Sherman I W
Bull World Health Organ. 1977;55(2-3):211-25.
In vitro studies have shown that exogenously supplied amino acids are transferred into the malaria-infected cell, where they are incorporated into proteins. Most amino acids appear to enter the cell by facilitated or simple diffusion; however, the high distribution ratios seen in Plasmodium knowlesi-infected cells are difficult to explain on this basis. The changes (leakiness) observed in amino acid transport in P. lophurae infected cells are probably the result of ATP depletion in the host cell as well as the elaboration of plasmodial substances. Depletion of isoleucine, methionine, and cysteine from the medium strikingly depresses the in vitro growth of P. knowlesi. The degree of amino acid incorporation into the malaria-infected cell is not correlated with the amount of a particular amino acid in the host cell haemoglobin, the decline of that amino acid in the plasma of infected animals, or the ratio of free amino acids of the erythrocyte to those of the plasma. In erythrocyte-"free" P. lophurae, carrier-mediated transport is apparently limited to a small number of amino acids; all others seem to enter by simple diffusion.Malaria-infected erythrocytes transport exogenously supplied purines at substantially higher rates than uninfected red cells. The preferred purines are adenosine, hypoxanthine, and inosine. The only pyrimidine incorporated is orotic acid. Thymidine, cytidine, and uridine do not readily enter the red cell, and incorporation does not take place because the parasites lack the appropriate enzyme for conversion to nucleotides. Erythrocyte-"free" P. berghei and P. lophurae take up purines and orotic acid. It has been suggested that in vivo the preferred purines are hypoxanthine and inosine, and that the transport locus for erythrocytes is specific for 6-oxopurines. Similar results of purine incorporation are reported for the insect stages of P. cynomolgi and P. berghei, although transport studies have not been carried out.
体外研究表明，外源供应的氨基酸会转移到受疟疾感染的细胞中，并在那里被整合到蛋白质中。大多数氨基酸似乎通过易化扩散或简单扩散进入细胞；然而，基于此很难解释诺氏疟原虫感染细胞中出现的高分布比率。在感染洛氏疟原虫的细胞中观察到的氨基酸转运变化（渗漏）可能是宿主细胞中ATP耗竭以及疟原虫物质分泌的结果。培养基中异亮氨酸、蛋氨酸和半胱氨酸的耗竭显著抑制了诺氏疟原虫的体外生长。氨基酸整合到受疟疾感染细胞中的程度与宿主细胞血红蛋白中特定氨基酸的含量、感染动物血浆中该氨基酸的下降情况或红细胞游离氨基酸与血浆游离氨基酸的比率均无关。在红细胞“游离”的洛氏疟原虫中，载体介导的转运显然仅限于少数几种氨基酸；其他所有氨基酸似乎都通过简单扩散进入。受疟疾感染的红细胞转运外源供应嘌呤的速率明显高于未感染的红细胞。首选的嘌呤是腺苷、次黄嘌呤和肌苷。唯一被整合的嘧啶是乳清酸。胸苷、胞苷和尿苷不易进入红细胞，且由于寄生虫缺乏转化为核苷酸的适当酶，所以不会发生整合。红细胞“游离”的伯氏疟原虫和洛氏疟原虫会摄取嘌呤和乳清酸。有人提出，在体内首选的嘌呤是次黄嘌呤和肌苷，红细胞的转运位点对6 - 氧嘌呤具有特异性。对于食蟹猴疟原虫和伯氏疟原虫的昆虫阶段，也报道了类似的嘌呤整合结果，尽管尚未进行转运研究。
