Linked Life Data

6438923

Source:http://linkedlifedata.com/resource/pubmed/id/6438923

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1985-1-3
pubmed:abstractText
Factors which determine the acetaminophen glucuronidation capacity in the male rat have been examined. Conditions previously shown to increase (streptozotocin diabetes) or decrease (a 24 h fast) the glucuronidation capacity in vivo did not alter the microsomal glucuronyl transferase activity, indicating that the amount of enzyme is not rate-limiting. Acetaminophen caused a rapid depletion of hepatic levels of the co-substrate, UDPGA; both the extent of depletion and the time required for recovery back to pre-drug levels were dependent on the dose of acetaminophen administered. The amount of UPDGA required for the glucuronidation of a therapeutic dose was nearly equal to the total content of UDPGA in the liver; after a toxic dose, the UDPGA demand was over 100-fold greater than the normal basal level. It is concluded that the glucuronidation capacity of the animals is determined by their capacity to synthesize UDPGA, which in turn is dependent on flux through the glucuronic acid pathway.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0049-8254
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
553-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Role of UDPGA flux in acetaminophen clearance and hepatotoxicity.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't