Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-3-18
pubmed:abstractText
Programmed cell death or apoptosis is characterized by typical morphological alterations. By transmission electron microscopy, apoptotic cells are identified by condensation of the chromatin in tight apposition to the nuclear envelope, alteration of the nuclear envelope and fragmentation of the nucleus, whereas integrity of the plasma membrane and organelles is preserved. Conversely cells undergoing necrosis display an early desintegration of cytoplasmic membrane and swelling of mitochondria. In this study we assessed by flow cytometry the sequential alterations of forward angle light scatter, 90 degrees light scatter, and fluorescence associated with fluorescein diacetate, rhodamine 123, and propidium iodide in two human B cell lines undergoing apoptosis induced by the topoisomerase II inhibitor VP-16. The kinetics of these modifications were compared to those of cells undergoing necrosis induced by sodium azide. At the same time intervals, cells were examined by transmission electron microscopy and by UV microscopy after staining with Hoechst 33342. We report that sequential changes in light scatters and fluorescein diacetate are similar in cells undergoing apoptosis or necrosis, whereas apoptosis is characterized by a slightly delayed decrease of mitochondrial activity as assessed by rhodamine 123 staining. Surprisingly a part of cells undergoing apoptosis displayed an early uptake of propidium iodide followed by a condensation and then a fragmentation of their nuclei. It is concluded that uptake of propidium iodide is a very early marker of cell death which does not discriminate between necrosis and apoptosis. Along with biochemical criteria, nuclear morphology revealed by staining with Hoechst 33342 would seem to be of the most simple and most discriminative assay of apoptosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0196-4763
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
275-83
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8582250-Animals, pubmed-meshheading:8582250-Apoptosis, pubmed-meshheading:8582250-Azides, pubmed-meshheading:8582250-Cell Hypoxia, pubmed-meshheading:8582250-Cell Membrane, pubmed-meshheading:8582250-Cell Nucleus, pubmed-meshheading:8582250-Cells, Cultured, pubmed-meshheading:8582250-Etoposide, pubmed-meshheading:8582250-Humans, pubmed-meshheading:8582250-Light, pubmed-meshheading:8582250-Mice, pubmed-meshheading:8582250-Mice, Inbred BALB C, pubmed-meshheading:8582250-Microscopy, Electron, pubmed-meshheading:8582250-Microscopy, Fluorescence, pubmed-meshheading:8582250-Mitochondria, pubmed-meshheading:8582250-Propidium, pubmed-meshheading:8582250-Scattering, Radiation, pubmed-meshheading:8582250-Sodium Azide, pubmed-meshheading:8582250-Thymus Gland, pubmed-meshheading:8582250-Tumor Cells, Cultured
pubmed:year
1995
pubmed:articleTitle
Kinetics of plasma membrane and mitochondrial alterations in cells undergoing apoptosis.
pubmed:affiliation
Centre Commun de Cytométric en Flux, Hôpital Edouard Hérriot, Lyon, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't