Cycloheximide enhanced porphyrin synthesis in chick embryo liver: Association with an increase in the hepatic glycine pool

Abstract

Cycloheximide 3 μ g injected into eggs with 15 day chick embryos prior to the administration of 3,5-diethoxycarbonyl-1,4-dihydro-2,4,6-trimethylpyridine (DDC) 2 caused a twofold increase in the hepatic porphyrin within 5 hr as compared with embryos given DDC alone. A corresponding increase in the level of δ-aminolevulinic acid (ALA) synthetase did not occur, nor was the conversion of exogenous ALA into porphyrin enhanced by the presence of cycloheximide. Glycine loading of chick embryos treated with DDC also raised the hepatic porphyrin level above that obtained when DDC alone was given. No further increase in porphyrin accompanied the use of cycloheximide at the time of glycine loading. A cycloheximidemediated rise in the hepatic glycine pool was demonstrated and it is proposed that this in turn caused an increase in the production of ALA, which was reflected in an enhanced porphyrin level.