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1
Release from the Crabtree effect by hypoxic cell radiosensitizers.缺氧细胞放射增敏剂对克氏效应的解除
Br J Cancer. 1979 Aug;40(2):295-9. doi: 10.1038/bjc.1979.178.
2
Effects of hypoxic cell radiosensitizers on the activity of ATPases.乏氧细胞放射增敏剂对ATP酶活性的影响。
Int J Radiat Biol Relat Stud Phys Chem Med. 1981 Dec;40(6):681-4. doi: 10.1080/09553008114551681.
3
Inhibition of glycolysis of mammalian cells by misonidazole and other radiosensitizing drugs. prevention by thiols.米索硝唑及其他放射增敏药物对哺乳动物细胞糖酵解的抑制作用。硫醇的预防作用。
Biochem Pharmacol. 1982 Jul 15;31(14):2345-51. doi: 10.1016/0006-2952(82)90528-7.
4
Effect of anoxic radiosensitizers on cellular and mitochondrial oxygen consumption and respiration control ratio.缺氧放射增敏剂对细胞和线粒体氧消耗及呼吸控制率的影响。
Br J Cancer Suppl. 1978 Jun;3:159-62.
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Misonidazole-induced biochemical alterations of mammalian cells: effects on glycolysis.甲硝唑诱导的哺乳动物细胞生化改变:对糖酵解的影响。
Int J Radiat Oncol Biol Phys. 1982 Mar-Apr;8(3-4):683-6. doi: 10.1016/0360-3016(82)90712-x.
6
Effect of misonidazole (Ro-07-0582) on the incidence of micronuclei in irradiated Ehrlich tumour ascites cells.米索硝唑(Ro-07-0582)对受照射的艾氏腹水癌细胞微核发生率的影响。
Int J Radiat Biol Relat Stud Phys Chem Med. 1978 Dec;34(6):589-93. doi: 10.1080/09553007814551281.
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Misonidazole and MTDQ in combination: cytotoxic and radiosensitizing properties in hypoxic mammalian cells.米索硝唑与MTDQ联合应用:对缺氧哺乳动物细胞的细胞毒性和放射增敏特性
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Radiosensitisation of cells in vitro with misonidazole: dependence on endogenous sulphydryl.米索硝唑对体外细胞的放射增敏作用:对内源性巯基的依赖性。
Br J Radiol. 1983 Nov;56(671):871-5. doi: 10.1259/0007-1285-56-671-871.
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Effects of misonidazole on purine metabolism in Ehrlich ascites tumor cells in vitro.甲硝唑对体外培养的艾氏腹水癌细胞嘌呤代谢的影响。
Biochem Pharmacol. 1980 Sep 15;29(18):2533-6. doi: 10.1016/0006-2952(80)90364-0.
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A comparison of two nitroimidazoles and a dihydroquinoline as radiosensitizers and cytotoxic agents.两种硝基咪唑和一种二氢喹啉作为放射增敏剂和细胞毒性剂的比较。
Int J Radiat Oncol Biol Phys. 1979 Oct;5(10):1781-6. doi: 10.1016/0360-3016(79)90561-3.

引用本文的文献

1
Hypoxia-induced increases in glucose uptake do not cause oxidative injury or advanced glycation end-product (AGE) formation in vascular endothelial cells.缺氧诱导的葡萄糖摄取增加不会在血管内皮细胞中引起氧化损伤或晚期糖基化终产物(AGE)的形成。
Physiol Rep. 2015 Jul;3(7). doi: 10.14814/phy2.12460.

本文引用的文献

1
The respiratory quotients of normal and tumour tissue.正常组织与肿瘤组织的呼吸商。
Biochem J. 1935 Nov;29(11):2433-41. doi: 10.1042/bj0292433.
2
Observations on the carbohydrate metabolism of tumours.关于肿瘤碳水化合物代谢的观察
Biochem J. 1929;23(3):536-45. doi: 10.1042/bj0230536.
3
RELATIONS BETWEEN TUMOR AND METASTASIS. I. ASPECTS OF THE CRABTREE EFFECT.肿瘤与转移的关系。一、克氏效应的各个方面。
Cancer. 1965 Aug;18:978-84. doi: 10.1002/1097-0142(196508)18:8<978::aid-cncr2820180809>3.0.co;2-s.
4
Inducers of the Crabtree effect and its release by uncouplers and other agents.克奈特瑞效应的诱导因素以及解偶联剂和其他试剂对其的解除作用
Cancer Res. 1963 May;23:600-6.
5
Metabolic control mechanisms. IV. The effect of glucose upon the steady state of respiratory enzymes in the ascites cell.代谢控制机制。IV. 葡萄糖对腹水细胞呼吸酶稳态的影响。
J Biol Chem. 1959 Sep;234:2421-7.
6
The Crabtree effect: a review.“克奈特瑞效应”综述
Cancer Res. 1961 Aug;21:829-41.
7
Differentiation, metabolic organization, and viability of the visual cell.视觉细胞的分化、代谢组织及生存能力。
AMA Arch Ophthalmol. 1958 Oct;60(4 Part 2):702-31; discussion 731-3. doi: 10.1001/archopht.1958.00940080722016.
8
[Respiration of cells and tissues in vitro as a physiological method and as a model-test procedure].[体外细胞和组织呼吸作为一种生理学方法及模型测试程序]
Z Gesamte Exp Med. 1956;127(1):1-15.
9
Carbohydrate metabolism in ascites tumor cells.腹水肿瘤细胞中的碳水化合物代谢
Ann N Y Acad Sci. 1956 Mar 14;63(5):1017-21. doi: 10.1111/j.1749-6632.1956.tb50909.x.
10
On the control of metabolism in ascites tumor cell suspensions.关于腹水肿瘤细胞悬液中代谢的控制
Ann N Y Acad Sci. 1956 Mar 14;63(5):1008-16. doi: 10.1111/j.1749-6632.1956.tb50908.x.

缺氧细胞放射增敏剂对克氏效应的解除

Release from the Crabtree effect by hypoxic cell radiosensitizers.

作者信息

Mustea I, Bara A

出版信息

Br J Cancer. 1979 Aug;40(2):295-9. doi: 10.1038/bjc.1979.178.

DOI:10.1038/bjc.1979.178
PMID:475972
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2010000/
Abstract

The Crabtree effect can be observed when the O2 consumption of tumour cells or of mammalian cells grown in culture is measured in physiological medium containing glucose. The effect of 2 hypoxic cell radiosensitizers, misonidazole and NDPP, on the O2 consumption of Ehrlich ascites tumour cells was compared in media with and without glucose. A stimulatory effect on O2 consumption was found for 5--20mM misonidazole as well as for 0.5mM NDPP, both in media containing 10(-2)M glucose. Thus glucose induced a Crabtree effect in Ehrlich tumour cells, expressed as 38--45% inhibition of O2 consumption relative to that in the same medium without glucose. The stimulatory effect of misonidazole and NDPP on O2 utilization in medium with glucose undoubtedly appeared as a release from the Crabtree effect.

摘要

当在含有葡萄糖的生理培养基中测量肿瘤细胞或培养的哺乳动物细胞的耗氧量时,可观察到克拉布特里效应。在含葡萄糖和不含葡萄糖的培养基中,比较了两种乏氧细胞放射增敏剂米索硝唑和NDPP对艾氏腹水瘤细胞耗氧量的影响。在含有10⁻²M葡萄糖的培养基中,发现5 - 20mM米索硝唑以及0.5mM NDPP对耗氧量有刺激作用。因此,葡萄糖在艾氏肿瘤细胞中诱导了克拉布特里效应,相对于不含葡萄糖的相同培养基,耗氧量受到38 - 45%的抑制。米索硝唑和NDPP对含葡萄糖培养基中氧利用的刺激作用无疑表现为从克拉布特里效应中释放出来。