Kruger-McDermott C, Balinska M, Galivan J
Cancer Lett. 1986 Jan;30(1):79-84. doi: 10.1016/0304-3835(86)90135-7.
H35 hepatoma cells can be rescued from exposure to an inhibitory pulse of methotrexate (MTX) by subsequent addition of folinic acid, dihydrofolate or thymidine. Both folinic acid and dihydrofolate cause the dissociation of methotrexate--dihydrofolate reductase complex although dihydrofolate rescues less effectively than folinic acid. Thymidine does not cause a measurable dissociation of the enzyme--inhibitor complex. The results suggest that the rescue of MTX treated cells by reduced folate coenzymes can be mediated at least in part by the generation of dihydrofolate which by itself can partially reverse MTX inhibition of cell growth.
通过随后添加亚叶酸、二氢叶酸或胸腺嘧啶核苷，H35肝癌细胞可从甲氨蝶呤（MTX）抑制性脉冲暴露中被挽救。亚叶酸和二氢叶酸均可导致甲氨蝶呤 - 二氢叶酸还原酶复合物解离，尽管二氢叶酸的挽救效果不如亚叶酸。胸腺嘧啶核苷不会导致酶 - 抑制剂复合物发生可测量的解离。结果表明，还原型叶酸辅酶对MTX处理细胞的挽救作用至少部分可由二氢叶酸的生成介导，而二氢叶酸自身可部分逆转MTX对细胞生长的抑制作用。
