[Recent advances in the molecular mechanism of action of bacterial toxins, in particular of diphtheria, cholera, coli, botulinum and shigella toxins as well as tetanospasmin and the toxins of staphylococcus aureus].

Great progress was achieved in the clarification of the molecular structure and the mechanism of action of the toxins of pathogenic forms of bacteria. Proportions of toxins of Corynebacterium diphtheriae and of Pseudomonas aeruginosa transfer from the NAD and ADP-ribose protein to an amino acid of the elongation factor 2. Thus the protein synthesis is much inhibited. The cholera toxin and the L-toxin from Escherichia coli have a similar structure. They transfer an ADP-ribose portion from NAD to the GTP-protein of the adenylate cyclase complex, by which means the GTPase activity is reduced. The increase of the cAMP content leads to an increase of the permeability of the cells of the intestinal epithelium. The tetanospasmin decreases the production of the inhibitingly acting neurotransmitters ( glycin ) from intermediate neurons and thus evokes spasms. The botulinum toxin inhibits the release of acetylcholine from the motor end-plates and leads to paralyses. Staphylococcus aureus and Clostridium perfringens form among others cytolysins which are injurious to membranes.