The effect of N-methylprotoporphyrin and succinyl-acetone on the regulation of heme biosynthesis in chicken hepatocytes in culture.
The essential features of hepatic protoporphyria, namely inhibition of ferrochelatase, accumulation of protoporphyrin and stimulation of 5-aminolevulinic acid synthase (ALA-S) were all obtained by treating chicken hepatocytes in culture with small doses of N-methylprotoporphyrin. Both N-methylprotoporphyrin and succinyl-acetone, another inhibitor of heme biosynthesis, stimulated ALA-S when given on their own and also enhanced the stimulation of ALA-S caused by phenobarbital.
D000624:5-Aminolevulinate Synthetase / Q000378:metabolism; D000818:Animals; D002642:Chick Embryo; D005294:Ferrochelatase / Q000037:antagonists & inhibitors; D006418:Heme / Q000096:biosynthesis*; D006537:Heptanoates / Q000494:pharmacology*; D006538:Heptanoic Acids / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D010634:Phenobarbital / Q000494:pharmacology; D011166:Porphyrins / Q000494:pharmacology*; D011524:Protoporphyrins / Q000494:pharmacology*
D006537:Heptanoates; D006538:Heptanoic Acids; D011166:Porphyrins; D011524:Protoporphyrins; D006418:Heme; C020804:succinylacetone; C028842:N-methylprotoporphyrin IX; D000624:5-Aminolevulinate Synthetase; D005294:Ferrochelatase; D010634:Phenobarbital