Bedoukian   RussellIPM   RussellIPM   Piezoelectric Micro-Sprayer


Home
Animal Taxa
Plant Taxa
Semiochemicals
Floral Compounds
Semiochemical Detail
Semiochemicals & Taxa
Synthesis
Control
Invasive spp.
References

Abstract

Guide

Alphascents
Pherobio
InsectScience
E-Econex
Counterpart-Semiochemicals
Print
Email to a Friend
Kindly Donate for The Pherobase

« Previous AbstractHS-SPME-GC/MS Analysis for Revealing Carob's Ripening    Next AbstractInverse relationship between systemic resistance of plants to microorganisms and to insect herbivory »

Toxicol Appl Pharmacol


Title:Chlorobenzene induces oxidative stress in human lung epithelial cells in vitro
Author(s):Feltens R; Mogel I; Roder-Stolinski C; Simon JC; Herberth G; Lehmann I;
Address:"UFZ- Helmholtz Centre for Environmental Research, Department of Environmental Immunology, Permoserstrasse 15, D-04318 Leipzig, Germany. ralph.feltens@ufz.de"
Journal Title:Toxicol Appl Pharmacol
Year:2010
Volume:20091002
Issue:1
Page Number:100 - 108
DOI: 10.1016/j.taap.2009.09.020
ISSN/ISBN:1096-0333 (Electronic) 0041-008X (Linking)
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-kappaB 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 pi1 (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"
Keywords:"Antioxidants/pharmacology Blotting, Western Cell Line Chemokine CCL2/biosynthesis/genetics Chlorobenzenes/*toxicity Epithelial Cells/*drug effects Glutathione/metabolism Glutathione S-Transferase pi/biosynthesis/genetics Heme Oxygenase-1/biosynthesis/gene;"
Notes:"MedlineFeltens, Ralph Mogel, Iljana Roder-Stolinski, Carmen Simon, Jan-Christoph Herberth, Gunda Lehmann, Irina eng 2009/10/06 Toxicol Appl Pharmacol. 2010 Jan 1; 242(1):100-8. doi: 10.1016/j.taap.2009.09.020. Epub 2009 Oct 2"

 
Back to top
 
Citation: El-Sayed AM 2024. The Pherobase: Database of Pheromones and Semiochemicals. <http://www.pherobase.com>.
© 2003-2024 The Pherobase - Extensive Database of Pheromones and Semiochemicals. Ashraf M. El-Sayed.
Page created on 22-11-2024