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Title (Primary) Chlorobenzene induces oxidative stress in human lung epithelial cells in vitro
Author Feltens, R.; Mögel, I.; Röder-Stolinski, C.; Simon, J.-C.; Herberth, G.; Lehmann, I.;
Journal Toxicology and Applied Pharmacology
Year 2010
Department IMMU; METABOX;
Volume 242
Issue 1
Language englisch;
Keywords Chlorobenzene; Volatile organic compound (VOC); Glutathione S-transferase p1 (GSTP1); Heme oxygenase 1 (HO-1); Superoxide dismutase 1 (SOD1); Prostaglandin-endoperoxide synthase 2 (PTGS2); Dual specificity phosphatase 1 (DUSP1); Monocyte chemoattractant protein-1 (MCP-1); Oxidative stress; N-(2-mercaptopropionyl)-glycine (MPG); Bucillamine
Abstract Chlorobenzene is a volatile organic compound (VOC) that is widely used as a solvent, degreasing agent and chemical intermediate in many industrial settings. Occupational studies have shown that acute and chronic exposure to chlorobenzene can cause irritation of the mucosa of the upper respiratory tract and eyes. Using in vitro assays, we have shown in a previous study that human bronchial epithelial cells release inflammatory mediators such as the cytokine monocyte chemoattractant protein-1 (MCP-1) in response to chlorobenzene. This response is mediated through the NF-?B signaling pathway. Here, we investigated the effects of monochlorobenzene on human lung cells, with emphasis on potential alterations of the redox equilibrium to clarify whether the chlorobenzene-induced inflammatory response in lung epithelial cells is caused via an oxidative stress-dependent mechanism. We found that expression of cellular markers for oxidative stress, such as heme oxygenase 1 (HO-1), glutathione S-transferase p1 (GSTP1), superoxide dismutase 1 (SOD1), prostaglandin-endoperoxide synthase 2 (PTGS2) and dual specificity phosphatase 1 (DUSP1), were elevated in the presence of monochlorobenzene. Likewise, intracellular reactive oxygen species (ROS) were increased in response to exposure. However, in the presence of the antioxidants N-(2-mercaptopropionyl)-glycine (MPG) or bucillamine, chlorobenzene-induced upregulation of marker proteins and release of the inflammatory mediator MCP-1 are suppressed. These results complement our previous findings and point to an oxidative stress-mediated inflammatory response following chlorobenzene exposure.
ID 9933
Persistent UFZ Identifier https://www.ufz.de/index.php?en=20939&ufzPublicationIdentifier=9933
Feltens, R., Mögel, I., Röder-Stolinski, C., Simon, J.-C., Herberth, G., Lehmann, I. (2010):
Chlorobenzene induces oxidative stress in human lung epithelial cells in vitro
Toxicol. Appl. Pharmacol. 242 (1), 100 - 108