Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

A possible mechanism for decrease in serum thyroxine level by polychlorinated biphenyls in Wistar and Gunn rats.

Yoshihisa Kato1, Shinichi Ikushiro, Koichi Haraguchi

  • 1School of Pharmaceutical Sciences, COE Program in the 21st Century, University of Shizuoka, 52-1, Yada, Shizuoka 422-8526, Japan. kato@ys7.u-shizuoka-ken.ac.jp

Toxicological Sciences : an Official Journal of the Society of Toxicology
|July 16, 2004
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Pilot study to assess the potential of oral myofunctional therapy for improving respiration during sleep.

Journal of prosthodontic research·2013
Same author

Multiple ferritins are vital to successful blood feeding and reproduction of the hard tick Haemaphysalis longicornis.

The Journal of experimental biology·2013
Same author

Efficacy of herpes virus helicase-primase inhibitor, ASP2151, for treating herpes simplex keratitis in mouse model.

The British journal of ophthalmology·2013
Same author

Identification and characterization of an interspersed repeat antigen of Babesia microti (BmIRA).

Experimental parasitology·2013
Same author

Pharmacokinetics and pharmacodynamics of ASP2151, a helicase-primase inhibitor, in a murine model of herpes simplex virus infection.

Antimicrobial agents and chemotherapy·2013
Same author

[Development of a home care educational program for community physicians and other professionals-a trial in Kashiwa City].

Gan to kagaku ryoho. Cancer & chemotherapy·2012

Polychlorinated biphenyls (PCBs) decrease serum thyroxine (T4) levels in rats, independent of UDP-glucuronosyltransferase (T4-UDP-GT) induction. Hydroxylated PCB metabolites may contribute to this T4 reduction.

Area of Science:

  • Environmental Toxicology
  • Endocrinology
  • Pharmacology

Background:

  • Polychlorinated biphenyls (PCBs) are known environmental contaminants that can disrupt thyroid hormone homeostasis.
  • Previous studies in mice showed PCB-induced thyroxine (T4) decrease without increased T4-UDP-GT, contrasting with rats where T4-UDP-GT induction was implicated.
  • Understanding the precise mechanisms of PCB-induced T4 reduction is crucial for assessing their toxicological impact.

Purpose of the Study:

  • To elucidate the relationship between PCB exposure, serum T4 levels, and UDP-glucuronosyltransferase (UGT1A) activity in rats.
  • To investigate the role of hepatic T4-UDP-GT induction versus other mechanisms in PCB-mediated T4 reduction.
  • To compare the effects of PCBs in Wistar rats and Gunn rats, a strain deficient in UGT1A isoforms.

Main Methods:

Related Experiment Videos

  • Wistar and Gunn rats were treated with PCBs (Kanechlor-500 or 2,2',4,5,5'-pentachlorobiphenyl).
  • Serum total T4, total triiodothyronine (T3), and thyroid-stimulating hormone levels were measured.
  • Hepatic T4-UDP-GT activity and level, hepatic type-I deiodinase activity, and PCB metabolite formation were analyzed.

Main Results:

  • Both PCB treatments significantly decreased serum T4 levels in Wistar and Gunn rats, with no significant difference between strains.
  • T4-UDP-GT activity and level increased in Wistar rats but not in Gunn rats following PCB treatment.
  • PCB treatment decreased hepatic type-I deiodinase activity in both rat strains and led to the formation of hydroxylated PCB metabolites.

Conclusions:

  • The decrease in serum T4 by PCBs in Gunn rats is not dependent on increased hepatic T4-UDP-GT activity.
  • Formation of hydroxylated PCB metabolites likely contributes to the PCB-mediated decrease in serum T4 levels.
  • In Wistar rats, PCB-induced T4 reduction may involve both increased hepatic T4-UDP-GT and the formation of hydroxylated metabolites.