2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a prototype for a large group of halogenated aromatic hydrocarbons, and is the most potent of these compounds. It is an unwanted by-product in the manufacture of some groups of herbicides as 2,4,5trichlorophenoxyacetic acid, and occurs during the incineration of some types of municipal wastes. TCDD is an environmental pollutant with exceptional toxicity for certain mammalian and avian species. The liver is one of the principal target organs affected by TCDD in the rat and other laboratory species (Poland et al., 1985). TCDD induces many functional, biochemical and pathological changes, including altered lipid metabolism in the liver. Chronic oral administration of TCDD to rats and mice results in hepatic porphyria (Goldstein et al., 1973). Depletion of body iron stores is effective therapy for porphyria, and iron deficiency protects mice against porphyria caused by TCDD (Rowley and Sweeney, 1984). Non-heme iron in the liver supports the hepatotoxic effects of dioxins (Jones et al., 1981). However, the mechanisms involved are unknown. Ferrous iron plays an important role in the initiation of lipid peroxidation (Morehouse et al., 1984). Ironois sequestered in healthy cells in ferritin as ferric iron (Fe ~+) to protect against iron toxicity (Munro and Linder, 1978). A proposed mechanism for the production of liver injury in chronic iron overload is that organelle damage leading to cell death occurs as a result of membrane lipid peroxidation initiated and promoted by intracellular iron (Bacon et al., 1985). The presence of iron in subcellular fractions in vitro may catalyze lipid peroxidation and produce membrane damage (Hultcrantz et al., 1982). Stohs et a]. (1983) have provided evidence for the occurrence of hepatic lipid peroxidation after TCDD administration. The purpose of this study was to determine if TCDD induced lipid peroxidation was associated with an increase in the iron content of liver and its subcellular fractions. The effect of TCDD administration on the iron content of whole homogenate, mierosomes, mitochondria, and cytosol of livers of female rats fed defined diets containing deficient, normal and excessive levels of iron for 17, 24 and 31 days was investigated.