大鼠脑突触终末质膜对抗坏血酸自由基的还原作用。

Reduction of ascorbate free radical by the plasma membrane of synaptic terminals from rat brain.

作者信息

Samhan-Arias Alejandro K, Duarte Rui O, Martín-Romero Francisco Javier, Moura Jose J G, Gutiérrez-Merino Carlos

机构信息

Department of Biochemistry and Molecular Biology, Faculty of Sciences, University of Extremadura, 06071 Badajoz, Spain.

出版信息

Arch Biochem Biophys. 2008 Jan 15;469(2):243-54. doi: 10.1016/j.abb.2007.10.004. Epub 2007 Oct 12.

DOI:10.1016/j.abb.2007.10.004

PMID:17963686

Abstract

Synaptic plasma membranes (SPMV) decrease the steady state ascorbate free radical (AFR) concentration of 1mM ascorbate in phosphate/EDTA buffer (pH 7), due to AFR recycling by redox coupling between ascorbate and the ubiquinone content of these membranes. In the presence of NADH, but not NADPH, SPMV catalyse a rapid recycling of AFR which further lower the AFR concentration below 0.05 microM. These results correlate with the nearly 10-fold higher NADH oxidase over NADPH oxidase activity of SPMV. SPMV has NADH-dependent coenzyme Q reductase activity. In the presence of ascorbate the stimulation of the NADH oxidase activity of SPMV by coenzyme Q(1) and cytochrome c can be accounted for by the increase of the AFR concentration generated by the redox pairs ascorbate/coenzyme Q(1) and ascorbate/cytochrome c. The NADH:AFR reductase activity makes a major contribution to the NADH oxidase activity of SPMV and decreases the steady-state AFR concentration well below the micromolar concentration range.

摘要

突触质膜（SPMV）可降低磷酸盐/EDTA缓冲液（pH 7）中1mM抗坏血酸的稳态抗坏血酸自由基（AFR）浓度，这是由于抗坏血酸与这些膜的泛醌含量之间通过氧化还原偶联实现AFR循环。在存在NADH而非NADPH的情况下，SPMV催化AFR的快速循环，使AFR浓度进一步降低至0.05 microM以下。这些结果与SPMV的NADH氧化酶活性比NADPH氧化酶活性高近10倍相关。SPMV具有NADH依赖性辅酶Q还原酶活性。在存在抗坏血酸的情况下，辅酶Q(1)和细胞色素c对SPMV的NADH氧化酶活性的刺激可归因于抗坏血酸/辅酶Q(1)和抗坏血酸/细胞色素c氧化还原对产生的AFR浓度的增加。NADH:AFR还原酶活性对SPMV的NADH氧化酶活性起主要作用，并将稳态AFR浓度降低至远低于微摩尔浓度范围。