Youn J H, Nam H W, Kim D J, Choi W Y
Department of Parasitology, Catholic University Medical College, Seoul, Korea.
Kisaengchunghak Chapchi. 1990 Jun;28(2):79-84. doi: 10.3347/kjp.1990.28.2.79.
Metabolic inhibitors which act in the process of pyrimidine salvage influenced on the uracil incorporation into nucleic acids of Toxoplasma. Inhibitors of dihydrofolate reductase, pyrimethamine and methotrexate, and inhibitors of thymidylate synthase, fluoro-uridine, fluoro-dUMP and fluoro-uracil, diminished isotopic uracil uptake in dose-dependent manners. Azauridine which suppresses de novo pyrimidine biosynthesis did not affect the salvage even in a relatively high dose. These results suggested that the activation of uracil salvage should be closely related with the function of TMP biosynthetic enzymes. The pattern of thymidine uptake had no differences between control HL-60 cells and Toxoplasma infected cells, which did not reflect the specific proliferation of Toxoplasma. It can be exploited to characterize the effects of various compounds related with the proliferation of Toxoplasma, especially its DNA synthesis.
作用于嘧啶补救途径的代谢抑制剂影响尿嘧啶掺入弓形虫核酸的过程。二氢叶酸还原酶抑制剂乙胺嘧啶和甲氨蝶呤，以及胸苷酸合成酶抑制剂氟尿苷、氟脱氧尿苷酸和氟尿嘧啶，以剂量依赖方式减少同位素尿嘧啶摄取。抑制嘧啶从头合成的阿扎尿苷即使在相对高剂量下也不影响补救途径。这些结果表明尿嘧啶补救途径的激活应与胸苷酸生物合成酶的功能密切相关。对照HL-60细胞和弓形虫感染细胞之间胸苷摄取模式没有差异，这并未反映弓形虫的特异性增殖。它可用于表征与弓形虫增殖尤其是其DNA合成相关的各种化合物的作用。
