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Neurotoxicity of polychlorinated biphenyls (PCBs) by disturbance of thyroid hormone-regulated genes

S A Roelens1, V Beck, G Aerts

  • 1Laboratory of Comparative Endocrinology, Katholieke Universiteit Leuven, Belgium. simon.roelens@bio.kuleuven.ac.be

Annals of the New York Academy of Sciences
|May 14, 2005
PubMed

Insights

Polychlorinated biphenyls (PCBs) alter thyroid hormone-regulated gene expression in the brain. This neurotoxicity is congener-specific, mimicking both hyperthyroid and hypothyroid effects.

Area of Science:

  • Neuroscience
  • Toxicology
  • Molecular Biology

Background:

  • Polychlorinated biphenyls (PCBs) are recognized neurotoxic compounds.
  • PCBs may exert neurotoxicity by altering thyroid hormone (TH)-regulated gene expression in the brain.

Purpose of the Study:

  • To identify genes regulated by TH that are affected by PCB exposure.
  • To investigate the relationship between PCB exposure, thyroid hormone levels, and gene expression in the brain.

Main Methods:

  • Comparative analysis of brain protein extracts from PCB-treated and hypo-/hyperthyroid embryonic models.
  • Utilized fluorescent 2D-difference gel electrophoresis (2D-DIGE) for protein expression profiling.

Main Results:

  • Identified 109 differentially expressed proteins.
  • Found 17 proteins that were differentially expressed in response to both PCB exposure and altered thyroid states (hypo- or hyperthyroidism).
  • Demonstrated that the interaction between PCBs and TH-regulated gene expression is specific to the PCB congener.

Conclusions:

  • PCB exposure can disrupt thyroid hormone-regulated gene expression in the brain.
  • PCB effects on gene expression can resemble both hyperthyroid and hypothyroid conditions.
  • The specific PCB congener influences the nature and extent of gene expression alterations.

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