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Journal Article

Strongly enhanced toxicity of the mushroom toxin α-amanitin by an amatoxin-specific Fab or monoclonal antibody

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Faulstich,  Heinz
Department of Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Kirchner,  Karin
Max Planck Institute for Medical Research, Max Planck Society;

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https://www.sciencedirect.com/science/article/pii/0041010188901882
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Citation

Faulstich, H., Kirchner, K., & Derenzini, M. (1988). Strongly enhanced toxicity of the mushroom toxin α-amanitin by an amatoxin-specific Fab or monoclonal antibody. Toxicon, 26(5), 491-499. doi:10.1016/0041-0101(88)90188-2.


Cite as: https://hdl.handle.net/21.11116/0000-000A-9FE4-2
Abstract
H. Faulstich, K. Kirchiner and M. Derenzini. Strongly enhanced toxicity of the mushroom toxin α-amanitin by an amatoxin-specific Fab or monoclonal antibody. Toxicon26, 491–499, 1988. — A monoclonal antibody, with high affinity against the mushroom toxin α-amanitin, was prepared. Administration of the Fab fragment of the monoclonal antibody to mice caused a 50-fold increase in α-amanitin toxicity. Electron micrographs showed normal appearance of hepatocytes but typical, amanitin-induced lesions in cells of the proximal convoluted tubules of the kidney. The pronounced nephrotoxicity is mainly explained by glomerular filtration and tubular reabsorption of the Fab-amatoxin complex and, to a lesser extent, of the immunoglobulin — amatoxin complex, which is still c. twice as toxic as free α-amanitin. To our knowledge this is the first reported case where immunoglobulins or their fragments enhance rather than decrease the activity of a toxin. Accordingly, immunotherapy of Amanita mushroom poisoning in humans does not appear promising.