Abstract
Experiments were carried out to investigate the possibility of inducing porphyria in human hepatocytes and HepG2 cells in culture. After treatment with hexachlorobenzene, 3-methylcholanthrene, phenobarbital or dimethyl sulfoxide, protoporphyrin was the predominating porphyrin accumulating in presence of delta-aminolevulinic acid. The typical uroporphyrin accumulation, as is seen in hexachlorobenzene-induced porphyria in vivo, was absent. In HepG2 cells, the activities of uroporphyrinogen decarboxylase and porphobilinogen deaminase were not influenced by cytochrome P-450 inducers, hexachlorobenzene or dimethyl sulfoxide during 48 h of culture. Therefore, the use of these cells in the study of porphyria cutanea tarda does not seem promising.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aminolevulinic Acid / pharmacology*
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Carcinoma, Hepatocellular
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Cells, Cultured
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Cytochrome P-450 Enzyme System / biosynthesis
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Cytochrome P-450 Enzyme System / metabolism*
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Dimethyl Sulfoxide / pharmacology
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Enzyme Induction
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Hexachlorobenzene / pharmacology
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Humans
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Hydroxymethylbilane Synthase / metabolism
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Liver / drug effects
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Liver / metabolism*
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Liver Neoplasms
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Methylcholanthrene / pharmacology
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Phenobarbital / pharmacology
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Porphyrins / biosynthesis*
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Tumor Cells, Cultured
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Uroporphyrinogen Decarboxylase / metabolism
Substances
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Porphyrins
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Hexachlorobenzene
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Methylcholanthrene
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Aminolevulinic Acid
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Cytochrome P-450 Enzyme System
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Hydroxymethylbilane Synthase
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Uroporphyrinogen Decarboxylase
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Dimethyl Sulfoxide
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Phenobarbital