Linked Life Data

8821817

Source:http://linkedlifedata.com/resource/pubmed/id/8821817

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-11-15
pubmed:abstractText
Hypoxia is considered to result in a necrotic form of cell injury. We examined the role of endonuclease activation, considered a feature of apoptosis, in DNA damage and cell death in hypoxic injury in LLC-PK1 cells. Hypoxia in LLC-PK1 cells was induced using a combination of glucose deprivation and a mitochondrial inhibitor, antimycin A (10 microM). Chemical hypoxia caused DNA damage as measured by the alkaline unwinding assay and internucleosomal DNA fragmentation that preceded cell death. Incubating protein extract of cells subjected to chemical hypoxia with calf thymus DNA resulted in oligonucleosome length fragments, which were prevented by an endonuclease inhibitor, aurintricarboxylic acid. Chemical hypoxia resulted in an increased DNA degrading activity with a molecular mass of approximately 15 kDa. Endonuclease inhibitors, aurintricarboxylic acid and Evans blue, prevented antimycin A-induced DNA strand breaks, fragmentation and cell death. We conclude that endonuclease activation plays an important role in chemical hypoxic injury to LLC-PK1 cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
355-61
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Endonuclease induced DNA damage and cell death in chemical hypoxic injury to LLC-PK1 cells.
pubmed:affiliation
Division of Nephrology, University of Arkansas for Medical Sciences, Little Rock, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't