Linked Life Data

10079838

Source:http://linkedlifedata.com/resource/pubmed/id/10079838

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-6-1
pubmed:abstractText
Studies in our laboratory indicate that extracellular ATP (ATP)o may induce cell death by reactive oxygen insults. We have also shown that the Ca(2+)-induced oxidative stress as elicited by ATP may lead to an activation of a specific AP-1 activity. Since early impairment of mitochondria constitutes a critical event of the apoptotic cell death, we have examined whether (ATP)o will affect mitochondrial damage and cell injury by using mitochondrial specific probes, dihydrorhodamine and 3-(4,5-dimethylthiazo-2-yl)-2,5-diphenyl tetrazolium bromide (MTT). We have found that (ATP)o induced cell death in a concentration dependent manner by MTT assay. The (ATP)o induced cell death correlated well with the reactive oxygen species (ROS) generation in mitochondria, since (ATP)o enhanced both cell death and ROS production and antioxidant blocked both of these processes. We found (ATP)o treatment led to apoptotic cell death by examining DNA laddering and the TUNEL assay. Interestingly, vitamin C and vitamin E combined treatment appeared to attenuate the (ATP)o-induced apoptosis. Results indicated that (ATP)o may cause oxidative damage of mitochondria leading to apoptotic cell death. Antioxidants may be useful in preventing apoptosis by preventing ROS formation in mitochondria.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0065-2598
pubmed:author
pubmed:issnType
Print
pubmed:volume
446
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
73-83
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Extracellular ATP-induced apoptosis in PC12 cells.
pubmed:affiliation
Department of Pharmacology, University of Missouri, Columbia 65212, USA. Pharmays@muccmail.missouri.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.