Cohen A, Barankiewicz J, Lederman H M, Gelfand E W
J Biol Chem. 1983 Oct 25;258(20):12334-40.
Purine and pyrimidine deoxyribonucleoside metabolism was studied in G1 and S phase human thymocytes and compared with that of the more mature T lymphocytes from peripheral blood. Both thymocyte populations have much higher intracellular deoxyribonucleoside triphosphate (dNTP) pools than peripheral blood T lymphocytes. The smallest dNTP pool in S phase thymocytes is dCTP (5.7 pmol/10(6) cells) and the largest is dTTP (48 pmol/10(6) cells), whereas in G1 thymocytes, dATP and dGTP comprise the smallest pools. While both G1 and S phase thymocytes have active deoxyribonucleoside salvage pathways, only S phase thymocytes have significant ribonucleotide reduction activity. We have studied ribonucleotide reduction and deoxyribonucleoside salvage in S phase thymocytes in the presence of extracellular deoxyribonucleosides. Based on these studies, we propose a model for the interaction of deoxyribonucleoside salvage and ribonucleotide reduction in S phase thymocytes. According to this model, extracellular deoxycytidine at micromolar concentrations is efficiently salvaged by deoxycytidine kinase. However, due to feedback inhibition of deoxycytidine kinase by dCTP, the maximal level of dCTP which can be achieved is limited. The salvage of both deoxyadenosine and deoxyguanosine (up to 10(-4) M) is completely inhibited in the presence of micromolar concentrations of deoxycytidine, whereas the salvage of thymidine is unregulated resulting in large increases in dTTP levels. Moreover, significant amounts of the salvaged deoxycytidine is used for dTTP synthesis resulting in further increase of dTTP pools. The accumulated dTTP inhibits the reduction of UDP and CDP while stimulating GDP reduction and subsequently also ADP reduction. The end result of the proposed model is that S phase thymocytes in the presence of a wide range of extracellular deoxyribonucleoside concentrations synthesize their pyrimidine dNTP by the salvage pathway, whereas purine dNTPs are synthesized primarily by ribonucleotide reduction. Using the proposed model, it is possible to predict the relative intracellular dNTP pools found in fresh S phase thymocytes.
在G1期和S期人胸腺细胞中研究了嘌呤和嘧啶脱氧核糖核苷代谢,并与外周血中更成熟的T淋巴细胞进行了比较。两个胸腺细胞群体的细胞内脱氧核糖核苷三磷酸(dNTP)池均比外周血T淋巴细胞高得多。S期胸腺细胞中最小的dNTP池是dCTP(5.7 pmol/10⁶个细胞),最大的是dTTP(48 pmol/10⁶个细胞),而在G1期胸腺细胞中,dATP和dGTP组成最小的池。虽然G1期和S期胸腺细胞都有活跃的脱氧核糖核苷补救途径,但只有S期胸腺细胞有显著的核糖核苷酸还原活性。我们研究了在细胞外脱氧核糖核苷存在的情况下S期胸腺细胞中的核糖核苷酸还原和脱氧核糖核苷补救。基于这些研究,我们提出了一个S期胸腺细胞中脱氧核糖核苷补救与核糖核苷酸还原相互作用的模型。根据这个模型,微摩尔浓度的细胞外脱氧胞苷可被脱氧胞苷激酶有效地补救。然而,由于dCTP对脱氧胞苷激酶的反馈抑制,能够达到的dCTP的最大水平是有限的。在微摩尔浓度的脱氧胞苷存在下,脱氧腺苷和脱氧鸟苷(高达10⁻⁴ M)的补救完全被抑制,而胸苷的补救不受调节,导致dTTP水平大幅增加。此外,大量补救的脱氧胞苷用于dTTP合成,导致dTTP池进一步增加。积累的dTTP抑制UDP和CDP的还原,同时刺激GDP还原,随后也刺激ADP还原。所提出模型的最终结果是,在广泛的细胞外脱氧核糖核苷浓度存在的情况下,S期胸腺细胞通过补救途径合成其嘧啶dNTP,而嘌呤dNTP主要通过核糖核苷酸还原合成。使用所提出的模型,可以预测新鲜S期胸腺细胞中相对的细胞内dNTP池。