PCB-induced oxidative stress in endothelial cells: Modulation by nutrients

Bernhard Hennig, Bruce D. Hammock, Rabih Slim, Michal Toborek, Viswanathan Saraswathi, Larry W. Robertson

Research output: Contribution to journalArticlepeer-review

84 Scopus citations


There is an increasing body of evidence suggesting that exposure to Superfund chemicals may have adverse consequences on many organ systems, as well as carcinogenic and atherogenic effects. This is particularly true for polyhalogenated aromatic hydrocarbons such as the polychlorinated biphenyls (PCBs). The vascular endothelium, which is constantly exposed to blood components including environmental contaminants, is extremely vulnerable to chemical insult as well as necrotic and apoptotic injury. Our recent studies suggest that certain PCBs, especially coplanar PCBs, can compromise normal functions of vascular endothelial cells by activating oxidative stress-sensitive signaling pathways and subsequent proinflammatory events critical in the pathology of atherosclerosis and cardiovascular disease. Our findings suggest that an increase in the level of cellular oxidative stress is a significant event in PCB-mediated endothelial cell dysfunction and that nutrients can modulate PCB-induced oxidative stress and endothelial toxicity. We have demonstrated that the dietary fat linoleic acid, the parent unsaturated fatty acid of the omega-6 family, can increase endothelial dysfunction induced by selected PCBs, probably by contributing to oxidative stress and as the result of the production of toxic metabolites called leukotoxins. The subsequent imbalance in the overall cellular oxidant/antioxidant status can activate oxidative stress- or redox-sensitive transcription factors, which in turn promote gene expression for inflammatory cytokines and adhesion molecules, intensifying the inflammatory response and endothelial cell dysfunction. Our data also suggest that antioxidant nutrients such as vitamin E can protect against endothelial cell damage mediated by PCBs or polyunsaturated dietary fats by interfering with oxidative stress-sensitive and proinflammatory signaling pathways. The concept that nutrition can modify or ameliorate the toxicity of Superfund chemicals is provocative and warrants further study as the implications for human health are significant. The information from such studies could be used to develop dietary recommendations and nutritional interventions for populations at high risk for exposure to PCBs, including communities living near Superfund sites and those exposed via occupation or diet.

Original languageEnglish
Pages (from-to)95-102
Number of pages8
JournalInternational Journal of Hygiene and Environmental Health
Issue number1-2
StatePublished - 2002

Bibliographical note

Funding Information:
Acknowledgements. We would like to thank Ms. Maureen Avakian for her excellent editorial assistance. Research reported by the authors is supported in part by grants from NIEHS ( P42 ES 07380 and 04699), NIEHS (RO1 ES02710 and P30 ES05707), NRICGP/USDA (97-35200-4231 and 00-35200-9101), DOD, and the Kentucky Agricultural Experimental Station. The contents of this paper are solely the responsibility of authors and do not necessarily represent the official view of the funding agencies.


  • Atherosclerosis
  • Endothelial cells
  • Fatty acids
  • Leukotoxins
  • Nutrition
  • Polychlorinated biphenyls

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health


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