Abstract
3,5-Diethoxycarbonyl-2,4,6-trimethylpyridine induces porphyrin biosynthesis in monolayer cultures of chick embryo liver cells, but not in the intact chick embryo while 3,5-diethoxycarbonyl-1,4-dihydro-2,4,6-trimethylpyridine induces porphyrin biosynthesis in both systems. To investigate the reason for this finding, 3,5-diethoxy-carbonyl-2,4,6-trimethylpyridine- 14C and 3,5-diethoxycarbonyl-1,4-dihydro-2,4,6-trimethylpyridine- 14C were prepared, injected into 17-day-old chick embryos and the total amount of drug and metabolite(s) in the livers measured at various time periods. 3,5-Diethoxycarbonyl-2,4,6-trimethylpyridine was found to undergo a more rapid metabolic degradation in liver than 3,5-diethoxycarbonyl-1,4-dihydro-2,4,6-trimethyl-pyridine, and its inactivity in the chick embryo was attributed to its rapid metabolic degradation. The fact that 3,5-diethoxycarbonyl-2,4,6-trimethylpyridine causes porphyrin accumulation in chick embryo liver cells is due to the inability of the cells to rapidly metabolize the drug.
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