在ρ(0)HL-60细胞中，质膜上辅酶Q10的增加会刺激抗坏血酸盐的稳定。

Ascorbate stabilization is stimulated in rho(0)HL-60 cells by CoQ10 increase at the plasma membrane.

作者信息

Gómez-Díaz C, Villalba J M, Pérez-Vicente R, Crane F L, Navas P

机构信息

Departamento de Biología Celular, Universidad de Córdoba, Spain.

出版信息

Biochem Biophys Res Commun. 1997 May 8;234(1):79-81. doi: 10.1006/bbrc.1997.6582.

DOI:10.1006/bbrc.1997.6582

PMID:9168964

Abstract

Long-term treatment with ethidium bromide of HL-60 cells induced a mitochondria-deficient rho degree cell line, where mitochondrial DNA can not be identified by PCR and cytochrome c oxidase activity was 80% decreased. These cells showed a progressive increase of ascorbate stabilization which was 52% higher in the established rho degree HL-60 cells. Both CoQ10 and NADH-ascorbate free radical reductase of the plasma membrane were increased in rho(0)HL-60 cells compared to parental cells, while NADH-cytochrome c reductase was unchanged. CoQ10 is a component of the ascorbate stabilization activity in the plasma membrane that would provide both a mechanism to deplete the excess of NADH produced in rho(0)HL-60 cells and for resistance to oxidative stress.

摘要

用溴化乙锭对HL-60细胞进行长期处理诱导出一种线粒体缺陷型ρ⁰细胞系，在此细胞系中，通过聚合酶链反应无法鉴定出线粒体DNA，且细胞色素c氧化酶活性降低了80%。这些细胞显示出抗坏血酸稳定性的逐渐增加，在已建立的ρ⁰HL-60细胞中，其抗坏血酸稳定性高出52%。与亲代细胞相比，ρ⁰HL-60细胞膜中的辅酶Q10和NADH-抗坏血酸自由基还原酶均增加，而NADH-细胞色素c还原酶则无变化。辅酶Q10是细胞膜中抗坏血酸稳定活性的一个组成部分，它既能为消耗ρ⁰HL-60细胞中产生的过量NADH提供一种机制，又能提供对氧化应激的抗性。