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A semiquantitative morphologic procedure has been applied to chlordecone potentiation of CHCl3-induced liver injury in male Sprague-Dawley rats. The distance of the injured area from the terminal hepatic venule (THV) to the portal area was measured and the damaged cells were classified by type. The results were plotted graphically, along with elevations in plasma enzyme activities (GPT and OCT), to depict the pattern of damage. Chlordecone pretreatment enhanced the severity of the CHCl3-induced cellular changes and increased the number of cells affected. Dosages of 5 mg/kg of chlordecone did not potentiate CHCl3 toxicity, but higher dosages (10-50 mg/kg) enhanced the toxic response in a dose-dependent manner.

In this experiment we aimed at developping a method of ready evaluation of lung alveolar toxic damage using morphometric measurements. Swiss-Webster mice were treated with different doses of diquat (i.p.) and the left lung was fixed at 0, 3, and 5 days after treatment. The technique of morphometry of histological sections embedded in glycol methacrylate (GMA) was used to quantify possible modifications of alveolar cells. Quantitative evaluation includes: alveolar macrophages, polymorphonuclear cells, type II and intermediate pneumocytes. The results indicate a lung dose-dependent response, observed in both inflammatory and epithelial regeneration components of the alveolar primary reaction. This method could be used to readily evaluate the pulmonary toxic potential of any substance.

Cultures of rat hepatocytes have been used to study the interaction of chrysotile asbestos fibers with epithelial cells. The hepatocytes were incubated for 20 h with chrysotile asbestos (UICC B and a preparation of short fibers: 90% less than 2 micron) at concentrations of 1 or 10 micrograms/ml. Morphologic studies were then performed by means of transmission electron microscopy. Fibers were incorporated into plasma membrane invaginations, cytoplasmic vacuoles and phagolysosomes. These observations demonstrate that rat hepatocytes can engage in phagocytosis of chrysotile fibers. The results are compared to those previously obtained with mesothelial cells and tracheobronchial epithelium, exposed to asbestos in vitro. The advantages of the hepatocyte model to investigate the effects on cells of the association of asbestos fibers with genotoxic agents in relation to carcinogenesis are discussed.