Cycloheximide and actinomycin D block the toxic effect of glutamic acid on PC12 cells.
Programmed cell death is considered to play a key role during development and also during physiopathological events such as neurodegenerative diseases and ischaemia. We have recently shown in PC12 cells that glutamate induces a progressive cytotoxicity which is only visible 8-10 h after incubation with glutamate for at least 4-6 h. We now present evidence that the toxic action of glutamate may correspond to programmed cell death because it is blocked by either actinomycin D or cycloheximide. This effect, however, may not be due to apoptosis since it is not blocked by aurintricarboxylic acid, a non-specific inhibitor of endonucleases, and neither chromatin condensation nor DNA fragmentation or liberation is seen after glutamate treatment.
Serghini
R
R
Laboratoire de Neurosciences, CNRS URA 1829, Caen, France.
Froissard
P
P
Sola
B
B
Duval
D
D
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001312:Aurintricarboxylic Acid / Q000494:pharmacology; D003513:Cycloheximide / Q000494:pharmacology*; D004249:DNA Damage; D003609:Dactinomycin / Q000494:pharmacology*; D018698:Glutamic Acid / Q000633:toxicity*; D016716:PC12 Cells; D051381:Rats
D003609:Dactinomycin; D018698:Glutamic Acid; D001312:Aurintricarboxylic Acid; D003513:Cycloheximide