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TCDD, dietary iron and hepatic iron distribution in female rats

Journal Article · · Bull. Environ. Contam. Toxicol.; (United States)
DOI:https://doi.org/10.1007/BF01606678· OSTI ID:6290295
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. 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. TCDD induces many functional, biochemical and pathological changes, including altered lipid metabolism in the liver. Ferrous iron plays an important role in the initiation of lipid peroxidation. 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. The presence of iron in subcellular fractions in vitro may catalyze lipid peroxidation and produce membrane damage. There is 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, microsomes, 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.
Research Organization:
Univ. of Nebraska Medical Center, Omaha
OSTI ID:
6290295
Journal Information:
Bull. Environ. Contam. Toxicol.; (United States), Journal Name: Bull. Environ. Contam. Toxicol.; (United States) Vol. 38:2; ISSN BECTA
Country of Publication:
United States
Language:
English