NDLI: DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats

Content Provider	Springer Nature Link
Author	Liu, Changjiang Zhao, Letian Wei, Li Li, Lianbing
Copyright Year	2015
Abstract	Di-(2-ethylhexyl) phthalate (DEHP) is used extensively in many personal care and consumer products, resulting in widespread nonoccupational human exposure through multiple routes and media. Limited studies suggest that exposure to DEHP may be associated with altered thyroid function, but detailed mechanisms are unclear. In order to elucidate potential mechanisms by which DEHP disturbs thyroid hormone homeostasis, Sprague-Dawley (SD) rats were dosed with DEHP by gavage at 0, 250, 500, and 750 mg/kg/day for 30 days and sacrificed within 24 h after the last dose. Gene expressions of thyroid hormone receptors, deiodinases, transthyretin, and hepatic enzymes were measured by RT-PCR; protein levels of transthyretin were also analyzed by Western blot. Results showed that DEHP caused histological changes in the thyroid and follicular epithelial cell hypertrophy and hyperplasia were observed. DEHP significantly reduced thyroid hormones (T3, T4) and thyrotropin releasing hormone (TRH) levels, whereas thyroid stimulating hormone (TSH) was not affected. After exposure to DEHP, biosynthesis of thyroid hormones was suppressed, and sodium iodide symporter (NIS) and thyroid peroxidase (TPO) levels were significantly reduced. Additionally, levels of deiodinases and transthyretin were also affected. TSH receptor (TSHr) level was downregulated, while TRH receptor (TRHr) level was upregulated. Metabolism of thyroid hormones was accelerated due to elevated gene expression of hepatic enzymes (UDPGTs and CYP2B1) by DEHP. Taken together, observed findings indicate that DEHP could reduce thyroid hormones through influencing biosynthesis, biotransformation, biotransport, receptor levels, and metabolism of thyroid hormones.
Starting Page	12711
Ending Page	12719
Page Count	9
File Format	PDF
ISSN	09441344
Journal	Environmental Science and Pollution Research
Volume Number	22
Issue Number	16
e-ISSN	16147499
Language	English
Publisher	Springer Berlin Heidelberg
Publisher Date	2015-04-28
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	DEHP Thyroid hormone Receptor Hepatic enzyme Deiodinase Transthyretin Biosynthesis Environment Environmental Chemistry Ecotoxicology Environmental Health Atmospheric Protection/Air Quality Control/Air Pollution Waste Water Technology Water Pollution Control Water Management Aquatic Pollution
Content Type	Text
Resource Type	Article
Subject	Environmental Chemistry Health, Toxicology and Mutagenesis Pollution Medicine

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

PCB153 and p,p′-DDE disorder thyroid hormones via thyroglobulin, deiodinase 2, transthyretin, hepatic enzymes and receptors

DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats.

Phthalate pollution in an Amazonian rainforest

Effects of diethylphthalate and di-(2-ethyl)hexylphthalate on the physiology and ultrastructure of cucumber seedlings

Meta-analysis of environmental contamination by phthalates

Lifetime cancer risk assessment for inhalation exposure to di(2-ethylhexyl) phthalate (DEHP)

Effects of bisphenol A, an environmental endocrine disruptor, on the endogenous hormones of plants

Effects of perfluoroalkyl acids on the function of the thyroid hormone and the aryl hydrocarbon receptor

Ant cuticular response to phthalate pollution

DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats

Similar Documents

PCB153 and p,p′-DDE disorder thyroid hormones via thyroglobulin, deiodinase 2, transthyretin, hepatic enzymes and receptors

DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats.

Phthalate pollution in an Amazonian rainforest

Effects of diethylphthalate and di-(2-ethyl)hexylphthalate on the physiology and ultrastructure of cucumber seedlings

Meta-analysis of environmental contamination by phthalates

Lifetime cancer risk assessment for inhalation exposure to di(2-ethylhexyl) phthalate (DEHP)

Effects of bisphenol A, an environmental endocrine disruptor, on the endogenous hormones of plants

Effects of perfluoroalkyl acids on the function of the thyroid hormone and the aryl hydrocarbon receptor

Ant cuticular response to phthalate pollution

DEHP reduces thyroid hormones via interacting with hormone synthesis-related proteins, deiodinases, transthyretin, receptors, and hepatic enzymes in rats