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Organic compounds in tire particle induce reactive oxygen species and heat-shock proteins in the human alveolar cell line A549

TitoloOrganic compounds in tire particle induce reactive oxygen species and heat-shock proteins in the human alveolar cell line A549
Tipo di pubblicazioneArticolo su Rivista peer-reviewed
Anno di Pubblicazione2008
AutoriGualtieri, Maurizio, Mantecca P., Cetta F., and Camatini M.
RivistaEnvironment International
Volume34
Paginazione437-442
Parole chiavearticle, cell death, Cell Line, cell membrane, Cell morphology, cell stress, cell viability, Chemical analysis, controlled study, cytology, Debris, Densitometers, densitometry, dichlorodihydrofluorescein diacetate, dichlorofluorescein, dose response, Dose-Response Relationship, Drug, Dust, Environmental stress, Epithelial Cells, Fine particles, Flow cytometry, Gene expression, heat shock, heat shock protein 70, Heat-Shock Proteins, human, human cell, Humans, industrial waste, lung alveolus cell, Mortality, motor vehicle tire, Organic Chemicals, organic compound, organic compounds, Parameter estimation, Particles (particulate matter), particulate matter, physiological response, priority journal, Protein, protein expression, Proteins, Pulmonary Alveoli, reactive oxygen metabolite, Reactive Oxygen Species, Reactive oxygen species (ROS), Time Factors, tire, Tire debris, Toxicity
Abstract

Debris produced from the attrition of tires of motor vehicles constitutes 5-7% of the atmospheric particulate matter (PM10). Debris particles are indeed small enough to enter human lung and thus morphological and chemical characterization has been performed. We demonstrated that the organic fraction of tire debris induces a dose-dependent increase in cell mortality, DNA damage, as well as a significant modification of cell morphology at the dose of 60 μg/ml, which may correspond to the quantity present in the air humans inhale daily. The present research aims at investigating if reactive oxygen species (ROS) production and Hsp70 expression are involved in the cascade of toxic effects produced on the A549 cell line, as it has been suggested for the ultrafine atmospheric particles and diesel exhaust. To this end, cells were exposed at the doses of 10, 50, 60, 75 μg/ml of TD organic extract (TDOE) and analyzed at different exposure time. ROS were detected by the oxidation of 2′7′-dichlorodihydrofluorescein diacetate to dichlorofluorescein, and fluorescence was measured by flow cytometry. Hsp70 protein expression was determined by immunochemical analysis, and protein expression quantification performed by optical densitometry. ROS production was analysed after 2 h of treatment. A statistically significant increase in fluorescence was observed and the intensity of the stress response was parallel to the increasing concentrations used. An evident increase of Hsp70 expression at lower doses (10, 50 μg/ml) and at longer exposure times (72 h) was observed, during the time that our previous studies showed that cell viability, plasma membrane integrity, and DNA molecules were not affected. Thus it can be deduced that the increase in Hsp70 expression protected the cells from those damages, which became evident at the higher doses, and that this parameter might be used as a sensitive indicator of exposure. These data suggest that ROS production may be the first event caused by A549 exposure to TDOE and this result is in line with other evidences provided for the role of ROS generation in ultrafine PM toxicity. It can be suggested that this event induces an overexpression of Hsp70 only at the lower doses and longer exposure time, when cells still appear unaffected. Subsequently when ROS generation reaches high levels, a general inhibition of protein synthesis probably occurs, culminating in cell toxicity. © 2007 Elsevier Ltd. All rights reserved.

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URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-43549099961&doi=10.1016%2fj.envint.2007.09.010&partnerID=40&md5=72cacb7d48332fc3b70ddc51bc2f38c8
DOI10.1016/j.envint.2007.09.010
Citation KeyGualtieri2008437