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Thyroid peroxidase as toxicity target for dithiocarbamates

M Marinovich1, M Guizzetti, F Ghilardi

  • 1Laboratory of Toxicology, University of Milan, Italy.

Archives of Toxicology
|January 1, 1997
PubMed
Summary

Ethylenebisdithiocarbamates and ETU are toxic to the thyroid. Researchers found that these compounds inhibit thyroid peroxidase (TPO) activity, explaining their in vivo toxicity.

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Area of Science:

  • Toxicology
  • Endocrinology
  • Molecular Biology

Background:

  • Ethylenebisdithiocarbamates (EBDCs) and their metabolite ethylenethiourea (ETU) are known to be toxic to the thyroid gland.
  • The primary mechanism of EBDC/ETU thyroid toxicity is suspected to involve inhibition of thyroid peroxidase (TPO).

Purpose of the Study:

  • To investigate the effects of EBDCs and ETU on the peroxidative activity of human thyroid peroxidase (TPO).
  • To determine if TPO inhibition by these compounds correlates with their known in vivo thyrotoxicity.

Main Methods:

  • Chinese hamster ovary (CHO) cells transfected with the human TPO gene were used.
  • Cells were treated with varying concentrations of ETU, ziram, zineb, and thiram.
  • Peroxidative activity and iodinating activity of TPO were measured.

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Main Results:

  • ETU, ziram, and zineb inhibited TPO peroxidative activity.
  • Zineb's inhibition was irreversible without iodide.
  • Only ETU and zineb significantly blocked TPO-catalyzed iodination.
  • Thiram showed no effect on TPO activity.

Conclusions:

  • The differential inhibition of TPO peroxidative and iodinating activities by EBDCs and ETU provides a molecular explanation for their varying in vivo thyrotoxic effects.
  • TPO is a key molecular target for the thyroid toxicity induced by these compounds.