PMID: 3442379Jan 1, 1987

Inhibitory effect of tetrachloro-p-hydroquinone and other metabolites of hexachlorobenzene on hepatic uroporphyrinogen decarboxylase activity with reference to the role of glutathione

Annals of the New York Academy of Sciences
G KossW Koransky

Abstract

Exposure of rats to HCB caused a dose-dependent depletion of GSH. Chlorophenolic and sulfur-containing metabolites of HCB incubated with GSH-free rat liver cytosolic protein drastically diminished the UROD activity. In addition, HCB also exhibited inhibitory potency. The most effective compounds studied were TCH and its oxidation product, chloranil. Incubation of liver cytosolic protein and of GSH with HCB and its metabolites yielded results that suggested interaction between the compounds and cell constituents--an interaction that may cause inhibition of the hepatic UROD activity in the HCB-exposed organism.

References

Jul 1, 1994·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·G KossA Seubert
Feb 1, 1992·Toxicology and Applied Pharmacology·M D'Amour, M Charbonneau
Sep 15, 1998·Immunopharmacology and Immunotoxicology·M L QueirozJ P Silveira
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Related Concepts

Uroporphyrinogen Decarboxylase Activity
UROD gene
August Rats
Sulfur
Hepatic
Carboxy-Lyases
Glutathione Measurement
Oxidation
Vulklor
Organism

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