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Title (Primary) Chlorinated benzenes cause concomitantly oxidative stress and induction of apoptotic markers in lung epithelial cells (A549) at non-acute toxic concentrations
Author Mörbt, N.; Feltens, R.; Tomm, J.; Kalkhof, S.; Mögel, I.; Vogt, C.; Lehmann, I.; von Bergen, M.;
Journal Journal of Proteome Research
Year 2011
Department IMMU; PROTEOM;
Volume 10
Issue 2
Language englisch;
Abstract In industrialized countries people spend more time indoors and are therefore increasingly exposed to volatile organic compounds that are emitted at working places and from consumer products, paintings and furniture, with chlorobenzene (CB) and 1,2 dichlorobenzene (DCB) being representatives of the halogenated arenes. To unravel the molecular effects of low concentrations typical for indoor and occupational exposure we exposed human lung epithelial cells to CB and DCB and analyzed the effects on the proteome level by 2-D DIGE, where 860 protein spots were detected. A set of 25 and 30 proteins were found to be significantly altered due to exposure to environmentally relevant concentrations of 10-2 g/m3 of CB or 10-3 g/m3 of DCB (2.2 ppm and 0.17 ppm), respectively. The most enriched pathways were cell death signalling, oxidative stress response, protein quality control and metabolism. The involvement of oxidative stress was validated by ROS measurement. Among the regulated proteins 28, e.g. voltage-dependent anion-selective channel protein 2, PDCD6IP protein, heat shock protein beta-1, proliferating cell nuclear antigen, nucleophosmin, seryl-tRNA synthetase, prohibitin and protein arginine N-methyltransferase 1 could be correlated with the molecular pathway of cell death signaling. Caspase 3 activation by cleavage was confirmed for both CB and DCB by immunoblotting. Treatment with CB or DCB also caused differential protein phosphorylation, e.g. at the proteins HNRNP C1/C2, serine-threonine receptor associated protein and transaldolase 1. Compared to previous results, where cells were exposed to styrene, for the chlorinated aromatic substances beside oxidative stress apoptosis was found as the predominant cellular response mechanism.
ID 10802
Persistent UFZ Identifier http://www.ufz.de/index.php?en=20939&ufzPublicationIdentifier=10802
Mörbt, N., Feltens, R., Tomm, J., Kalkhof, S., Mögel, I., Vogt, C., Lehmann, I., von Bergen, M. (2011):
Chlorinated benzenes cause concomitantly oxidative stress and induction of apoptotic markers in lung epithelial cells (A549) at non-acute toxic concentrations
J. Proteome Res. 10 (2), 363 - 378