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Main Title Experimental Hepatic Porphyria Induced by Polychlorinated Biphenyls.
Author Goldstein, Joyce A. ; Hickman, Patricia ; Jue., Danny L. ;
CORP Author Environmental Protection Agency, Chamblee, Ga. Chamblee Toxicology Lab.
Year Published 1973
Stock Number PB-278 101
Additional Subjects Toxicology ; Liver ; Porphyria ; Enzymes ; Chlorine aromatic compounds ; Metabolic diseases ; Porphyrins ; Hemoglobins ; Metabolism ; Organic compounds ; Contaminants ; Rats ; Laboratory animals ; Bioassay ; Ingestion(Biology) ; Dosage ; Dose rate ; Biphenyl/chloro ; Toxic substances ; Reprints
Library Call Number Additional Info Location Last
NTIS  PB-278 101 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 12p
Aroclor 1254, which consists of a mixture of polychlorinated biphenyls (PCBs) containing 54% chlorine, produced an experimental hepatic porphyria in rats resembling hexachlorobenzene poisoning and human porphyria cutanea tarda. The PCB-induced porphyria is characterized by delayed development, increased excretion of urinary uroporphyrins, accumulation of 8- and 7-carboxyporphyrins in the liver and increased drug-metabolizing capacity of the liver. Cytochrome P-450 and microsomal heme were increased maximally at 1 week, in the absence of an increase in the rate-limiting enzyme in heme synthesis, delta-aminolevulinic acid (ALA) synthetase. Induction of ALA synthetase and porphyria occurred later, after2-7 months' exposure to PCBs. No induction of ALA synthetase could be demonstrated prior to the onset of porphyria. Marked induction of ALA synthetase occurred 5 hr after large single doses of Aroclor 1254; however, the doses required were larger than those used to produce porphyria when administered chronically, and induction appeared to be related to the marked increase in cytochrome P-450 seen 24 hr after administration of the drug.