We have investigated how a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects thyroid hormone regulation, especially in relation to the localization of thyroid stimulating hormone (TSH) in the pituitary and that of thyroxin (T4) of the thyroid in the rat. Female Sprague-Dawley rats were given a single oral administration of TCDD ranging from 1.0 to 4.0 microg/kg body weight (bw), and then tissue specimens were removed on day 7 post-administration. Thyroid hormone concentrations were measured in serum, and the expression of the TCDD-responsive genes, UDP-glucuronosyltransferase-1 (UGT1) and cytochrome P4501A1 (CYP1A1) were examined in the liver. TCDD administration resulted in an increase in both immunostaining intensity and the number of TSH-positive cells in the anterior pituitary. T4 was found to localize only in the follicular lumen of the thyroid in vehicle-treated control rats, while TCDD administration caused a foamy change in the colloid of some follicles, an indication of accelerating the biosynthesis of T4 in the thyroid. By morphometrical analysis, the ratio of parenchymal/lumenal area of the thyroid was found to increase in response to TCDD. TCDD treatment as low as 2.0 microg TCDD/kg bw induced a significant decrease in both serum total T4 (TT4) and free T4 (FT4) concentrations in the rats, with a significant increase in serum TSH levels in the 4.0 microg TCDD/kg bw rats. Serum total triiodothyronine (TT3) level was unchanged in all groups. The UGT1 gene was significantly induced at a TCDD dose as low as 1.0 microg/kg bw in a dose-dependent manner. TCDD concentrations in the serum, liver and adipose tissues were detected in a dose-related fashion. The present immunohistochemical results clearly support the earlier biochemical findings on the perturbation of the thyroid-pituitary axis by TCDD and suggest that UGT1 is an immediate target of a low TCDD exposure that triggers the perturbation.
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http://dx.doi.org/10.1016/s0300-483x(01)00559-5 | DOI Listing |
Ecotoxicol Environ Saf
January 2025
Department of Stomatology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, No. 242, Guangji Road, Suzhou, Jiangsu Province 215000, China. Electronic address:
Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in utero can result in osteogenic defect during palatogenesis, but the effects on other craniofacial bones and underlying mechanisms remain to be characterized. By treating pregnant mice with TCDD (40 μg/kg) at the vital craniofacial patterning stages (embryonic day 8.5, 10.
View Article and Find Full Text PDFUnlabelled: Quantitative understanding of mitochondrial heterogeneity is necessary for elucidating the precise role of these multifaceted organelles in tumor cell development. We demonstrate an early mechanistic role of mitochondria in initiating neoplasticity by performing quantitative analyses of structure-function of single mitochondrial components coupled with single cell transcriptomics. We demonstrate that the large Hyperfused-Mitochondrial-Networks (HMNs) of keratinocytes promptly get converted to the heterogenous Small-Mitochondrial-Networks (SMNs) as the stem cell enriching dose of the model carcinogen, TCDD, depolarizes mitochondria.
View Article and Find Full Text PDFJ Mol Histol
December 2024
Department of Stomatology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, No.51, Weiliu Road, Jinan, Shandong Province, 250021, China.
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an important environmental pollutant that disturbs the immune balance of the maternal-fetal interface (MFI) and is also a common environmental factor for the formation of cleft palate (CP). Therefore, the purpose is to investigate whether TCDD can cause CP by disrupting the immune balance of the maternal-fetal interface. Fifteen C57BL/6J mice were randomly assigned to three groups: control group, TCDD group, and TCDD plus Freund's complete adjuvant (FCA) (TCDD + FCA) group.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.
Exposure to environmental contaminants can result in profound effects on the host immune system. One class of environmental toxicants, known as dioxins, are persistent environmental contaminants termed "forever chemicals". The archetype toxicant from this group of chemicals is 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), an immunotoxicant that activates the aryl-hydrocarbon receptor pathway leading to a variety of changes in immune cell responses.
View Article and Find Full Text PDFSci Total Environ
January 2025
Department of Environmental Science, Rutgers, the State University of New Jersey, United States of America. Electronic address:
Polychlorinated dibenzo-p-dioxins and -furans (PCDD/Fs) are contaminants of concern in the New York/New Jersey Harbor and in the organisms of the Newtown Creek Superfund site, which lies within the harbor. Because PCDD/Fs are never intentionally produced, identifying their sources can be challenging. In this work, sources of PCDD/Fs to the sediment of Newtown Creek were investigated using Positive Matrix Factorization (PMF) to analyze two data sets containing data on concentrations of (1) PCDD/Fs and (2) PCDD/Fs plus polychlorinated biphenyls (PCBs).
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