Danazol, a new steroidal inducer of delta-aminolevulinic acid synthetase

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This study demonstrates that danazol induces hepatic delta-aminolevulinic acid synthetase and increases porphyrin production in a chick embryo model, explaining clinical exacerbations of acute intermittent porphyria.

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Abstract

Danazol (a derivative of 17 alpha-ethinyl testosterone) has recently been reported to cause clinical exacerbations of acute intermittent porphyria. In the present study, we demonstrate that danazol is an inducer of hepatic delta-aminolevulinic acid synthetase and that it increases hepatocyte porphyrin production using a chick embryo model. The findings provide an explanation for the clinical observations. Although danazol is a porphyrinogenic agent in the chick embryo and humans it has been reported to be ineffective as a porphyrinogen in rats. The present findings, therefore, also confirm the superiority of the chick embryo as a model system for the screening of drugs and chemicals which may have the potential to cause clinical exacerbations of porphyria.

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MeSH descriptors

5-Aminolevulinate Synthetase Danazol Pregnadienes 5-Aminolevulinate Synthetase Animals Cells, Cultured Chick Embryo Danazol Enzyme Induction Enzyme Induction Liver Liver Liver Pregnadienes Protoporphyrins Protoporphyrins

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last seen: 2026-05-10T10:44:52.684890+00:00
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last seen: 2026-10-08T21:58:49.153990+00:00
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