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Abstract
Male rats were given aflatoxin B 1 (7 mg/kg) and the resulting hepatic lesion was studied ultrastructurally at 9, 12, 18, 24 and 48 h. Within the periportal zone of necrosis there is a gradual disruption of the liver cell plates leaving fragments of liver cells containing autophagic vacuoles and a few macrophages. In the surviving liver cells autophagy is seen in all cells but is most marked in those cells adjacent to the zone of necrosis and least in the centrilobular cells. The other most noticeable changes are seen in the rough and smooth endoplasmic reticulum. The rough endoplasmic reticulum (RER) is partially disorganized in all cells at 9 h but by 18 h the centrilobular zone is normal. The smooth endoplasmic reticulum (SER) shows steady increase from 18 and 24 h to 48 h and is preceded by the formation of foci of ribosome-like particles arranged as loose whorls and rows which may be interpreted as either polysomes or ‘reticulosomes’. The formation of new smooth membrane occurs in cells with segregated nucleoli which has been correlated with an inhibition of RNA polymerase activity. It is not possible in this experiment to distinguish the specific cellular changes which lead to necrosis from those of nonlethal damage.
Published Version
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