Cycloheximide can rescue heat-shocked L cells from death by blocking stress-induced apoptosis.
Cultured mouse L cells undergo apoptosis upon 1 h heat shock at 43 and 45 degrees C. Morphologically characteristic apoptotic cells begin to appear soon after the shock. Immunohistochemistry with anti-transglutaminase antibody shows that in most treated cells the enzyme is induced. Its activation results in the formation of highly cross-linked detergent-resistant apoptotic bodies during recovery. Cycloheximide added during hyperthermic stress inhibits the appearance of apoptotic bodies, showing that heat-shock-induced apoptosis is dependent on protein neosynthesis. The analysis of colony-forming ability of heat-shocked L cells shows a survival of 5% at 43 degrees C and less than 0.02% at 45 degrees C. When protein synthesis is inhibited during heat shock the fraction of surviving cells increases to 23% at 43 degrees C and 0.9% at 45 degrees C. This suggest that part of the cells that die upon heat shock are not heavily damaged and would have survived in the presence of a block in protein synthesis.
Ghibelli
L
L
Dipartimento di Biologia, Università di Roma Tor Vergata, Italy.
Nosseri
C
C
Oliverio
S
S
Piacentini
M
M
Autuori
F
F
D000818:Animals; D000906:Antibodies; D016923:Cell Death / Q000187:drug effects*; D003513:Cycloheximide / Q000494:pharmacology*; D004790:Enzyme Induction; D006358:Hot Temperature; D007739:L Cells / Q000737:chemistry / Q000187:drug effects*; D051379:Mice; D011503:Transglutaminases / Q000032:analysis
D000906:Antibodies; D003513:Cycloheximide; D011503:Transglutaminases