dc.contributor.author | Esteban, Javier | |
dc.contributor.author | Sánchez, Ismael | |
dc.contributor.author | Hamscher, Gerd | |
dc.contributor.author | Miettinen, Hanna M | |
dc.contributor.author | Korkalainen, Merja | |
dc.contributor.author | Viluksela, Matti | |
dc.contributor.author | Pohjanvirta, Raimo | |
dc.contributor.author | Håkansson, Helen | |
dc.date.accessioned | 2021-06-01T08:10:06Z | |
dc.date.available | 2021-06-01T08:10:06Z | |
dc.date.issued | 2021 | |
dc.identifier.uri | https://erepo.uef.fi/handle/123456789/25312 | |
dc.description.abstract | 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. | |
dc.language.iso | englanti | |
dc.publisher | Elsevier BV | |
dc.relation.ispartofseries | Reproductive toxicology | |
dc.relation.uri | http://dx.doi.org/10.1016/j.reprotox.2021.02.004 | |
dc.rights | CC BY 4.0 | |
dc.subject | aryl hydrocarbon receptor | |
dc.subject | 2,3,7,8-Tetrachlorodibenzo-p-dioxin | |
dc.subject | TCDD | |
dc.subject | genetically modified organisms | |
dc.subject | retinoids | |
dc.subject | vitamin A | |
dc.title | 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 | |
dc.description.version | published version | |
dc.contributor.department | School of Pharmacy, Activities | |
dc.contributor.department | Ympäristö- ja biotieteiden laitos / Toiminta | |
uef.solecris.id | 77003161 | en |
dc.type.publication | Tieteelliset aikakauslehtiartikkelit | |
dc.relation.doi | 10.1016/j.reprotox.2021.02.004 | |
dc.description.reviewstatus | peerReviewed | |
dc.format.pagerange | 33-49 | |
dc.relation.issn | 0890-6238 | |
dc.relation.volume | 101 | |
dc.rights.accesslevel | openAccess | |
dc.type.okm | A1 | |
uef.solecris.openaccess | Hybridijulkaisukanavassa ilmestynyt avoin julkaisu | |
dc.rights.copyright | © 2021 The Authors | |
dc.type.displayType | article | en |
dc.type.displayType | artikkeli | fi |
dc.rights.url | https://creativecommons.org/licenses/by/4.0/ | |