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-AminolevulinicDanazol,Acid SynthetaseDepartments of Pharmacology and Medicine, Cornell University Medical College, New York,New York 10021
Address requests for reprints to: Miranda J. Hughes, Department of Pharmacology, Cornell University Medical College, 1300 York Avenue, New York, New York 10021.
Danazol (a derivative of 17
-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
-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.
Received July 29, 1980.
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