The Effects on Rat Thyroid Function of an Hepatic Microsomal Enzyme Inducer

1993 ◽  
Vol 12 (2) ◽  
pp. 153-158 ◽  
Author(s):  
S. Johnson ◽  
D. McKillop ◽  
J. Miller ◽  
I.K. Smith
Keyword(s):  
Hepatic Clearance ◽  
Liver Weight ◽  
Thyroid Stimulating Hormone ◽  
Albino Rats ◽  
Histopathological Changes ◽  
Hepatic Microsomal Enzyme ◽  
Pituitary Thyroid Axis ◽  
Related Enzyme ◽  
Rat Thyroid ◽  
Follicular Epithelial

1 Following daily administration to male albino rats for 2 weeks, β-naphthoflavone (25 and 60 mg kg-1, i.p.) and phenobarbitone (100 mg kg-1, p.o.) produced their characteristic patterns of induction of P450-related enzyme activities. β-naphthoflavone also induced p-nitrophenol glucuronidation by 160% over controls, while phenobarbitone produced only a 45% induction of this conjugation activity. 2 β-Naphthoflavone produced significant reductions in plasma thyroxine (T4) concentrations on days 4 and 16 and also decreased tri-iodothyronine (T3) on day 4. Thyroid-stimulating hormone (TSH) was significantly increased on day 16 by the higher dose of β-naphthoflavone. Thyroid weight was significantly increased at both dose levels on day 16 and liver weight was significantly increased on both days 4 and 16. No histopathological changes were seen in the liver or pituitary, but 30% of the animals showed minimal to mild follicular epithelial hypertrophy of the thyroid gland. 3 Phenobarbitone had no effect on T4 concentrations, but significantly decreased T3 on day 4. TSH increased by 60% on day 16, but was not statistically significant compared with controls. Thyroid weight was significantly increased on day 16 and liver weight was significantly increased on days 4 and 16. Mild to moderate thyroid follicular epithelial hypertrophy and moderate hepatocyte hypertrophy occurred in all animals. No histopathological changes were seen in the pituitary. 4 The early changes in T4 and/or T3 were probably due to increased hepatic clearance by induction of thyroxine glucuronidation with both compounds. Thyroid hypertrophy would be expected to follow as a result of activation of the hypothalamic-pituitary-thyroid axis. Data for the two compounds suggest some variation in the precise mechanism of action, which has not yet been fully elucidated.

The Herbicide Metolachlor Induces Liver Cytochrome P450s 2B1/2 and 3A1/2, but Not Thyroxine-Uridine Dinucleotide Phosphate Glucuronosyltransferase and Associated Thyroid Gland Activity

2003 ◽  
Vol 22 (4) ◽  
pp. 287-295 ◽  
Author(s):  
Shana R. Dalton ◽  
Richard T. Miller ◽  
Sharon A. Meyer
Keyword(s):  
Thyroid Gland ◽  
Epithelial Cell ◽  
Thyroid Stimulating Hormone ◽  
Cytochrome P450s ◽  
Tumor Promoter ◽  
Sprague Dawley ◽  
Follicular Epithelial Cell ◽  
Rat Thyroid ◽  
Thyroid Gland Activity ◽  
Follicular Epithelial

Metolachlor (2-chloro- N-(2-ethyl-6-methylphenyl)- N-(2-methoxy-1-methylethyl) acetamide) is widely used internationally as a corn and cotton herbicide. The metolachlor effects noted in rats during testing for U.S. pesticide registration include increased liver weight and hepatocarcinogenicity associated with eosinophilic foci. These properties, plus nongenotoxicity, are also characteristic of the prototypical rat liver tumor promoter, phenobarbital. Phenobarbital induces hepatic cytochrome P450s CYP2B1/2 and CYP3A1/2 and thyroxine (T4)-UDP-glucuronosyltransferase (T4-UGT), which enhances thyroxine clearance and thus indirectly increases thyroid gland activity. Because other chloroacetanilide herbicides are known to similarly affect rat thyroid gland, this study tested the hypothesis that metolachlor would have these additional phenobarbital-like effects on liver, especially that of T4-UGT induction with consequential stimulation of thyroid gland. Effects of metolachlor, fed to male Sprague-Dawley rats for 14 days at the carcinogenic dose of 3000 ppm, were compared to those of equimolar phenobarbital. Liver microsomal CYP2B1/2 and CYP3A1/2 were probed by immunoblotting and T4-UGT was measured enzymat-ically. Serum T4, triiodothyronine (T3), and thyroid-stimulating hormone (TSH) and thyroid follicular epithelial cell morphology and proliferation were used to assess thyroid gland activity. Metolachlor induced CYP2B1/2 and CYP3A1/2 proteins, but unlike phenobarbital, did not affect T4-UGT activity. In agreement, serum T4, T3, or TSH were unaffected by metolachlor. Also, no significant effects of metolachlor on thyroid gland morphology or follicular epithelial cell height or proliferation were observed. These data demonstrate that metolachlor is an inducer of hepatic CYP2B1/2 activity. But unlike the prototypical CYP2B1/2 inducer phenobarbital, metolachlor does not cause an increase in T4-glucuronidation and thyroid gland activation.

Imidacloprid induced oxidative stress and histopathological changes in liver of rats

2017 ◽  
Author(s):  
Archana Lohiya ◽  
Vinod Kumar ◽  
J. S. Punia
Keyword(s):  
Oxidative Stress ◽  
Membrane Proteins ◽  
Reduced Glutathione ◽  
Liver Weight ◽  
Albino Rats ◽  
Histopathological Changes ◽  
Control Groups ◽  
Gum Acacia ◽  
Wistar Albino Rats ◽  
Dose Levels

Imidacloprid was evaluated for its effect on oxidative stress and histopathological changes in liver of Wistar albino rats at two dose levels (19 and 38 mg/kg/day) administered orally for 10, 20 and 30 days. Effects were compared with respective control groups administered with 2% gum acacia (1ml/100g). Different parameters undertaken were liver weight, oxidative stress parameters viz. activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and levels of reduced glutathione (GSH) and malondialdehyde (MDA), cytoplasmic and membrane proteins and histopathological changes in liver. Imidacloprid at 38 mg/kg dose significantly increased (p less than 0.05) organ weight and levels of MDA in 20 and 30 days group. There was significant decreased (p less than 0.05) in levels of cytoplasmic and membrane proteins and activities of enzymes SOD and GPx at 38 mg/kg dose administered for 20 and 30 days. GSH levels were decreased significantly (p less than 0.05) at 38 mg/kg dose administered for 30 days. Degenerative changes in hepatocytes were observed at 38 mg/kg dose administered orally for 20 and 30 days.

scholarly journals OctylPhenol (OP) Alone and in Combination with NonylPhenol (NP) Alters the Structure and the Function of Thyroid Gland of the Lizard Podarcis siculus

2021 ◽  
Vol 80 (3) ◽  
pp. 567-578 ◽  
Author(s):  
Rosaria Sciarrillo ◽  
Mariana Di Lorenzo ◽  
Salvatore Valiante ◽  
Luigi Rosati ◽  
Maria De Falco
Keyword(s):  
Thyroid Gland ◽  
Endocrine Disrupting Chemicals ◽  
Thyroid Stimulating Hormone ◽  
Control Group ◽  
Type Ii ◽  
Endocrine Disrupting ◽  
Pituitary Thyroid Axis ◽  
Podarcis Siculus ◽  
Thyroid Axis ◽  
By Products

Abstract Different environmental contaminants disturb the thyroid system at many levels. AlkylPhenols (APs), by-products of microbial degradation of AlkylPhenol Polyethoxylates (APEOs), constitute an important class of Endocrine Disrupting Chemicals (EDCs), the two most often used environmental APs being 4-nonylphenol (4-NP) and 4-tert-octylphenol (4-t-OP). The purpose of the present study was to investigate the effects on the thyroid gland of the bioindicator Podarcis siculus of OP alone and in combination with NP. We used radioimmunoassay to determine their effects on plasma 3,3′,5-triiodo-L-thyronine (T3), 3,3′,5,5′-L-thyroxine (T4), thyroid-stimulating hormone (TSH), and thyrotropin-releasing hormone (TRH) levels in adult male lizards. We also investigated the impacts of AP treatments on hepatic 5′ORD (type II) deiodinase and hepatic content of T3 and T4. After OP and OP + NP administration, TRH levels increased, whereas TSH, T3, and T4 levels decreased. Lizards treated with OP and OP + NP had a higher concentration of T3 in the liver and 5′ORD (type II) activity, whereas T4 concentrations were lower than that observed in the control group. Moreover, histological examination showed that the volume of the thyroid follicles became smaller in treated lizards suggesting that that thyroid follicular epithelial cells were not functionally active following treatment. This data collectively suggest a severe interference with hypothalamus–pituitary–thyroid axis and a systemic imbalance of thyroid hormones. Graphic Abstract

scholarly journals Effects of the domestic thyroid stimulating hormone receptor (TSHR) variant on the hypothalamic-pituitary-thyroid axis and behavior in chicken

Genetics ◽  
2021 ◽  
Vol 217 (1) ◽  
Author(s):  
Amir Fallahshahroudi ◽  
Martin Johnsson ◽  
Enrico Sorato ◽  
S J Kumari A Ubhayasekera ◽  
Jonas Bergquist ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hormone Receptor ◽  
Thyroid Stimulating Hormone ◽  
Phenotypic Traits ◽  
Wild Type ◽  
Data Set ◽  
Red Junglefowl ◽  
Pituitary Thyroid Axis ◽  
And Behavior ◽  
Stimulating Hormone

Abstract Domestic chickens are less fearful, have a faster sexual development, grow bigger, and lay more eggs than their primary ancestor, the red junglefowl. Several candidate genetic variants selected during domestication have been identified, but only a few studies have directly linked them with distinct phenotypic traits. Notably, a variant of the thyroid stimulating hormone receptor (TSHR) gene has been under strong positive selection over the past millennium, but it’s function and mechanisms of action are still largely unresolved. We therefore assessed the abundance of the domestic TSHR variant and possible genomic selection signatures in an extensive data set comprising multiple commercial and village chicken populations as well as wild-living extant members of the genus Gallus. Furthermore, by mean of extensive backcrossing we introgressed the wild-type TSHR variant from red junglefowl into domestic White Leghorn chickens and investigated gene expression, hormone levels, cold adaptation, and behavior in chickens possessing either the wild-type or domestic TSHR variant. While the domestic TSHR was the most common variant in all studied domestic populations and in one of two red junglefowl population, it was not detected in the other Gallus species. Functionally, the individuals with the domestic TSHR variant had a lower expression of the TSHR in the hypothalamus and marginally higher in the thyroid gland than wild-type TSHR individuals. Expression of TSHB and DIO2, two regulators of sexual maturity and reproduction in birds, was higher in the pituitary gland of the domestic-variant chickens. Furthermore, the domestic variant was associated with higher activity in the open field test. Our findings confirm that the spread of the domestic TSHR variant is limited to domesticated chickens, and to a lesser extent, their wild counterpart, the red junglefowl. Furthermore, we showed that effects of genetic variability in TSHR mirror key differences in gene expression and behavior previously described between the red junglefowl and domestic chicken.

Stimulation of Na(+)-K(+)-ATPase by thyrotropin in cultured thyroid follicular cells

1995 ◽  
Vol 268 (5) ◽  
pp. C1252-C1258 ◽  
Author(s):  
T. A. Pressley ◽  
S. C. Higham ◽  
L. A. Joson ◽  
D. W. Mercer
Keyword(s):  
Thyroid Stimulating Hormone ◽  
Follicular Cells ◽  
Hormone Synthesis ◽  
Metabolic Turnover ◽  
Striking Increase ◽  
Thyroid Follicular Cells ◽  
A Cell ◽  
Messenger System ◽  
Rat Thyroid ◽  
Stimulation Of

Thyroid-stimulating hormone (TSH; thyrotropin) produces a pleiotropic response in the thyroid gland, accelerating nearly every aspect of metabolic turnover within the follicular epithelia. We examined the effects of TSH on expression of Na(+)-K(+)-ATPase in FRTL-5 cells, a cell line derived from rat thyroid. TSH (10 mU/ml) produced a nearly twofold increase in abundance of the mRNA encoding the catalytic alpha 1-subunit within 6 h of treatment. With the four mRNAs encoding the beta 1-subunit, TSH produced a striking increase in abundance, but this regulation was discoordinate, and some species increased more than others. Similar increases in mRNA abundance were elicited by activators of the adenosine 3',5'-cyclic monophosphate second messenger system. In contrast to the alpha 1- and beta 1-mRNAs, the abundance of the mRNA encoding the beta 2-subunit was unchanged with TSH after 6 h, indicating that the effects of thyrotropin were not universal or indiscriminate. Thyrotropin also caused a 76% increase in Na(+)-K(+)-ATPase activity and a 46% increase in pump-mediated transport after 48 h. These studies suggest that the changes in metabolic turnover initiated by TSH during hormone synthesis include upregulation of the N(+)-K+ pump.

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