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

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

Author information

1
Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, PA 15261.

Abstract

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.

PMID:
8160188
[Indexed for MEDLINE]

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