Cycloheximide in sublethal doses caused apoptosis in liver cells in vivo, inducing c-myc, c-fos, c-jun and p53 genes and accumulation of sphingosine, a toxic product of the sphingomyelin cycle. These data support the hypothesis that continuous synthesis of labile protective proteins is required to restrain apoptosis in liver; sphingosine might be important in mediating cycloheximide-induced apoptosis as an endogenous modulator of protein kinase C activity.
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Alessenko et al. (1997) studied this question.
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