Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2002-12-19
pubmed:abstractText
Oxidative stress is considered to be an important pathogenic event in ischemia-reperfusion injury, leading to apoptosis or necrosis. We show acute cytotoxicity upon exposure to hydrogen peroxide (H(2)O(2)) in BEAS-2B cells and A549 cells. Single-cell gel electrophoresis showed formation of large comet tails from DNA upon oxidant exposure suggestive of DNA damage. The ATP content of the cells decreased upon exposure to H(2)O(2). Preincubation with 3-aminobenzamide (3-ABA), an inhibitor of poly (ADP-ribosyl) polymerase (PARP), prevented the cytotoxicity. The decrease in the ATP content of the cells was also prevented by 3-ABA. Increase in PARP activity was further confirmed by measuring incorporation of [(32)P]-NAD into nuclear proteins in presence of the cell extracts. Markers of apoptosis were not seen in cells treated with H(2)O(2) with or without 3-ABA pretreatment. These studies suggest that DNA damage is one of the primary reasons for oxidant-induced cell death and that PARP plays an important role in cell death due to its consumption of ATP. Further elaboration of this and other pathways that consume ATP may help prevent oxidant-mediated acute lung injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0190-2148
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
591-607
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Oxidant-induced cell death in respiratory epithelial cells is due to DNA damage and loss of ATP.
pubmed:affiliation
Critical Care Medicine Department, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892, USA.
pubmed:publicationType
Journal Article