Beck J T, Ullman B
Department of Biochemistry and Molecular Biology, Oregon Health Sciences University, Portland 97201-3098.
Mol Biochem Parasitol. 1991 Nov;49(1):21-8. doi: 10.1016/0166-6851(91)90126-q.
The ability of Leishmania donovani promastigotes to proliferate in folate-deficient medium supplemented with pterins suggests that pterins can serve as a source of folate in these parasites [16]. Using reversed-phase high-performance liquid chromatography, the ability of intact L. donovani to transform [3H]biopterin into tetrahydrofolates was demonstrated. Radioactivity was primarily associated with 5-methyltetrahydrofolate and 10-formyltetrahydrofolate. A mutant strain of L. donovani, MTXA5, that was genetically deficient in folate transport capacity and incapable of growing in pterin-supplemented folate-deficient growth medium, exhibited a greatly reduced capacity to metabolize [3H]biopterin to reduced folates. These data indicated that wild-type L. donovani promastigotes, unlike mammalian cells, were able to convert biopterin to tetrahydrofolates and supported the hypothesis that folate transport deficiency in mutant organisms is associated with an inability to transform pterins to reduced folates.
杜氏利什曼原虫前鞭毛体在补充了蝶呤的叶酸缺乏培养基中增殖的能力表明，蝶呤可作为这些寄生虫的叶酸来源[16]。使用反相高效液相色谱法，证明了完整的杜氏利什曼原虫将[3H]生物蝶呤转化为四氢叶酸的能力。放射性主要与5-甲基四氢叶酸和10-甲酰基四氢叶酸相关。杜氏利什曼原虫的一个突变株MTXA5，其在叶酸转运能力上存在基因缺陷，且无法在补充了蝶呤的叶酸缺乏生长培养基中生长，该突变株将[3H]生物蝶呤代谢为还原型叶酸的能力大大降低。这些数据表明，与哺乳动物细胞不同，野生型杜氏利什曼原虫前鞭毛体能够将生物蝶呤转化为四氢叶酸，并支持了以下假设：突变生物体中的叶酸转运缺陷与无法将蝶呤转化为还原型叶酸有关。
