Stimulation of the pathway of porphyrin synthesis in the liver of rats and mice by griseofulvin, 3,5-Diethoxycarbonyl-1,4-dihydrocollidine and related drugs: evidence for two basically different mechanisms.
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.
D000818:Animals; D003997:Dicarbethoxydihydrocollidine / Q000494:pharmacology*; D006118:Griseofulvin / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D011166:Porphyrins / Q000096:biosynthesis*; D011524:Protoporphyrins / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology*; D051381:Rats
D011166:Porphyrins; D011524:Protoporphyrins; D011725:Pyridines; D006118:Griseofulvin; D003997:Dicarbethoxydihydrocollidine