Citation

Faulstich H, Kirchner K, Derenzini M. Toxicon 1988; 26(5): 491-499.

Affiliation

Max-Planck-Institut für Medizinische Forschung, Heidelberg, F.R.G.

Copyright

(Copyright © 1988, Elsevier Publishing)

DOI

unavailable

PMID

3188055

Abstract

A monoclonal antibody, with high affinity against the mushroom toxin alpha-amanitin, was prepared. Administration of the Fab fragment of the monoclonal antibody to mice caused a 50-fold increase in alpha-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 alpha-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.

Language: en