Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1997-8-27
pubmed:abstractText
It has been proposed that nongenotoxic peroxisome proliferators may cause hepatocellular cancer by an oxidative damage-mediated mechanism(s). The argument for this hypothesis is based mainly on the noted ability of peroxisome proliferators to induce significantly H2O2-producing peroxisomal beta-oxidation while causing a minimal induction of H2O2-degrading catalase. The recent discovery, accurate determination, and use of isoprostanes as a sensitive indicator of oxidative damage prompted us to investigate whether induction of hepatic peroxisomal beta-oxidation in male B6C3F1 mice is accompanied by elevated levels of isoprostanes in those livers. The data show that while 7 days of feeding mice a diet containing 100 ppm [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (WY-14,643) increased peroxisomal beta-oxidation by 16-fold and catalase activity by only 2-fold, hepatic levels of esterified F2-isoprostanes were not altered. These levels were 2.8 +/- 0.5 ng/g liver in control mice and 2.4 +/- 0.1 ng/g liver in mice fed the experimental diet for 7 days. Consequently, it is concluded that oxidative stress does not appear to occur in response to peroxisome proliferation, as evidenced by the lack of increase in hepatic levels of F2-isoprostanes in livers of mice treated with the potent peroxisome proliferator WY-14,643.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1369-74
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Evidence against peroxisome proliferation-induced hepatic oxidative damage.
pubmed:affiliation
Division of Pharmacology, University of Missouri-Kansas City, 64108, U.S.A.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't