Retinal ischemia leads to apoptosis which is ameliorated by aurintricarboxylic acid.
Transient retinal ischemia results in a delayed cell death of the inner retinal layers. This study demonstrates that this ischemic cell death occurs, at least in part, through apoptosis. The general endonuclease inhibitor, aurintricarboxylic acid, protected rat retinal cells from ischemic cell damage when administered before the onset of ischemia and, more importantly, when administered 6 hr after the insult. Thus, the demonstration that transient retinal ischemia results in cell damage as a result of apoptosis opens new therapeutic strategies aimed at lessening retinal damage as a result of this process.
Rosenbaum
D M
DM
Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Rosenbaum
P S
PS
Gupta
A
A
Michaelson
M D
MD
Hall
D H
DH
Kessler
J A
JA
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001312:Aurintricarboxylic Acid / Q000627:therapeutic use*; D053938:DNA Fragmentation; D005819:Genetic Markers; D007511:Ischemia / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008854:Microscopy, Electron; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000502:physiology* / Q000648:ultrastructure
D005819:Genetic Markers; D001312:Aurintricarboxylic Acid