Olivares J, Rossi A
Laboratoire de Physiologie Cellulaire Cardiaque URA CNRS 632, Université Joseph Fourier, Grenoble, France.
J Mol Cell Cardiol. 1988 Apr;20(4):313-22. doi: 10.1016/s0022-2828(88)80065-8.
Plasma contains micromolar concentrations of pyrimidine bases and nucleosides: uracil 1.9 +/- 0.1 (n = 29), cytosine 1.1 +/- 0.01 (n = 29), uridine 1.2 +/- 0.1 (n = 56) and cytidine 5.4 +/- 0.1 (n = 59) (means +/- S.E.M.). Accordingly, we postulated that these compounds could be used as the main precursors for myocardial pyrimidine nucleotide synthesis. The kinetics of the incorporation of blood plasma bases and nucleosides into myocardial nucleotides was studied by in vivo radio-isotopic studies in rats. The clearance of the radiolabelled compounds in blood plasma and the incorporation of radiolabelled precursors into liver nucleotides was also investigated. The results can be summarized as follows: (1) The pyrimidine radioactive bases were only very slightly incorporated into heart nucleotides 1 h after injection: thus 1 h after injection any incorporation of radiolabelled cytosine into nucleotides remained undetectable and for radioactive uracil the ratio of the specific radioactivity of uracil nucleotides to that of plasma uracil remained below 0.7%. (2) Radiolabelled plasma uridine was subject to a far more rapid catabolism than radiolabelled plasma cytidine. (3) The labelling of myocardial uracil nucleotides from plasma uridine was very slight. Their specific radioactivity represented less than 16% of plasma uridine specific radioactivity. (4) When the tracer was cytidine the specific radioactivity of cytosine nucleotides reached that of precursor within 30 min after injection and uracil nucleotides were also labeled (10% of cytidine nucleotides specific radioactivity). These results, and other previous data, suggest the possibility that the pyrimidine nucleotide synthesis in the rat heart may be largely achieved via the phosphorylation of blood plasma cytidine.
尿嘧啶1.9±0.1（n = 29），胞嘧啶1.1±0.01（n = 29），尿苷1.2±0.1（n = 56），胞苷5.4±0.1（n = 59）（均值±标准误）。因此，我们推测这些化合物可能是心肌嘧啶核苷酸合成的主要前体。通过对大鼠进行体内放射性同位素研究，探讨了血浆碱基和核苷掺入心肌核苷酸的动力学。同时还研究了放射性标记化合物在血浆中的清除情况以及放射性标记前体掺入肝脏核苷酸的情况。结果总结如下：（1）注射后1小时，嘧啶放射性碱基仅极少量掺入心脏核苷酸：因此，注射后1小时，未检测到放射性胞嘧啶掺入核苷酸，对于放射性尿嘧啶，尿嘧啶核苷酸的比放射性与血浆尿嘧啶的比放射性之比仍低于0.7%。（2）放射性标记的血浆尿苷的分解代谢比放射性标记的血浆胞苷快得多。（3）血浆尿苷对心肌尿嘧啶核苷酸的标记作用非常微弱。其比放射性不到血浆尿苷比放射性的16%。（4）当示踪剂为胞苷时，注射后30分钟内胞嘧啶核苷酸的比放射性即达到前体的比放射性，尿嘧啶核苷酸也被标记（为胞嘧啶核苷酸比放射性的10%）。这些结果以及之前的其他数据表明，大鼠心脏中的嘧啶核苷酸合成很可能主要通过血浆胞苷的磷酸化来实现。
