C2 toxin is composed of two subunits: a binding component recognizing specific receptors on a variety of eukaryotic cells, and an enzyme component that ADP-ribosylates intracellular non-muscular G actin. This protein normally forms the microfilaments of the cytoskeleton; its ADP-ribosylation causes loss of the cell shape, an increase in vascular permeability, and enterotoxic and cytotoxic effects. C2 toxin may help the diffusion of the botulinum neurotoxin in the body by increasing vascular permeability, but it does not produce the symptoms of botulism. Although it is lethal in mice, its clinical significance for humans is unclear (139).
C3 toxin acts by ADP-ribosylating low molecular mass GTP-binding proteins of the Rho family, found in many types of host cells. The GTP-binding proteins regulate the eukaryotic cells metabolism and so C3 toxin might interfere with this regulation. However, the total lack of lethality makes the pathological significance of C3 toxin even more uncertain than that of C2 (139).
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