Folate metabolism in malaria.
Folate metabolism in malaria.
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疟疾中的叶酸代谢。
DOI：
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发表时间：
1977
影响因子：
11.1
通讯作者：
R. Ferone
中科院分区：
文献类型：
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作者：
R. Ferone
众所周知，疟疾寄生虫被磺胺类和抗叶酸化合物抑制，生长需要4-氨基苯甲酸，对完整的叶酸和叶酸只有部分反应。过去十年间关于核酸前体合成和疟疾中叶酸酶的生化数据支持疟疾寄生虫类似于从头合成叶酸辅助因子的微生物的假说。磺胺类药物抑制原虫二氢翼酸合成酶(EC 2.5.1.15)。乙胺嘧啶和许多其他抗叶酸化合物与寄生虫的四氢叶酸脱氢酶(EC 1.5.1.3)结合得比与宿主酶更紧密。然而，由于药物抑制而导致的叶酸辅助因子耗尽的代谢后果尚不清楚。其他有待研究的领域包括叶酸的蝶啶部分的起源，谷氨酸(S)在叶酸辅因子生物合成中的添加，完整的外源叶酸影响疟疾生长的方式，以及涉及N(5)-甲基四氢叶酸的酶和反应的演示。
It is known that malaria parasites are inhibited by sulfonamides and antifolate compounds, require 4-aminobenzoic acid for growth, and respond only partly to intact folic and folinic acids. Biochemical data obtained during the last decade on the synthesis of nucleic acid precursors and on folate enzymes in malaria support the hypothesis that malaria parasites are similar to microorganisms that synthesize folate cofactors de novo. Sulfa drugs inhibit plasmodial dihydropteroate synthase (EC 2.5.1.15). Pyrimethamine and many other antifolate compounds bind to tetrahydrofolate dehydrogenase (EC 1.5.1.3) of the parasite more tightly than to the host enzyme. However, the metabolic consequences of the depletion of folate cofactors as a result of drug inhibition are not yet known. Other areas to be studied are the origin of the pteridine moiety of folates, the addition of glutamate(s) in folate cofactor biosynthesis, the means by which intact, exogenous folates affect malarial growth, and demonstration of the enzymes and reactions involving N(5)-methyl tetrahydrofolate.