Abstract

Liver cell necrosis produced in rats by injection of the triterpenoid glycoside albitocin was studied with the electron microscope. Coagulative necrosis was of two distinct types. The first was characterized by the presence of clumps of calcium-associated, electron-opaque granules in the matrix of mitochondria, the changes closely resembling those described in necrosis due to various other toxins. However, in the second, clumps of matrix granules were absent and the appearances were like those seen in ischaemic necrosis and in in vitro autolysis. It is probable that this second type of necrosis resulted from sinusoidal obstruction, which followed the development of the first type of necrosis in the peripheral parts of the lobules. Mitochondria1 abnormalities provided the best indication of the development of coagulative necrosis, but the findings cast doubt on the importance of calcium accumulation within mitochondria as a causative factor in the initiation of necrosis. Shrinkage necrosis involved cellular condensation followed by fission into multiple, membrane-bounded cytoplasmic fragments. Some of these were ingested by parenchymal cells and histiocytes. Others probably underwent a process akin to coagulative necrosis.

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