Modulation of cell death pathways to apoptosis and necrosis of H2O2-treated rat thymocytes by lipocortin I

Biochem Biophys Res Commun. 1996 Mar 27;220(3):643-7. doi: 10.1006/bbrc.1996.0457.


Lipocortin I, also called annexin I, a calcium and phospholipid binding protein, protected rat thymocytes from H2O2-elicited necrosis and facilitated H2O2-induced apoptosis, while anti-lipocortin I antibody enhanced H202-elicited necrosis by blocking H202-induced apoptosis. Essentially similar results were obtained with phospholipase A2 inhibitors and activators such as 3,4-octyadecyl-benzylacrylic acid and melittin, respectively. Available evidence suggests that lipocortin I modulates signals for cell death pathways of H2O2-treated rat thymocytes to apoptosis and necrosis by regulating cellular phospholipase A2 activities but not by inhibiting membrane lipid peroxidation.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Annexin A1 / immunology
  • Annexin A1 / pharmacology*
  • Antibodies / pharmacology
  • Apoptosis / drug effects*
  • Arachidonic Acid / metabolism
  • Cell Death / drug effects*
  • Cells, Cultured
  • DNA / drug effects
  • Dose-Response Relationship, Drug
  • Hydrogen Peroxide / toxicity*
  • Lipid Peroxidation / drug effects
  • Male
  • Melitten / pharmacology
  • Necrosis
  • Phospholipids / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Thymus Gland / drug effects*
  • Thymus Gland / pathology
  • Thymus Gland / physiology


  • Annexin A1
  • Antibodies
  • Phospholipids
  • Melitten
  • Arachidonic Acid
  • DNA
  • Hydrogen Peroxide