Granström E, Hansson G
Adv Prostaglandin Thromboxane Res. 1976;1:215-9.
The metabolism of three analogues of PGF2alpha was studied in the Cynomolgus monkey and in the human, viz., 15-methyl-PGF2alpha, 16,16-dimethyl PGF2alpha, and 17-phenyl-18,19,20-trinor-PGF2alpha. The half-lives of the three compounds in the human circulation was considerably longer than that of PGF2alpha. The dehydrogenation of the secondary alcohol group at C-15 was completely blocked in the two first-mentioned compounds. These were degraded mainly by beta-oxidation, and their main metabolites, both in plasma and urine, were dinor-15-methyl-PGF2alpha and dinor-16,16-dimethyl-PFG2alpha, respectively. 17-Phenyl-18,19,20-trinor-PGF2alpha, finally, was metabolized to some extent by dehydrogenation at C-15, and also by reduction of the delta13 double bond and by beta-oxidation.
在食蟹猴和人体中研究了三种前列腺素F2α类似物的代谢情况，即15-甲基前列腺素F2α、16,16-二甲基前列腺素F2α和17-苯基-18,19,20-三降前列腺素F2α。这三种化合物在人体循环中的半衰期比前列腺素F2α长得多。在上述前两种化合物中，C-15位仲醇基的脱氢反应完全受阻。它们主要通过β-氧化降解，其在血浆和尿液中的主要代谢产物分别是二降-15-甲基前列腺素F2α和二降-16,16-二甲基前列腺素F2α。最后，17-苯基-18,19,20-三降前列腺素F2α在一定程度上通过C-15位脱氢、δ13双键还原以及β-氧化进行代谢。
