Clostridium perfringens enterotoxin acts by producing small molecule permeability alterations in plasma membranes

Toxicology. 1994 Feb 28;87(1-3):43-67. doi: 10.1016/0300-483x(94)90154-6.


Clostridium perfringens enterotoxin (CPE) appears to utilize a unique mechanism of action to directly affect the plasma membrane permeability of mammalian cells. CPE action involves a multi-step action which culminates in cytotoxicity. Initially CPE binds to a protein receptor on mammalian plasma membranes. The membrane-bound CPE then becomes progressively more resistant to release by proteases (a phenomenon consistent with the insertion of CPE into membranes). This 'inserted' CPE then participates in the formation of a large complex in plasma membranes which contains one CPE: one 70 kDa membrane protein: one 50 kDa membrane protein. Upon formation of large complex, plasma membranes become freely permeable to small molecules such as ions and amino acids. This CPE-induced disruption of the cellular colloid-osmotic equilibrium then causes secondary cellular effects and cell death.

Publication types

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

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Cell Membrane / drug effects*
  • Cell Membrane Permeability / drug effects
  • Clostridium perfringens / chemistry
  • Clostridium perfringens / pathogenicity*
  • Enterotoxins / chemistry
  • Enterotoxins / toxicity*
  • Humans
  • Molecular Sequence Data
  • Molecular Weight


  • Enterotoxins