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Inhibitory Effect of Tetrachloro‐ p ‐Hydroquinone and Other Metabolites of Hexachlorobenzene on Hepatic Uroporphyrinogen Decarboxylase Activity with Reference to the Role of Glutathione a
Author(s) -
KOSS GÜNTER,
LOSEKAM MARGA,
SEIDEL JUTTA,
STEINBACH KLAUS,
KORANSKY WOLFGANG
Publication year - 1987
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1987.tb48769.x
Subject(s) - uroporphyrinogen iii decarboxylase , chemistry , hexachlorobenzene , cytosol , incubation , potency , biochemistry , glutathione , inhibitory postsynaptic potential , hydroquinone , endocrinology , enzyme , in vitro , biology , heme , organic chemistry , pollutant
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.