PMID- 21544203
OWN - NLM
STAT- MEDLINE
DCOM- 20110825
LR  - 20240313
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 6
IP  - 4
DP  - 2011 Apr 22
TI  - Thyroid disruption by Di-n-butyl phthalate (DBP) and mono-n-butyl phthalate (MBP) 
      in Xenopus laevis.
PG  - e19159
LID - 10.1371/journal.pone.0019159 [doi]
LID - e19159
AB  - BACKGROUND: Di-n-butyl phthalate (DBP), a chemical widely used in many consumer 
      products, is estrogenic and capable of producing seriously reproductive and 
      developmental effects in laboratory animals. However, recent in vitro studies 
      have shown that DBP and mono-n-butyl phthalate (MBP), the major metabolite of 
      DBP, possessed thyroid hormone receptor (TR) antagonist activity. It is therefore 
      important to consider DBP and MBP that may interfere with thyroid hormone system. 
      METHODOLOGY/PRINCIPAL FINDINGS: Nieuwkoop and Faber stage 51 Xenopus laevis were 
      exposed to DBP and MBP (2, 10 or 15 mg/L) separately for 21 days. The two test 
      chemicals decelerated spontaneous metamorphosis in X. laevis at concentrations of 
      10 and 15 mg/L. Moreover, MBP seemed to possess stronger activity. The effects of 
      DBP and MBP on inducing changes of expression of selected thyroid hormone 
      response genes: thyroid hormone receptor-beta (TRbeta), retinoid X receptor gamma 
      (RXRgamma), alpha and beta subunits of thyroid-stimulating hormone (TSHalpha and TSHbeta) 
      were detected by qPCR at all concentrations of the compounds. Using mammalian 
      two-hybrid assay in vitro, we found that DBP and MBP enhanced the interactions 
      between co-repressor SMRT (silencing mediator for retinoid and thyroid hormone 
      receptors) and TR in a dose-dependent manner, and MBP displayed more markedly. In 
      addition, MBP at low concentrations (2 and 10 mg/L) caused aberrant methylation 
      of TRbeta in head tissue. CONCLUSIONS: The current findings highlight potential 
      disruption of thyroid signalling by DBP and MBP and provide data for human risk 
      assessment.
FAU - Shen, Ouxi
AU  - Shen O
AD  - The Center for Disease Control and Prevention of Suzhou Industrial Park, Suzhou, 
      China.
FAU - Wu, Wei
AU  - Wu W
FAU - Du, Guizhen
AU  - Du G
FAU - Liu, Renping
AU  - Liu R
FAU - Yu, Lugang
AU  - Yu L
FAU - Sun, Hong
AU  - Sun H
FAU - Han, Xiumei
AU  - Han X
FAU - Jiang, Yi
AU  - Jiang Y
FAU - Shi, Wei
AU  - Shi W
FAU - Hu, Wei
AU  - Hu W
FAU - Song, Ling
AU  - Song L
FAU - Xia, Yankai
AU  - Xia Y
FAU - Wang, Shoulin
AU  - Wang S
FAU - Wang, Xinru
AU  - Wang X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110422
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Phthalic Acids)
RN  - 0 (Receptors, Thyroid Hormone)
RN  - 0 (Retinoid X Receptor gamma)
RN  - 0 (Thyroid Hormone Receptors beta)
RN  - 2286E5R2KE (Dibutyl Phthalate)
RN  - 9002-71-5 (Thyrotropin)
RN  - ZI46LWZ45G (monobutyl phthalate)
SB  - IM
MH  - Animals
MH  - Dibutyl Phthalate/*pharmacology
MH  - Phthalic Acids/*pharmacology
MH  - Protein Binding/drug effects
MH  - Receptors, Thyroid Hormone/antagonists & inhibitors
MH  - Retinoid X Receptor gamma/genetics/metabolism
MH  - Thyroid Gland/*drug effects/*metabolism
MH  - Thyroid Hormone Receptors beta/genetics/metabolism
MH  - Thyrotropin/genetics/metabolism
MH  - Xenopus laevis
PMC - PMC3081329
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2011/05/06 06:00
MHDA- 2011/08/27 06:00
PMCR- 2011/04/22
CRDT- 2011/05/06 06:00
PHST- 2010/12/02 00:00 [received]
PHST- 2011/03/28 00:00 [accepted]
PHST- 2011/05/06 06:00 [entrez]
PHST- 2011/05/06 06:00 [pubmed]
PHST- 2011/08/27 06:00 [medline]
PHST- 2011/04/22 00:00 [pmc-release]
AID - PONE-D-10-05815 [pii]
AID - 10.1371/journal.pone.0019159 [doi]
PST - epublish
SO  - PLoS One. 2011 Apr 22;6(4):e19159. doi: 10.1371/journal.pone.0019159.