Linked Life Data

10573525

Source:http://linkedlifedata.com/resource/pubmed/id/10573525

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1999-12-16
pubmed:abstractText
The purpose of this study was to examine distribution and time history of oxidative stress during the hyperacute period of reperfusion in the liver grafts undergoing cold ischemia and to investigate roles of Kupffer cells as a potential oxidant source. Rat livers were harvested at 4 degrees C in University of Wisconsin solution and followed by reperfusion with Krebs-Henseleit buffer under monitoring bile excretion. To investigate oxidative changes, laser-confocal microfluorography was performed in reperfused livers preloaded with dichlorodihydrofluorescein diacetate succinimidyl ester, a fluorescence precursor sensing intracellular hydroperoxide generation. Livers undergoing the 16-hour cold storage displayed an impaired recovery of bile acid-dependent bile output concurrent with a marked increase in hydroperoxide generation in hepatocytes, which occurred as early as 5 minutes after the onset of reperfusion, whereas the status of lobular perfusion was well maintained. Pretreatment with liposome-encapsulated dichloromethylene diphosphonate, a Kupffer cell-depleting reagent, did neither alter the reperfusion-induced periportal oxidative changes nor improve the recovery of bile output in the graft. On the other hand, EPCK, a hepatotropic antioxidant composed of vitamin E phosphate ester bound to vitamin C, not only diminished the oxidative changes but also improved the reduction of bile acid-dependent bile output. Furthermore, the reagent was capable of inhibiting H(2)O(2)-induced oxidative stress in cultured hepatocytes. These results suggest that hepatocytes constitute a major site of the oxidative insult triggered through Kupffer cell-independent mechanisms and serve as an important cellular component to be protected by antioxidant therapeutics.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1454-63
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10573525-Animals, pubmed-meshheading:10573525-Antioxidants, pubmed-meshheading:10573525-Ascorbic Acid, pubmed-meshheading:10573525-Bile, pubmed-meshheading:10573525-Clodronic Acid, pubmed-meshheading:10573525-Cold Temperature, pubmed-meshheading:10573525-Deferoxamine, pubmed-meshheading:10573525-Fluoresceins, pubmed-meshheading:10573525-Hydrogen Peroxide, pubmed-meshheading:10573525-Kupffer Cells, pubmed-meshheading:10573525-Liver, pubmed-meshheading:10573525-Liver Transplantation, pubmed-meshheading:10573525-Male, pubmed-meshheading:10573525-Mitochondria, Liver, pubmed-meshheading:10573525-Oxidative Stress, pubmed-meshheading:10573525-Rats, pubmed-meshheading:10573525-Rats, Wistar, pubmed-meshheading:10573525-Reperfusion Injury, pubmed-meshheading:10573525-Taurocholic Acid, pubmed-meshheading:10573525-Vitamin E
pubmed:year
1999
pubmed:articleTitle
Kupffer cell-independent acute hepatocellular oxidative stress and decreased bile formation in post-cold-ischemic rat liver.
pubmed:affiliation
Department of Surgery and Department of Biochemistry, Keio University School of Medicine, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't