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Related Experiment Videos

Exposure to polychlorinated biphenyls causes endothelial cell dysfunction

M Toborek1, S W Barger, M P Mattson

  • 1Department of Nutrition and Food Science, University of Kentucky, Lexington 40506-0054, USA.

Journal of Biochemical Toxicology
|August 1, 1995
PubMed
Summary

Certain polychlorinated biphenyls (PCBs) disrupt endothelial barrier function, increasing atherosclerosis risk. PCB 77 and PCB 114 caused oxidative stress and calcium changes, unlike PCB 153, suggesting specific PCB interactions contribute to vascular dysfunction.

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Area of Science:

  • Environmental toxicology
  • Cardiovascular research
  • Cellular biology

Background:

  • Environmental chemicals like polychlorinated biphenyls (PCBs) are suspected contributors to atherosclerosis.
  • Vascular endothelial cells are critical for maintaining vascular health and integrity.

Purpose of the Study:

  • To investigate the atherogenic potential of specific PCBs by examining their effects on endothelial cell function.
  • To determine if varying aryl hydrocarbon (Ah) receptor binding affinities influence PCB-induced endothelial dysfunction.

Main Methods:

  • Porcine pulmonary artery endothelial cells were exposed to different concentrations of PCB 77, PCB 114, and PCB 153 for up to 24 hours.
  • Assessed endothelial barrier function via albumin transfer.
  • Measured cellular oxidative stress (DCF fluorescence, lipid hydroperoxides) and intracellular calcium ([Ca2+]i).

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  • Quantified cytochrome P450 1A activity and content, and vitamin E levels.
  • Main Results:

    • PCB 77 and PCB 114, but not PCB 153, dose-dependently impaired endothelial barrier function, increasing albumin permeability.
    • These PCBs induced significant oxidative stress and elevated intracellular calcium levels.
    • Increased cytochrome P450 1A activity and content, along with decreased vitamin E, were observed in cells exposed to PCB 77 and PCB 114.

    Conclusions:

    • Specific PCBs (77 and 114) can induce endothelial cell dysfunction, characterized by barrier disruption, oxidative stress, and altered calcium homeostasis.
    • These findings suggest a role for certain PCBs in atherosclerosis development, potentially mediated by Ah receptor interaction and cytochrome P450 1A activation.
    • PCB 153, with lower Ah receptor binding affinity, did not elicit similar detrimental effects, highlighting the importance of PCB structure in toxicity.