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glutathione-s-transferase p-form 8-tetrachlorodibenzo-p-dioxin-induced oxidative stress glutathione s-transferases act month download article/chapter 9-cis-retinoyl-β-d-glucuronide 8-tetrachlorodibenzo-p-dioxin-treated rats cellular retinol-binding protein line solid-phase extraction 100 µg/kg body weight retinoic-acid-induced gene expression cellular retinoid-binding proteins retinoyl-β-d-glucuronide 9-3h]dibenzo-p-dioxin noninduced microsomal udp-glucuronosyltransferases tgf-β mediated fibrogenesis p450 isozyme-selective inhibitors 13-di-cis-retinoic acid dioxin-resistant mice treated aromatic hydrocarbon receptor christina trossvik & helen håkansson 4-oxo-13-cis-retinoic acid 13-cis-4-oxo-retinoic acid cytochrome-p-450-dependent metabolism sprague-dawley rats induced male sprague-dawley rats vitamin a-free diet microcolumn liquid chromatography trans-retinoic acid 4-hydroxylation found dose-dependent elevation 9-cis-retinoic acid catalyzed exerts retinoid-mimetic effects tissue transglutaminase stimulation rat phenol udp-glucuronosyltransferase full article pdf oxidative stress induced rat recombinant udp 8-tetrachlorodibenzo-p-dioxin tetrachlorodibenzo-p-dioxin vitamin a-sufficient rats oxidative stress response retinoid-binding proteins privacy choices/manage cookies retinoyl-β-glucuronide human p-450 cytochromes 13-di-cis-ra high embryonic concentrations strategic environmental research polychlorinated biphenyl congeners tissue-specific constitutive hl60 cells transfected

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         description:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is known to influence vitamin A homeostasis. In order to investigate the mechanism behind this retinoid disruption, male Sprague-Dawley rats were exposed to TCDD at doses ranging from 0.1 to 100 µg/kg body weight, and were killed 3 days after exposure. Additional groups of rats were killed 1 and 28 days after a single oral dose of 10 µg TCDD/kg body weight. Serum, kidney, and liver were investigated for retinoid levels, as well as gene expression and enzyme activities relevant for retinoid metabolism. Besides the well known effects of TCDD on apolar retinoids, i.e. decreased hepatic and increased renal retinyl ester (RE) levels, we have found dose-dependent elevation of all-trans-retinoic acid (all-trans-RA) levels in all investigated tissues. In the liver, 9-cis-4-oxo-13,14-dihydro-RA was drastically decreased by TCDD in a dose-dependent manner. In serum, cis-isomers of all-trans-RA, including 9,13-di-cis-RA, were significantly reduced already at the lowest dose level. Protein and mRNA levels of cellular retinol binding protein I (CRBP-I) in liver or kidneys were not significantly altered by TCDD exposure at doses at which retinoid levels were affected, making CRBP-I an unlikely candidate to account for the alterations in retinoid metabolism caused by TCDD. The expression and activities of relevant cytochrome P450 (CYP) enzymes with potential roles in all-trans-RA synthesis and/or degradation (CYP1A1, 1A2, and 2B1/2) were also monitored. A possible role of CYP1A1 in TCDD-induced all-trans-RA synthesis is suggested from the time-course relationship between CYP1A1 activity and all-trans-RA levels in liver and kidney. The significant alteration of the all-trans-RA metabolism has the potential to contribute significantly to the toxicity of TCDD.
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