Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1988-4-20
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
514
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
148-59
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Inhibitory effect of tetrachloro-p-hydroquinone and other metabolites of hexachlorobenzene on hepatic uroporphyrinogen decarboxylase activity with reference to the role of glutathione.
pubmed:affiliation
Institute of Toxicology and Pharmacology, Philipps University, Marburg, Federal Republic of Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't