Cobra cardiotoxin-induced cell death in fetal rat cardiomyocytes and cortical neurons: different pathway but similar cell surface target

Toxicon. 2005 Sep 15;46(4):430-40. doi: 10.1016/j.toxicon.2005.06.012.

Abstract

Cobra cardiotoxins (CTXs) are basic polypeptides with diverse pharmacological functions that are cytotoxic to many different cell types through both necrotic and apoptotic cell death pathways. In this comparative study of the action of CTX A3 from the Taiwan cobra (Naja atra) on fetal rat cardiomyocytes and cortical neurons, it was shown that CTX A3 induced different patterns of elevation of intracellular Ca2+ concentration ([Ca2+]i), CTX internalization, caspase-3 activity and viability. Application of an anti-sulfatide monoclonal antibody, O4 specific for 3-sulfo-galactose lipid, but not in the control experiments using anti-GM3 monoclonal antibody, reduces CTX-induced [Ca2+]i elevation, CTX internalization and toxicity. Therefore, CTX may target similar sulfo-containing cell surface receptors in both fetal rat cardiomyocytes and cortical neurons, but induce cell death through different pathways specific to each cell type.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal
  • Calcium / metabolism
  • Caspase 3
  • Caspases / metabolism
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Cell Nucleus / drug effects
  • Cobra Cardiotoxin Proteins / toxicity*
  • Fetus / drug effects*
  • Mass Spectrometry
  • Myocardium / pathology*
  • Necrosis / chemically induced*
  • Neurons / drug effects
  • Neurons / pathology*
  • Rats
  • Rats, Wistar
  • Taiwan

Substances

  • Antibodies, Monoclonal
  • Cobra Cardiotoxin Proteins
  • Casp3 protein, rat
  • Caspase 3
  • Caspases
  • Calcium