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肿瘤细胞线粒体中的质子-阳离子转运

Proton-cation translocation in tumor cell mitochondria.

作者信息

Papa S, Capuano F, Capitanio N, Lorusso M, Galeotti T

出版信息

Cancer Res. 1983 Feb;43(2):834-8.

PMID:6848196
Abstract

The capacity of mitochondria isolated from tumor cells to conserve the transmembrane electrochemical proton gradient set up by respiration has been studied. In a K+ medium, mitochondria from Ehrlich ascites tumor cells exhibit a capacity to conserve aerobic delta microH comparable to that displayed by normal rat liver mitochondria. Mitochondria from Morris hepatoma 3924A show a decreased capacity to store delta microH+, which is principally due to lowering of delta pH. In a Na+ medium, both species of tumor mitochondria show a significant decrease of aerobic delta pH, while delta psi is the same, with respect to rat liver mitochondria. Experiments on passive swelling show that mitochondria from ascites tumor cells have an enhanced permeability to chloride salts of monovalent cations and increased activity of the Na+ (K+)-H+ exchange system of the mitochondrial membrane with respect to normal mitochondria. The enhanced activity of this system in ascites cells is also shown by the characteristics of respiration-linked proton translocation in submitochondrial particles and subsequent anaerobic proton diffusion. It is concluded that the decreased capacity of mitochondria from tumor cells to conserve aerobic delta pH is due to enhanced cyclic flow of Na+ across the membrane.

摘要

对从肿瘤细胞中分离出的线粒体维持呼吸作用所建立的跨膜电化学质子梯度的能力进行了研究。在钾离子培养基中,艾氏腹水瘤细胞的线粒体维持需氧质子动力势差的能力与正常大鼠肝脏线粒体相当。莫里斯肝癌3924A的线粒体储存质子动力势差的能力下降,这主要是由于pH值差降低所致。在钠离子培养基中,相对于大鼠肝脏线粒体,两种肿瘤线粒体的需氧pH值差均显著降低,而膜电位相同。被动肿胀实验表明,腹水瘤细胞的线粒体对单价阳离子的氯化物盐的通透性增强,且线粒体膜的钠(钾)-氢交换系统的活性相对于正常线粒体有所增加。线粒体亚基颗粒中呼吸相关质子转运以及随后的厌氧质子扩散的特性也表明,腹水细胞中该系统的活性增强。得出的结论是,肿瘤细胞线粒体维持需氧pH值差的能力下降是由于钠离子跨膜循环流量增加所致。

相似文献

1
Proton-cation translocation in tumor cell mitochondria.肿瘤细胞线粒体中的质子-阳离子转运
Cancer Res. 1983 Feb;43(2):834-8.
2
Transport of pyruvate in mitochondria from different tumor cells.丙酮酸在来自不同肿瘤细胞的线粒体中的转运。
Cancer Res. 1983 Nov;43(11):5068-71.
3
Low mitochondrial proton leak due to high membrane cholesterol content and cytosolic creatine kinase as two features of the deviant bioenergetics of Ehrlich and AS30-D tumor cells.低线粒体质子泄漏归因于高膜胆固醇含量和胞质肌酸激酶,这是艾氏腹水瘤细胞和AS30 - D肿瘤细胞异常生物能量学的两个特征。
Cancer Res. 1992 Sep 15;52(18):4935-41.
4
Ehrlich ascites tumour cells have a more active mitochondrial polyamine transporter than that of rat liver.艾氏腹水瘤细胞的线粒体多胺转运体比大鼠肝脏的更活跃。
Biochem Mol Biol Int. 1995 Feb;35(2):329-36.
5
Kinetic properties of mitochondrial H+-adenosine triphosphatase in Morris hepatoma 3924A.莫里斯肝癌3924A中线粒体H⁺-腺苷三磷酸酶的动力学特性
Cancer Res. 1989 Dec 1;49(23):6547-50.
6
[Induction of hydrogen ion transport in mitochondrial membranes].
Biofizika. 1982 Jan-Feb;27(1):52-7.
7
[Stabilization of delta mu H+ in Escherichia coli upon K+ and Na+ transmembrane gradient dissipation].[大肠杆菌中K⁺和Na⁺跨膜梯度耗散时ΔμH⁺的稳定化]
Biokhimiia. 1982 Jan;47(1):137-44.
8
Magnesium and octylguanidinium inhibition of monovalent cation translocation in mitochondria.镁和辛基胍对线粒体单价阳离子转运的抑制作用
Acta Physiol Pharmacol Latinoam. 1986;36(3):217-32.
9
[Respiration and ion permeability of the inner membrane in rat "sodium" liver mitochondria].[大鼠“钠”肝线粒体内膜的呼吸作用与离子通透性]
Tsitologiia. 1997;39(11):1046-54.
10
Effect of magnesium on ATP-generating and ATP-utilizing reactions in Ehrlich ascites tumour cells.镁对艾氏腹水癌细胞中ATP生成和ATP利用反应的影响。
Acta Biol Med Ger. 1979;38(8):1101-14.

引用本文的文献

1
Oxidative phosphorylation enzymes in normal and neoplastic cell growth.正常与肿瘤细胞生长中的氧化磷酸化酶
J Bioenerg Biomembr. 1997 Aug;29(4):379-84. doi: 10.1023/a:1022402915431.
2
Proton/electron stoichiometry of mitochondrial bc1 complex. Influence of pH and transmembrane delta pH.线粒体bc1复合物的质子/电子化学计量。pH值和跨膜ΔpH值的影响。
J Bioenerg Biomembr. 1995 Feb;27(1):101-8. doi: 10.1007/BF02110337.