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Mechanisms of cycloheximide-induced apoptosis in liver cells

A V Alessenko1, Boikov PYa, G N Filippova

  • 1Institute of Biochemical Physics RAS, Moscow, Russia. aless@center.chph.ras.ru

FEBS Letters
|November 22, 1997
PubMed

Insights

Sublethal cycloheximide induces liver cell apoptosis by activating key genes and accumulating toxic sphingosine. This suggests protective proteins are vital for preventing liver cell death, with sphingosine potentially modulating protein kinase C.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Toxicology

Background:

  • Apoptosis, or programmed cell death, is a critical cellular process.
  • The role of specific genes and metabolic products in regulating apoptosis requires further elucidation.
  • Understanding liver cell apoptosis is crucial for addressing various liver diseases.

Purpose of the Study:

  • To investigate the effects of sublethal cycloheximide on liver cells in vivo.
  • To identify the molecular mechanisms underlying cycloheximide-induced apoptosis.
  • To explore the potential role of sphingosine in mediating this apoptotic process.

Main Methods:

  • Administration of sublethal doses of cycloheximide to liver cells in vivo.
  • Gene expression analysis to detect induction of c-myc, c-fos, c-jun, and p53.
  • Measurement of sphingosine accumulation within liver cells.

Main Results:

  • Cycloheximide treatment triggered apoptosis in liver cells.
  • Key apoptosis-related genes (c-myc, c-fos, c-jun, p53) were induced.
  • Significant accumulation of sphingosine, a toxic sphingomyelin cycle product, was observed.

Conclusions:

  • Continuous synthesis of labile protective proteins may be necessary to prevent liver apoptosis.
  • Sphingosine accumulation could play a role in mediating cycloheximide-induced liver cell apoptosis.
  • Sphingosine may act as an endogenous modulator of protein kinase C activity in this context.

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