Boss G R, Ragsdale R A, Zettner A, Seegmiller J E
J Lab Clin Med. 1980 Nov;96(5):783-9.
PGA administered in doses up to 1000 mg orally a day did not significantly lower the serum urate concentration nor decrease the urinary urate or total oxypurine excretion in five hyperuricemic subjects. The folate was well absorbed, as reflected by marked increases in the serum and erythrocyte folate concentrations, and up to 50% of the administered folate could be recovered in the urine. There was no evidence of clinical or laboratory toxicity at these high doses of folate. PGA is a weak inhibitor of human liver xanthine oxidase in vitro, and much of its inhibitory effect is secondary to trace contamination by pterin-6-aldehyde, a potent inhibitor of the enzyme.
对五名高尿酸血症患者口服给予高达1000毫克/天剂量的PGA，并未显著降低血清尿酸盐浓度，也未减少尿尿酸或总氧嘌呤排泄。叶酸吸收良好，血清和红细胞叶酸浓度显著升高就反映了这一点，且高达50%的摄入叶酸可在尿液中回收。在这些高剂量叶酸下，没有临床或实验室毒性的证据。PGA在体外是人类肝脏黄嘌呤氧化酶的弱抑制剂，其大部分抑制作用继发于蝶呤-6-醛的微量污染，蝶呤-6-醛是该酶的强效抑制剂。
