PMID- 19800902
OWN - NLM
STAT- MEDLINE
DCOM- 20091230
LR  - 20161125
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 242
IP  - 1
DP  - 2010 Jan 1
TI  - Chlorobenzene induces oxidative stress in human lung epithelial cells in vitro.
PG  - 100-8
LID - 10.1016/j.taap.2009.09.020 [doi]
AB  - 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.
FAU - Feltens, Ralph
AU  - Feltens R
AD  - UFZ- Helmholtz Centre for Environmental Research, Department of Environmental 
      Immunology, Permoserstrasse 15, D-04318 Leipzig, Germany. ralph.feltens@ufz.de
FAU - Mogel, Iljana
AU  - Mogel I
FAU - Roder-Stolinski, Carmen
AU  - Roder-Stolinski C
FAU - Simon, Jan-Christoph
AU  - Simon JC
FAU - Herberth, Gunda
AU  - Herberth G
FAU - Lehmann, Irina
AU  - Lehmann I
LA  - eng
PT  - Journal Article
DEP - 20091002
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Antioxidants)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chlorobenzenes)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
RN  - EC 2.5.1.18 (GSTP1 protein, human)
RN  - EC 2.5.1.18 (Glutathione S-Transferase pi)
RN  - GAN16C9B8O (Glutathione)
RN  - K18102WN1G (chlorobenzene)
SB  - IM
MH  - Antioxidants/pharmacology
MH  - Blotting, Western
MH  - Cell Line
MH  - Chemokine CCL2/biosynthesis/genetics
MH  - Chlorobenzenes/*toxicity
MH  - Epithelial Cells/*drug effects
MH  - Glutathione/metabolism
MH  - Glutathione S-Transferase pi/biosynthesis/genetics
MH  - Heme Oxygenase-1/biosynthesis/genetics
MH  - Humans
MH  - Lung/*cytology/drug effects
MH  - Oxidative Stress/*drug effects
MH  - Reactive Oxygen Species/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Up-Regulation/drug effects
EDAT- 2009/10/06 06:00
MHDA- 2009/12/31 06:00
CRDT- 2009/10/06 06:00
PHST- 2009/05/26 00:00 [received]
PHST- 2009/09/11 00:00 [revised]
PHST- 2009/09/28 00:00 [accepted]
PHST- 2009/10/06 06:00 [entrez]
PHST- 2009/10/06 06:00 [pubmed]
PHST- 2009/12/31 06:00 [medline]
AID - S0041-008X(09)00412-8 [pii]
AID - 10.1016/j.taap.2009.09.020 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2010 Jan 1;242(1):100-8. doi: 10.1016/j.taap.2009.09.020. 
      Epub 2009 Oct 2.