*correspondence: m. ghazi-khansari. ph.d., department ofpharmacology,

2,3,7,8-tetrachlorodibenzo-p-dioxin (tcdd) is a by-product o f t he trichlorophenol (herbicide) production and is also produced through a variety of combustion processes. it appears that tcdd is a ubiquitous chemical, particularly in industrialised countries, and the liver is the target organ of its toxicity. the prominent hepatotoxic effect of tcdd is progressive centrilobular necrosis. the isolated rat liver perfusion system approaches the normal physiology of the liver and is ideal for studying biochemical alterations of the liver since hepatocytes are easily exposed to various concentrations of chemicals with minimum neural-hormonal effects. in this study, the liver was perfused with krebs-henseleit butfer containing different concentrations of tcdd (0.3, 3, 20 and 30).lg/l). during the perfusion many factors including gross liver appearance, bile formation, and aminotransferase activities were assessed as indicators of liver viability. consequently, sections of liver tissue were examined for any histopathological changes. the results showed that histopathological changes in liver tissues were related in a dose-dependent manner to tcdd concentrations. in this instance doses of 20 and 30 ).lgll caused a significant (p<0.05) histopathological change in liver sections. liver necrosis and hemorrhage were also increased significantly in a dose-dependent manner.