The effects of amanitin poisoning on mouse kidney.

The effect of α- and β-amanitin on mouse kidney and rat kidney have been studied. The experiments on adult male mice show that (1) an MLD of α- or β-amanitin always produces necrosis in the kidneys but never in the liver; (2) with the doses used (up to 3 MLD) necrosis of the kidneys never appears less than 3 days after injection; (3) necrosis of the liver only appears with doses above MLD and generally within 2 days. No lesions were found in rat kidney after injection of amanitin. Mice injected with the conjugate of β-amanitin with albumin from rabbit serum all died from necrosis of the liver without any lesions in the kidney, 3 days after i.p. injection. It has been deduced that amanitin poisoning in mouse kidney depends on reabsorption in the tubules, that either the liver or the kidney can be the target organ of amanitin (depending on the dose) and that in rats nephrosis is prevented because there is no reabsorption of amanitin in the kidney tubules. The earliest ultrastructural changes occur in nuclei. First there is fragmentation of nucleoli and segregation of its granular and fibrillar components. At a second stage these fragments fall in number and then tend to disappear. At the same time there is a temporary increase in the number of perichromatin granules. Chromatin condensates at the borders of the nucleus and there is a big increase in numbers of interchromatin granules at the centre. Changes in the cytoplasm appear just before necrosis sets in.