Send to

Choose Destination
Toxicology. 1994 Feb 28;87(1-3):43-67.

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

Author information

Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, PA 15261.


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.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center