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Thus, when this conflict was prevented by serum depletion, apoptosis was suppressed.
The presence of apoptotic cells was prevented completely by benzyloxycarbonyl‐Val‐Ala‐fluoromethyl ketone (a nonspecific caspase inhibitor), indicating that apoptosis was mediated by caspase activation.
Apoptosis can be blocked by caspase inhibitors.
Apoptosis could be accelerated or prevented by modifying culture conditions or cell density, indicating that extracellular signals influenced the epimastigote decision between life and death.
Moreover, induction of apoptosis could be prevented by treating cells with an inhibitor of casp-8.
However, apoptosis can be inhibited by adding protein synthesis inhibitors, indicating de novo protein synthesis may be partially responsible for apoptosis.
As in many other cellular lineages susceptible to apoptosis, these degenerative changes can be prevented by treatment with the endonuclease antagonist, aurintricarboxylic acid, or by inhibiting de novo RNA or protein synthesis.
Apoptosis can be prevented by inhibitors of transcription or translation, suggesting a need for macromolecular synthesis in the apoptotic process.
Terminal apoptosis was thus prevented.
Apoptosis and barrier dysfunction could be prevented by caspase inhibition.

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