PMID: 6412692Jul 15, 1983Paper

Effects of polychlorinated biphenyl compounds, 2,3,7,8-tetrachlorodibenzo-p-dioxin, phenobarbital and iron on hepatic uroporphyrinogen decarboxylase. Implications for the pathogenesis of porphyria

The Biochemical Journal
H De VerneuilA Kappas

Abstract

Treatment of cultured chick embryo hepatocytes with phenobarbital, polychlorinated biphenyl compounds and 2,3,7,8-tetrachlorodibenzo-p-dioxin resulted in increased delta-aminolaevulinate synthase and decreased uroporphyrinogen decarboxylase activities and porphyrin accumulation; uroporphyrin and heptacarboxyporphyrin predominated. Iron had no effect on these changes. Simultaneous treatment of cultures with dioxin and phenobarbital produced a synergistic response in delta-aminolaevulinate synthase induction, uroporphyrinogen decarboxylase inhibition and porphyrin accumulation. These data suggest that an inhibitor of uroporphyrinogen decarboxylase may be generated in the liver from polychlorinated biphenyl compounds or dioxin by metabolic activation. Additionally these findings bear on the postulated role of these and related chemicals in determining the low levels of uroporphyrinogen decarboxylase activity in porphyria cutanea tarda patients.

Citations

May 1, 1987·American Journal of Hematology·P S WisselA Kappas
Jan 1, 1987·Annals of the New York Academy of Sciences·M O Doss
Jan 1, 1987·Annals of the New York Academy of Sciences·G H ElderA J Urquhart
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Aug 1, 1989·American Journal of Hematology·J M RiberaC Rozman
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Nov 7, 1998·Nature Genetics·H WangS Lin
Jan 1, 1987·Annals of the New York Academy of Sciences·S SassaO Sugita
May 15, 2007·Canadian Journal of Microbiology·Angela B JuárezMaría Del C Ríos de Molina
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Jan 1, 1989·Disease-a-month : DM·J R Bloomer, H L Bonkovsky
Nov 15, 1989·Archives of Biochemistry and Biophysics·L E RodmanL W Robertson

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