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Role of aryl hydrocarbon receptor (AHR) in overall retinoid metabolism: Response comparisons to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure between wild-type and AHR knockout mice


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Título :
Role of aryl hydrocarbon receptor (AHR) in overall retinoid metabolism: Response comparisons to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure between wild-type and AHR knockout mice
Autor :
Esteban Mozo, Javier
Sánchez Pérez, Ismael
Hamscher, Gerd  
Miettinen, Hanna  
Korkalainen, Merja  
Viluksela, Matti  
Pohjanvirta, Raimo  
Hakansson, Helen
Editor :
Elsevier
Departamento:
Departamentos de la UMH::Biología Aplicada
Fecha de publicación:
2021-02-16
URI :
https://hdl.handle.net/11000/37573
Resumen :
Young adult wild-type and aryl hydrocarbon receptor knockout (AHRKO) mice of both sexes and the C57BL/6J background were exposed to 10 weekly oral doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; total dose of 200 μg/kg bw) to further characterize the observed impacts of AHR as well as TCDD on the retinoid system. Unexposed AHRKO mice harboured heavier kidneys, lighter livers and lower serum all-trans retinoic acid (ATRA) and retinol (REOH) concentrations than wild-type mice. Results from the present study also point to a role for the murine AHR in the control of circulating REOH and ATRA concentrations. In wild-type mice, TCDD elevated liver weight and reduced thymus weight, and drastically reduced the hepatic concentrations of 9-cis-4-oxo-13,14- dihydro-retinoic acid (CORA) and retinyl palmitate (REPA). In female wild-type mice, TCDD increased the hepatic concentration of ATRA as well as the renal and circulating REOH concentrations. Renal CORA concentrations were substantially diminished in wild-type male mice exclusively following TCDD-exposure, with a similar tendency in serum. In contrast, TCDD did not affect any of these toxicity or retinoid system parameters in AHRKO mice. Finally, a distinct sex difference occurred in kidney concentrations of all the analysed retinoid forms. Together, these results strengthen the evidence of a mandatory role of AHR in TCDD-induced retinoid disruption, and suggest that the previously reported accumulation of several retinoid forms in the liver of AHRKO mice is a line-specific phenomenon. Our data further support participation of AHR in the control of liver and kidney development in mice.
Palabras clave/Materias:
Aryl hydrocarbon receptor
2,3,7,8-Tetrachlorodibenzo-p-dioxin
TCDD
Genetically modified organisms
Retinoids
Vitamin A
Área de conocimiento :
CDU: Ciencias puras y naturales: Biología
Tipo de documento :
info:eu-repo/semantics/article
Derechos de acceso:
info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
DOI :
https://doi.org/10.1016/j.reprotox.2021.02.004
Publicado en:
Reproductive Toxicology, Volume 101, April 2021, Pages 33-49
Aparece en las colecciones:
Artículos Biología Aplicada



Creative Commons La licencia se describe como: Atribución-NonComercial-NoDerivada 4.0 Internacional.