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Omeprazole induces apoptosis in jurkat cells

L Scaringi1, P Cornacchione, E Ayroldi

  • 1Department of Clinical and Experimental Medicine, General Pathology and Immunology Section, General Hospital, University of Perugia, Perugia, Italy. scaringi@unipg.it

International Journal of Immunopathology and Pharmacology
|October 6, 2004
PubMed

Insights

Omeprazole induces apoptosis in Jurkat cells via lysosomal destabilization and caspase activation. Both caspases and cysteine cathepsins play a role in this cell death pathway.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Pharmacology

Background:

  • Omeprazole is a proton pump inhibitor.
  • Its potential to induce apoptosis is not well understood.

Purpose of the Study:

  • To investigate the apoptotic effects of omeprazole (OM) on Jurkat cells.
  • To elucidate the molecular mechanisms underlying OM-induced apoptosis.

Main Methods:

  • Jurkat cells were treated with varying concentrations of OM.
  • Apoptosis, caspase cleavage (caspase 3, PARP), lysosomal stability, and protease activity were assessed.
  • Inhibitors of caspases (DEVD-CHO, ZVAD-fmk) and lysosomal enzymes (E64d) were used.

Main Results:

  • OM induced time- and concentration-dependent apoptosis in Jurkat cells.
  • OM caused rapid cleavage of caspase 3 and PARP.
  • Lysosomal destabilization occurred early and correlated with apoptosis.
  • Caspase inhibition partially blocked apoptosis, while lysosomal enzyme inhibition showed strong protection.
  • A general caspase inhibitor (ZVAD-fmk) that also inhibits cathepsins provided complete protection.

Conclusions:

  • Omeprazole exhibits a potent apoptotic effect on Jurkat cells.
  • Both caspases and lysosomal cysteine cathepsins are critically involved in the execution phase of omeprazole-induced apoptosis.

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