De Matteis F, Gibbs A H
Biochem J. 1975 Jan;146(1):285-7. doi: 10.1042/bj1460285.
Griseofulvin and isogriseofulvin cause, like 3,5-diethoxycarbonyl-1,4-dihydrocollidine, a fall in the activity of the hepatic enzyme porphyrin-metal chelatase and accumulation of protoporphyrin in the liver. Analogues of either griseofulvin or 3,5-diethoxycarbonyl-1,4-dihydrocollidine which do not decrease the chelatase activity are not porphyrogenic on their own, but can potentiate the porphyria caused by 3,5-diethoxycarbonyl-1,4-dihydrocollidine. This suggests the existence of two basically different mechanisms by which drugs stimulate the pathway of porphyrin synthesis in the liver.
灰黄霉素和异灰黄霉素与3,5 - 二乙氧基羰基 - 1,4 - 二氢可力丁一样，会导致肝脏酶卟啉 - 金属螯合酶的活性下降以及肝脏中原卟啉的积累。灰黄霉素或3,5 - 二乙氧基羰基 - 1,4 - 二氢可力丁的类似物若不会降低螯合酶活性，则自身不具有致卟啉症的作用，但可增强由3,5 - 二乙氧基羰基 - 1,4 - 二氢可力丁引起的卟啉症。这表明存在两种基本不同的机制，药物可通过这些机制刺激肝脏中卟啉合成途径。
