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ToxSci Advance Access published online on June 12, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg149
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received March 13, 2003; accepted May 6, 2003
© 2003 Society of Toxicology

Environmental Toxicology

PCB 104-Induced Proinflammatory Reactions in Human Vascular Endothelial Cells: Relationship to Cancer Metastasis and Atherogenesis

Wangsun Choi 1, Sung Yong Eum 1, Yong Woo Lee 1, Bernhard Hennig 2, Larry W. Robertson 3, and Michal Toborek 1*

1 Department of Surgery, University of Kentucky, Lexington, KY 40536
2 College of Agriculture, University of Kentucky, Lexington, KY 40536; Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536
3 Department of Occupational & Environmental Health, University of Iowa, Iowa City, IA 52242

* To whom correspondence should be addressed. E-mail: mjtobo00{at}uky.edu.


  Abstract

Polychlorinated biphenyls (PCBs) are widespread environmental contaminants which are known to induce carcinogenic and possibly atherogenic events. Recent evidence suggests that selected PCBs may be potent developmental agents of vascular inflammatory responses by inducing cellular oxidative stress and activating redox-responsive transcription factors. Therefore, the aim of the present study was to investigate PCB-induced proinflammatory reactions in human vascular endothelial cells. To determine proinflammatory effects, cellular oxidative stress and expression of genes encoding for monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules, such as E-selectin and intercellular adhesion molecule-1 (ICAM-1), were assessed in human umbilical vein endothelial cells (HUVEC) exposed to 2,2',4,6,6'-pentachlorobiphenyl (PCB 104), a representative of ortho-substituted, non-coplanar PCB congeners. PCB 104 increased oxidative stress in endothelial cells, as determined by increased 2',7'-dichlorofluorescein (DCF) and rhodamine 123 fluorescence. In addition, PCB 104 markedly upregulated expression of MCP-1, E-selectin and ICAM-1 both at mRNA and protein levels. These effects were time- and concentration-dependent. The maximum expression of inflammatory genes was observed in endothelial cells exposed to 20 µM of PCB 104 for 1 or 2 h, depending on the specific gene. In addition, PCB 104 elevated the adhesion of THP-1 cells (a human acute monocytic leukemia cell line) to endothelial cell monolayers. These results indicate that PCB 104 is a potent stimulant of inflammatory mediators in human vascular endothelial cells. We hypothesize that these proinflammatory processes may contribute to the development of cancer metastasis and/or atherogenesis in patients exposed to PCBs.

Key Words: PCB, endothelial cells, inflammation, metastasis, atherosclerosis, vascular disease .


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