Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1992-4-2
pubmed:abstractText
Biochemical characteristics relevant to the differential susceptibilities of liver, heart, and intestine to acute Adriamycin toxicity were examined in female CD-1 mice with and without intravenous Adriamycin (dose range 23-30 mg/kg). The liver which, unlike heart and intestine, is relatively resistant to Adriamycin toxicity, had high levels of glutathione and glutathione peroxidase, and exhibited a sharp decline in non-protein thiol concentrations within 1-3 hr with rebound by 6 hr after Adriamycin. Covalent binding to Adriamycin or its metabolites could not account quantitatively for the loss of non-protein thiols, implicating an oxidative mechanism. No lipid peroxidation was observed in the liver, apparently due to effective utilization of antioxidant defenses. Adriamycin caused significant increases in cardiac lipid peroxides, indicative of oxidative tissue damage, which would be expected to exacerbate cardiotoxicity. However, non-protein thiol concentrations did not decrease in heart or in intestine in response to Adriamycin. Both heart and intestine had extremely low levels of glutathione peroxidase activity, which may limit glutathione utilization for protection against oxidative toxicity. The activity of DT diaphorase, which may have an activating role in Adriamycin metabolism, was high in heart and intestine and was induced 4-fold in liver in response to Adriamycin.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
831-6
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Biochemical determinants of Adriamycin toxicity in mouse liver, heart and intestine.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock 72205-7199.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.