Abstract
Cultured rat hepatocytes exposed to tunicamycin, a substance biologically indistinguishable from the corynetoxin responsible for a toxic hepatocerebral disorder in Australian ruminant livestock, had degenerative changes characterized by marked cytoplasmic lipid accumulation and dilatation of cisternae of rough endoplasmic reticulum or necrosis. The findings, which resemble those found previously in vivo after tunicamycin administration, suggest that, after gaining ready access to liver parenchyma via leaky hepatic sinusoids, tunicamycin directly damages the hepatocytes.
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