||Hepatic Porphyria Induced by 2,3,7,8-Tetrachlorodibenzo-P-Dioxin in the Mouse.
Goldstein, J. A. ;
Hickman, P. ;
Bergman, H. ;
Vos., J. G. ;
||Environmental Protection Agency, Chamblee, Ga. Office of Pesticides Programs.
Nitrogen organic compounds ;
Chlorine organic compounds ;
Metabolic diseases ;
Lethal dosage ;
Laboratory animals ;
Experimental data ;
Physiological effects ;
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
||Oral administration of 4 weekly doses of 25 micrograms/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin resulted in induction of delta-aminolevulinic acid synthetase and hepatic porphyria in mice. There was a 2,000-fold increase in the liver content of 8- and 7-carboxyporphyrins. A single lethal oral dose of 150 micrograms/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin also resulted in a 4,000-fold increase in uroporphyrins in the liver. Doses of tetrachlorofibenzo-p-dioxin which resulted in porphyria also resulted in microscopic evidence of marked liver damage and a moderate increase in the total iron content of the liver. At this time, 2,3,7,8-tetrachlorodibenzo-p-dioxin, a contaminant of a variety of environmenal chemicals, is the most potent porphyrogenic chemical known.
||Pub. in Research Communications in Chemical Pathology and Pharmacology, v6 n3 p919-928, Nov 73.
||Included in the report, Journal Articles on Toxicology. Group 16, PB-280 830.
|PUB Date Free Form
||6T; 57Y; 68E; 68G
||(Order as PB-280 830, MF A01)