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Induction of cell death by the lysosomotropic detergent MSDH

W Li1, X Yuan, G Nordgren

  • 1Division of Pathology II, Faculty of Health Sciences, University of Linköping, S-581 85, Linköping, Sweden.

FEBS Letters
|March 21, 2000
PubMed

Insights

Lysosomal rupture induced by O-methyl-serine dodecylamide hydrochloride (MSDH) triggers apoptosis via caspase activation or necrosis. This suggests lysosomal proteases can directly cause cell death.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Toxicology

Background:

  • Lysosomes are crucial cellular organelles involved in degradation.
  • Lysosomal membrane integrity is vital for cell homeostasis.
  • Dysfunctional lysosomes are implicated in various pathologies.

Purpose of the Study:

  • To investigate the role of lysosomal rupture in programmed cell death.
  • To explore the mechanism by which lysosomal damage induces apoptosis and necrosis.
  • To characterize the effects of O-methyl-serine dodecylamide hydrochloride (MSDH) on lysosomal stability and cell fate.

Main Methods:

  • Utilized macrophage-like cells rich in lysosomes.
  • Applied varying concentrations of the synthetic detergent O-methyl-serine dodecylamide hydrochloride (MSDH).
  • Monitored for lysosomal rupture, pro-caspase-3 activation, apoptosis, mitochondrial potential changes, and necrosis.

Main Results:

  • Low MSDH concentrations caused partial lysosomal rupture, leading to delayed pro-caspase activation and apoptosis.
  • Mitochondrial transmembrane potential declined early in apoptosis, secondary to lysosomal destabilization.
  • High MSDH concentrations induced extensive lysosomal rupture, resulting in necrosis.

Conclusions:

  • Controlled lysosomal rupture can initiate apoptosis through caspase activation.
  • Released lysosomal proteases may directly trigger apoptosis or indirectly cause cell death via mitochondrial damage.
  • MSDH serves as a tool to study lysosomal function and its role in cell death pathways.

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