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1
Purinogenic immunodeficiency diseases: selective toxicity of deoxyribonucleosides for T cells.嘌呤生成性免疫缺陷疾病:脱氧核糖核苷对T细胞的选择性毒性。
Proc Natl Acad Sci U S A. 1978 Oct;75(10):5011-4. doi: 10.1073/pnas.75.10.5011.
2
Deoxyadenosine triphosphate as a mediator of deoxyguanosine toxicity in cultured T lymphoblasts.三磷酸脱氧腺苷作为培养的T淋巴母细胞中脱氧鸟苷毒性的介质。
J Clin Invest. 1986 Nov;78(5):1261-9. doi: 10.1172/JCI112710.
3
Biochemical basis for the enhanced toxicity of deoxyribonucleosides toward malignant human T cell lines.脱氧核糖核苷对恶性人T细胞系毒性增强的生化基础。
Proc Natl Acad Sci U S A. 1979 May;76(5):2430-3. doi: 10.1073/pnas.76.5.2430.
4
Purinogenic immunodeficiency diseases. Differential effects of deoxyadenosine and deoxyguanosine on DNA synthesis in human T lymphoblasts.嘌呤生成性免疫缺陷疾病。脱氧腺苷和脱氧鸟苷对人T淋巴母细胞DNA合成的不同影响。
J Clin Invest. 1979 Nov;64(5):1475-84. doi: 10.1172/JCI109606.
5
Deoxyribonucleoside toxicity in adenosine deaminase and purine nucleoside phosphorylase deficiency: implications for the development of new immunosuppressive agents.腺苷脱氨酶和嘌呤核苷磷酸化酶缺乏时的脱氧核糖核苷毒性:对新型免疫抑制剂开发的启示
Ciba Found Symp. 1978(68):115-33. doi: 10.1002/9780470720516.ch8.
6
S-adenosylhomocysteine hydrolase inactivation and purine toxicity in cultured human T- and B-lymphoblasts.培养的人T淋巴细胞和成淋巴细胞中S-腺苷同型半胱氨酸水解酶失活与嘌呤毒性
J Lab Clin Med. 1984 Jul;104(1):86-95.
7
B cells as well as T cells form deoxynucleotides from either deoxyadenosine or deoxyguanosine.B细胞和T细胞均可利用脱氧腺苷或脱氧鸟苷形成脱氧核苷酸。
Clin Exp Immunol. 1984 Apr;56(1):39-48.
8
Possible metabolic basis for the different immunodeficient states associated with genetic deficiencies of adenosine deaminase and purine nucleoside phosphorylase.与腺苷脱氨酶和嘌呤核苷磷酸化酶基因缺陷相关的不同免疫缺陷状态的可能代谢基础。
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9
Purine deoxyribonucleosides counteract effects of hydroxyurea on deoxyribonucleoside triphosphate pools and DNA synthesis.嘌呤脱氧核糖核苷可抵消羟基脲对三磷酸脱氧核糖核苷池和DNA合成的影响。
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10
On the mechanism of deoxyribonucleoside toxicity in human T-lymphoblastoid cells. Reversal of growth inhibition by addition of cytidine.关于脱氧核糖核苷对人T淋巴母细胞毒性的机制。添加胞苷可逆转生长抑制作用。
Eur J Biochem. 1985 Aug 1;150(3):429-34. doi: 10.1111/j.1432-1033.1985.tb09038.x.

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本文引用的文献

1
Further studies on the effect of deoxyadenosine on the accumulation of deoxyadenosine triphosphate and inhibition of deoxyribonucleic acid synthesis in Ehrlich ascites tumor cells in vitro.关于脱氧腺苷对体外培养的艾氏腹水癌细胞中三磷酸脱氧腺苷积累及脱氧核糖核酸合成抑制作用的进一步研究。
Biochim Biophys Acta. 1962 Dec 31;61:885-96. doi: 10.1016/0926-6550(62)90005-1.
2
Regulation of mammalian deoxyribonucleotide biosynthesis by nucleotides as activators and inhibitors.核苷酸作为激活剂和抑制剂对哺乳动物脱氧核糖核苷酸生物合成的调控。
J Biol Chem. 1966 Oct 25;241(20):4802-9.
3
A rapid quantitative determination of deoxyribonucleoside triphosphates based on the enzymatic synthesis of DNA.基于DNA酶促合成的脱氧核糖核苷三磷酸快速定量测定。
Biochim Biophys Acta. 1969 Feb 18;174(2):585-90. doi: 10.1016/0005-2787(69)90288-3.
4
Effects of thymidine on deoxyribonucleoside triphosphate pools and deoxyribonucleic acid synthesis in Chinese hamster ovary cells.胸苷对中国仓鼠卵巢细胞中脱氧核糖核苷三磷酸库及脱氧核糖核酸合成的影响。
J Biol Chem. 1973 Jun 10;248(11):3904-9.
5
Childhood lymphoblastic lymphoma, a cancer of thymus-derived lymphocytes.儿童淋巴细胞白血病,一种源自胸腺淋巴细胞的癌症。
Cancer Res. 1974 Mar;34(3):521-5.
6
Cytogenetic study of human lymphoid T-cell lines derived from lymphocytic leukemia.源自淋巴细胞白血病的人T淋巴细胞系的细胞遗传学研究
J Natl Cancer Inst. 1974 Sep;53(3):655-60. doi: 10.1093/jnci/53.3.655.
7
The deoxyribonucleoside transport systems of cultured Novikoff rat hepatoma cells.培养的诺维科夫大鼠肝癌细胞的脱氧核糖核苷转运系统。
J Cell Physiol. 1974 Jun;83(3):337-43. doi: 10.1002/jcp.1040830303.
8
Adenosine-deaminase deficiency in two patients with severely impaired cellular immunity.两名细胞免疫严重受损患者的腺苷脱氨酶缺乏症。
Lancet. 1972 Nov 18;2(7786):1067-9. doi: 10.1016/s0140-6736(72)92345-8.
9
Inhibition of maturation of human precursor lymphocytes by coformycin, an inhibitor of the enzyme adenosine deaminase.腺苷脱氨酶抑制剂助间霉素对人前体淋巴细胞成熟的抑制作用。
J Exp Med. 1976 May 1;143(5):1271-6. doi: 10.1084/jem.143.5.1271.
10
The effect of external deoxyribonucleosides on deoxyribonucleoside triphosphate concentrations in human lymphocytes.外源性脱氧核苷对人淋巴细胞中三磷酸脱氧核苷浓度的影响。
Biochem Pharmacol. 1975 Aug 15;24(16):1495-8. doi: 10.1016/0006-2952(75)90025-8.

嘌呤生成性免疫缺陷疾病:脱氧核糖核苷对T细胞的选择性毒性。

Purinogenic immunodeficiency diseases: selective toxicity of deoxyribonucleosides for T cells.

作者信息

Mitchell B S, Mejias E, Daddona P E, Kelley W N

出版信息

Proc Natl Acad Sci U S A. 1978 Oct;75(10):5011-4. doi: 10.1073/pnas.75.10.5011.

DOI:10.1073/pnas.75.10.5011
PMID:311004
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC336252/
Abstract

Deoxyadenosine at low concentrations and in the presence of an inhibitor of adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4) is markedly toxic to lymphoblast cell lines of T cell origin but does not impair growth of B cell lines. Deoxyguanosine is also more toxic for T lymphoblasts. In the presence of deoxyadenosine or deoxyguanosine, elevation of the corresponding deoxyribonucleoside triphosphate (dATP or dGTP) occurs in T cell, but not in B cell, lines. The addition of deoxycytidine or dipyridamole results in lower dATP and dGTP levels and prevents deoxyribonucleoside toxicity. These findings provide a molecular basis for the immunodeficiency observed in individuals with several inborn errors of purine metabolism.

摘要

低浓度的脱氧腺苷在腺苷脱氨酶(腺苷氨基水解酶,EC 3.5.4.4)抑制剂存在的情况下,对T细胞来源的淋巴母细胞系具有显著毒性,但不影响B细胞系的生长。脱氧鸟苷对T淋巴母细胞也更具毒性。在脱氧腺苷或脱氧鸟苷存在的情况下,T细胞系中相应的脱氧核糖核苷三磷酸(dATP或dGTP)水平会升高,但B细胞系中不会。添加脱氧胞苷或双嘧达莫会导致dATP和dGTP水平降低,并防止脱氧核糖核苷毒性。这些发现为患有几种嘌呤代谢先天性缺陷的个体中观察到的免疫缺陷提供了分子基础。