Polychlorinated biphenyls suppress thyroid hormone-induced transactivation

Polychlorinated biphenyls suppress thyroid hormone-induced transactivation Polychlorinated biphenyls (PCBs) have been known as environmental endocrine disrupting chemical that causes various abnormalities in many organs including the central nervous system (CNS). To examine the effect of PCBs on thyroid hormone (T3)-mediated transcription, transfection-based reporter assays were performed. Surprisingly, as low as 10 −10 M of 4(OH)-2 ′ ,3,3 ′ ,4 ′ ,5 ′ -pentachloro biphenyl suppressed T3-induced transactivation by thyroid hormone receptor (TR) in various cell lines. Interestingly, among the cell lines that we tested, brain-derived cell line TE671 cells showed strong suppression by the PCB. The suppression of TR action by the PCB was not likely due to the ligand competition with T3. Various compounds of PCBs showed similar suppression. However, PCBs did not suppress glucocorticoid receptor-mediated transcription. Finally, we showed that PCBs suppress TR/coactivator (SRC-1) complex-mediated transactivation. In summary, our results suggest that very low dose of PCBs can potentially interfere with TR-mediated transactivation by influencing on TR/coactivator complex. As such, PCBs may disturb growth and development of TH target organ, particularly in the CNS. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biochemical and Biophysical Research Communications Elsevier

Polychlorinated biphenyls suppress thyroid hormone-induced transactivation

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Publisher
Elsevier
Copyright
Copyright © 2002 Elsevier Science (USA)
ISSN
0006-291x
DOI
10.1016/S0006-291X(02)02659-1
Publisher site
See Article on Publisher Site

Abstract

Polychlorinated biphenyls (PCBs) have been known as environmental endocrine disrupting chemical that causes various abnormalities in many organs including the central nervous system (CNS). To examine the effect of PCBs on thyroid hormone (T3)-mediated transcription, transfection-based reporter assays were performed. Surprisingly, as low as 10 −10 M of 4(OH)-2 ′ ,3,3 ′ ,4 ′ ,5 ′ -pentachloro biphenyl suppressed T3-induced transactivation by thyroid hormone receptor (TR) in various cell lines. Interestingly, among the cell lines that we tested, brain-derived cell line TE671 cells showed strong suppression by the PCB. The suppression of TR action by the PCB was not likely due to the ligand competition with T3. Various compounds of PCBs showed similar suppression. However, PCBs did not suppress glucocorticoid receptor-mediated transcription. Finally, we showed that PCBs suppress TR/coactivator (SRC-1) complex-mediated transactivation. In summary, our results suggest that very low dose of PCBs can potentially interfere with TR-mediated transactivation by influencing on TR/coactivator complex. As such, PCBs may disturb growth and development of TH target organ, particularly in the CNS.

Journal

Biochemical and Biophysical Research CommunicationsElsevier

Published: Dec 6, 2002

References

  • Physiological and molecular basis of thyroid hormone action
    Yen, P.M.
  • The mechanism of action of thyroid hormones
    Zhang, J.; Lazar, M.A.

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