Activation of calpain precedes morphological alterations during hydrogen peroxide-induced apoptosis in neuronally differentiated mouse embryonal carcinoma P19 cell line

Neurosci Lett. 2000 Jan 28;279(2):97-100. doi: 10.1016/s0304-3940(99)00960-x.

Abstract

In order to reveal neurodegeneration elicited by reactive oxygen intermediates (ROI), neuronally differentiated cells from mouse embryonal carcinoma P19 cell line were exposed to hydrogen peroxide (H2O2). Enhanced protein-phosphorylation on tyrosine residues was detectable within 5 min of exposure to H2O2, and gradual rises in intracellular free Ca2+ level and in calpain activity were observed. Furthermore, H2O2 stimulation of differentiated P19 cells for 24 h resulted in morphological alterations in somas as well as neurites. Also, within 6 h of H2O2 treatment DNA fragmentation has been detected. Taken together, these results suggest that oxidative stress induces degradation of cytoskeletal proteins presumably resulting from increased intracellular Ca2+ concentration and subsequent activation of calpain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Calcium / metabolism
  • Calpain / metabolism*
  • Carcinoma, Embryonal
  • Cell Differentiation
  • Enzyme Activation
  • Hydrogen Peroxide / pharmacology*
  • Kinetics
  • Mice
  • Neurons / cytology
  • Neurons / drug effects*
  • Neurons / physiology
  • Oxidative Stress
  • Phosphoproteins / metabolism
  • Phosphotyrosine
  • Tumor Cells, Cultured

Substances

  • Phosphoproteins
  • Phosphotyrosine
  • Hydrogen Peroxide
  • Calpain
  • Calcium