; Dopp, Elke

doi:10.1016/j.mrgentox.2003.11.003

Cited by 46 publications

(34 citation statements)

References 37 publications

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“…All experiments were repeated 4 times. Cytotoxicity and genotoxicity analyses were investigated intensively in various cell systems for crocidolite and chrysotile (18)(19)(20)(21), titanium dioxide (22,23) and hematite (22,24). Based on the results of the above study, the particle concentrations did not show any loss of viability in the BEAS-2B cell line.…”

Section: Methodsmentioning

confidence: 99%

Induction of altered mRNA expression profiles caused by fibrous and granular dust

Helmig

Dopp

Wenzel

et al. 2013

Molecular Medicine Reports

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Section: Methodsmentioning

confidence: 99%

Induction of altered mRNA expression profiles caused by fibrous and granular dust

Helmig

Dopp

Wenzel

et al. 2013

Molecular Medicine Reports

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“…It is assumed that the latter may have the pivotal malignancy inducing role in the mesothelium, especially in cells with asbestos damaged DNA. 24 Asbestos fibres easily penetrate inside a cell, where they induce extensive DNA damage. The fibres generate genotoxic reactive oxygen and nitrogen species, cathalyse the synthesis of nitrotyrosine and induce DNA strand breaks.…”

Section: Asbestos and Sv40 Co-carcinogenitymentioning

confidence: 99%

“…The strong affinity of Tag for binding and inactivating p53 results in the cell avoiding key cell cycle checkpoints, thus surviving the otherwise fatal DNA damage and undergoing mitosis. 24,25 By escaping apoptosis and surviving, asbestos-damaged SV40 infected mesothelial cells pave the way to malignant transformation. It is very likely that asbestos fibres and viral Tag and tag interact and synergistically activate cellular signalling pathways, especially the ERK/ AP-1 pathway, that lead to cell proliferation, malignant transformation and invasion.…”

Section: Asbestos and Sv40 Co-carcinogenitymentioning

confidence: 99%

Presence and role of Simian Virus 40 (SV40) in malignant pleural mesothelioma

Hmeljak¹,

Cör²

2009

Radiology and Oncology

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Background. Evidence of a possible role of viruses in cancer first emerged in the early 1900s and was confirmed after the discovery of Epstein-Barr virus (EBV) in Conclusions. Simian virus 40 (SV40) is a small DNA virus from the genus polyomavirus, closely related to human polyomaviruses John Cunningham virus (JCV) and BK virus (BKV) and is highly oncogenic for rodents. The virus accidentally entered the human population through contaminated early batches of polio vaccine in the 1960s. After the discovery of SV40-like

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“…Asbestos induces cytotoxicity and apoptosis in HMCs (20,21), as well as in other lung cell types (3,4), and in such an effect the generation of superoxide and hydroxyl radicals has been deeply implicated. Some evidence suggests that cytotoxicity and mutagenesis induced by asbestos fibers are prevented by antioxidants and radical scavengers (22,23), such as in lung epithelial (24,25) and mesothelial cells (26).…”

Section: Discussionmentioning

confidence: 99%

Antioxidants Prevent the RhoA Inhibition Evoked by Crocidolite Asbestos in Human Mesothelial and Mesothelioma Cells

Aldieri

Riganti²,

Silvagno³

et al. 2011

Am J Respir Cell Mol Biol

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Asbestos is a naturally occurring fibrous silicate, whose inhalation is highly related to the risk of developing malignant mesothelioma (MM), and crocidolite is one of its most oncogenic types. The mechanism by which asbestos may cause MM is unclear. We have previously observed that crocidolite in human MM (HMM) cells induces NF-kB activation and stimulates the synthesis of nitric oxide by inhibiting the RhoA signaling pathway. In primary human mesothelial cells (HMCs) and HMM cells exposed to crocidolite asbestos, coincubated or not with antioxidants, we evaluated cytotoxicity and oxidative stress induction (lipid peroxidation) and the effect of asbestos on the RhoA signaling pathway (RhoA GTP binding, Rho kinase activity, RhoA prenylation, hydroxy-3-methylglutharyl-CoA reductase activity). In this paper we show that the reactive oxygen species generated by the incubation of crocidolite with primary HMCs and three HMM cell lines mediate the inhibition of 3-hydroxy-3-methylglutharyl-CoA reductase (HMGCR). The coincubation of HMCs and HMM cells with crocidolite together with antioxidants, such as Tempol, Mn-porphyrin, and the association of superoxide dismutase and catalase, prevented the cytotoxicity and lipoperoxidation caused by crocidolite alone as well as the decrease of HMGCR activity and restored the RhoA/RhoA-dependent kinase activity and the RhoA prenylation. The same effect was observed when the oxidizing agent menadione was administrated to the cells in place of crocidolite. Such a mechanism could at least partly explain the effects exerted by crocidolite fibers in mesothelial cells.

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Effects of asbestos on initiation of DNA damage, induction of DNA-strand breaks, P53-expression and apoptosis in primary, SV40-transformed and malignant human mesothelial cells

Cited by 46 publications

References 37 publications

Induction of altered mRNA expression profiles caused by fibrous and granular dust

Induction of altered mRNA expression profiles caused by fibrous and granular dust

Presence and role of Simian Virus 40 (SV40) in malignant pleural mesothelioma

Antioxidants Prevent the RhoA Inhibition Evoked by Crocidolite Asbestos in Human Mesothelial and Mesothelioma Cells

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