Mechanisms of cycloheximide‐induced apoptosis in liver cells

Abstract
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.