2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) poisoning in Victor Yushchenko: identification and measurement of TCDD metabolites

@article{Sorg20092378tetrachlorodibenzopdioxinP,
  title={2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) poisoning in Victor Yushchenko: identification and measurement of TCDD metabolites},
  author={Olivier Sorg and Markus Zennegg and Peter Schmid and Raisa M. Fedosyuk and R Valikhnovskyi and O Gaide and V Kniazevych and Jean Hilaire Saurat},
  journal={The Lancet},
  year={2009},
  volume={374},
  pages={1179-1185}
}
BACKGROUND 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has a long half-life of 5-10 years in human beings as a result of its high lipophilicity, and little or no metabolism. [...] Key Method We identified TCDD and its metabolites, and monitored their levels for 3 years using gas chromatography and high-resolution mass spectrometry in samples of blood serum, adipose tissue, faeces, skin, urine, and sweat, after they were extracted and cleaned with different organic solvents. Expand
Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain
TLDR
A reverse set of changes in the AHR protein and mRNA response to TCDD and feed restriction is demonstrated, suggesting that AHR might function also as a physiological regulator, possibly involved in the maintenance of energy balance.
2,3,7,8-Tetrachlorodibenzo-p-Dioxin Alters Lipid Metabolism and Depletes Immune Cell Populations in the Jejunum of C57BL/6 Mice.
TLDR
Results suggest TCDD elicits changes that support hepatic lipid accumulation, macrophage migration, and the progression of hepatic steatosis to steatohepatitis.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-elicited effects on bile acid homeostasis: Alterations in biosynthesis, enterohepatic circulation, and microbial metabolism
TLDR
Results suggest that systemic alterations in enterohepatic circulation, as well as host and microbiota bile acid metabolism, favor bile acids accumulation that contributes to AhR-mediated hepatotoxicity.
A new method for identification of in vitro metabolites of 2,3,7,8-TCDD with rat liver microsomes by using liquid chromatography-mass spectrometry
2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) is known as a highly toxic environmental contaminant and poses potential risks to human and animal health. As a persistent organic pollutant,
2,3,7,8 Tetrachlorodibenzo-p-dioxin-induced RNA abundance changes identify Ackr3, Col18a1, Cyb5a and Glud1 as candidate mediators of toxicity
TLDR
Time course and dose–response analyses of mRNA abundance following TCDD insult indicate that eight genes are similarly regulated in livers of both strains of rat, suggesting that they are not central to the severe L–E-specific T CDD-induced toxicities.
2,3,7,8-Tetrachlorodibenzo-p-dioxin elicited decreases in cobalamin inhibits methylmalonyl-CoA mutase activity redirecting propionyl-CoA metabolism to the β–oxidation-like pathway resulting in hepatic accumulation of the toxic intermediate acrylyl-CoA
TLDR
Results suggest MUT activity was impaired due to Cbl depletion by TCDD causing propionyl-CoA metabolism to be redirected to the alternate Cbl-independent β–oxidation-like pathway resulting in hepatic acrylyl- CoA accumulation.
Characterization of the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-provoked strong and rapid aversion to unfamiliar foodstuffs in rats.
TLDR
It is indicated that temporal proximity to TCDD exposure is a requisite for the avoidance response which emerges rapidly and may linger on for extended periods, but is not strictly confined to any specific food type.
Serum 2,3,7,8-Tetrachlorodibenzo-p-dioxin Levels and Their Association With Age, Body Mass Index, Smoking, Military Record-based Variables, and Estimated Exposure to Agent Orange in Korean Vietnam Veterans
TLDR
The average serum TCDD levels in the Korean Vietnam veterans were lower than those reported for other occupationally or environmentally exposed groups and US Vietnam veterans, and their use as an objective marker of Agent Orange exposure may have some limitations.
2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin alters sebaceous gland cell differentiation in vitro
TLDR
Evidence is provided that TCDD effects on human sebocytes are mediated through the AhR signalling pathway, which affects the differentiation of sebaceous gland cells probably by switching humanSebaceous into keratinocyte‐like differentiation.
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Abstract. In spring 1998, two women were diagnosed with severe 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) intoxication. Over the following 3 years, TCDD levels were monitored under various attempts
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Human feces samples from a self-dosing experiment were analyzed by gas chromatography/mass spectrometry (GC/MS) for [3H]-2,3,7,8-tetrachlorodibenzo-p-dioxin (3H-2378-TCDD) to determine that 36-44% of
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TLDR
Tritiated TCDD is used to search for metabolites in the bile of rats and marked changes in lipophilicity and mobility in TLC of the excreted radioactivity are found, hinting at the formation of phenolic hydroxyl groups in the dioxin molecule.
The effect of pretreatment on the biliary excretion of 2,3,7,8-tetrachlorodibenzo-p-dioxin, 2,3,7,8-tetrachlorodibenzofuran, and 3,3',4,4'-tetrachlorobiphenyl in the rat.
TLDR
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TLDR
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TLDR
Biliary excretion of radioactivity in both male and female juvenile rats was similar to that of adult males; senescent male rats excreted less, and Pretreatment with PB, DEX, or ABT resulted in similar decrease in biliaryexcretion of TCDD-derived radioactivity as observed in senescentmale rats.
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TLDR
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TLDR
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