J Environ Pathol Toxicol Oncol 1995 Jan 01;142:69-82.

A morphological study of liver lesions in Xenopus larvae exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with special reference to apoptosis of hepatocytes.

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Edema formation is a consistent feature of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) poisoning in experimental animals. Xenopus embryos exposed to 200 ppb of TCDD for 5 days from shortly after fertilization to early larval stage developed edema of the head, thorax, and abdomen, including ascites, from several days after the end of exposure. There has been no reports on liver lesions in TCDD-exposed anuran larvae. To elucidate the participation of liver in the edema formation, light and electron microscopic alterations in the livers from larvae that developed edema were examined. The marked change induced by TCDD was degeneration of the hepatocytes. Three types of degenerating hepatocytes were distinguished. The first type showed morphological features characteristic of apoptosis, including peripherally aggregated nuclear chromatin and overall cytoplasmic condensation; the cytoplasmic organelles retained their integrity and cytoplasmic blebbing. A considerable number of degenerating hepatocytes undergoing apoptosis and numerous apoptotic bodies derived from hepatocytes were observed by electron microscopy. The second type could not be determined as to which type of cell death it belonged to, and the third type was necrosis. Other alterations consisted of disturbances of the usual meshwork architecture of the liver, enlargements of bile canaliculi and the space of Disse, lipid accumulation, and appearance of phagocytizing macrophages. These morphological alterations in the liver generally correlated with the severity of edema with a few exception. These findings suggest that depressed hepatic function mainly due to hepatocyte death participates in the edema formation.

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