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American Journal of Pathology, Vol 109, 133-144, Copyright © 1982 by American Society for Investigative Pathology

REGULAR ARTICLES

Ultrastruct pathology of phalloidin-intoxicated hepatocytes in the presence and absence of extracellular calcium

MA Russo, AB Kane and JL Farber

The killing of cultured hepatocytes by phalloidin can be dissociated into two phases by manipulation of the Ca2+ concentration of the medium. In the absence of extracellular Ca2+, hepatocytes are injured but not killed by phalloidin. Addition of 1.8 mM Ca2+ to the culture medium kills 60-70% of the cells by three hours. As an initial attempt to identify the mechanisms whereby Ca2+ ions irreversibly injure phalloidin-damaged hepatocytes, we have examined the ultrastructural pathology of phalloidin-intoxicated liver cells in the presence or absence of extracellular Ca2+. In the absence of extracellular Ca2+ ions, the morphologic manifestations of phalloidin intoxication reflect entirely the interaction between phalloidin, microfilaments, and the plasma membrane. In the presence of Ca2+ ions, the morphologic manifestations of the lethal effects of Ca2+ are described: the swelling of mitochondria accompanied by the accumulation of dense, amorphous precipitates; a supercontracture of microfilaments, and a loss of volume control with intracellular edema and a change in cell shape. These alterations can be attributed to the known biologic actions of Ca2+ ions on cellular structure and function. The present study allows, therefore, a preliminary identification of mechanisms by which extracellular Ca2+ ions may mediate cell death in this as well as in other similar situations.


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Copyright © 1982 by the American Society for Investigative Pathology.