Kotin A M, Chebotar' N A
Biokhimiia. 1976 May;41(5):801-6.
Teratogenic doses of antimalaria preparation, 2,4-diamino-5-p-chlorophenyl-6-ethylpyrimidine (chloridine), known in biochemistry as a specific inhibitor of dihydrofolate reductase, result in the decrease of 32P-phosphate incorporation into ATP and ADP, coupled with the inhibitions of DNA synthesis, in rat embryo and placenta on 13th day of development, while the incorporation of 14C-formiate into free nucleotides of acid soluble embryo and placenta fractions (at the same intervals after teratogen injections), is the same as in the control. These data show that the primary blocking of folate cycle and DNA biosynthesis in 13 days old embryos with induced anomalies of development is some way coupled with disturbances of ATP metabolism.
致畸剂量的抗疟疾制剂2,4-二氨基-5-对氯苯基-6-乙基嘧啶（氯胍），在生物化学中作为二氢叶酸还原酶的特异性抑制剂为人所知，会导致发育第13天的大鼠胚胎和胎盘中32P-磷酸盐掺入ATP和ADP减少，同时伴有DNA合成受到抑制，而14C-甲酸掺入酸溶性胚胎和胎盘组分的游离核苷酸中（在注射致畸剂后的相同时间间隔），与对照组相同。这些数据表明，发育异常的13天大胚胎中叶酸循环和DNA生物合成的初级阻断在某种程度上与ATP代谢紊乱有关。
