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首页> 外文期刊>Biochimica et biophysica acta: international journal of biochemistry and biophysics >Sensitivity of the synaptic membrane Na+/Ca2+ exchanger and the expressed NCX1 isoform to reactive oxygen species.
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Sensitivity of the synaptic membrane Na+/Ca2+ exchanger and the expressed NCX1 isoform to reactive oxygen species.

机译：突触膜Na + / Ca2 +交换子和表达的NCX1亚型对活性氧的敏感性。

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摘要

Two plasma membrane proteins, the Na+/Ca2+ exchanger (NCX) and the Ca2+-ATPase, are major regulators of free intraneuronal Ca2+ levels as they are responsible for extrusion of Ca2+ from the intracellular to the extracellular medium. Because disruption of cellular Ca2+ regulation plays a role in damage occurring under conditions of oxidative stress, studies were conducted to assess the sensitivity of the NCX to reactive oxygen species (ROS). Exchanger activity in brain synaptic plasma membranes and in transfected CHO-K1 cells was inhibited following brief exposure to the peroxyl radical generating azo initiator 2,2'-azobis(2-amidinopropane)dihydrochloride (AAPH) and to peroxynitrite. Incubation with hydrogen peroxide did not alter NCX activity, even at 800 microM concentration. In CHO-K1 cells transiently transfected with the NCX1 isoform of the exchanger, AAPH treatment decreased the maximal transport capacity (Vmax), whereas the K(act) remained unchanged. Peroxynitrite led to an increase in K(act) with no change in Vmax. Loss of activity following exposure to either AAPH or peroxynitrite was associated with the formation of high molecular weight aggregates of NCX, and AAPH also caused fragmentation of the exchanger protein. These findings suggest that the NCX is sensitive to biologically relevant ROS and could be involved in the loss of Ca2+ homeostasis observed under oxidative stress.
机译：Na + / Ca2 +交换子（NCX）和Ca2 + -ATPase这两种质膜蛋白是游离神经内Ca2 +水平的主要调节剂，因为它们负责Ca2 +从细胞内向细胞外介质的挤出。由于细胞Ca2 +调节的破坏在氧化应激条件下发生的损伤中起作用，因此进行了研究以评估NCX对活性氧（ROS）的敏感性。短暂暴露于产生过氧自由基的偶氮引发剂2,2'-偶氮二（2-ami基丙烷）二盐酸盐（AAPH）和过氧亚硝酸盐后，大脑突触质膜和转染的CHO-K1细胞中的交换子活性受到抑制。即使在800 microM浓度下，过氧化氢孵育也不会改变NCX活性。在交换器的NCX1亚型瞬时转染的CHO-K1细胞中，AAPH处理降低了最大转运能力（Vmax），而K（act）保持不变。过氧亚硝酸盐导致K（act）增加，而Vmax不变。暴露于AAPH或过氧亚硝酸盐后的活性降低与NCX的高分子量聚集体的形成有关，并且AAPH也导致交换蛋白断裂。这些发现表明，NCX对生物学相关的ROS敏感，并且可能参与了在氧化应激下观察到的Ca2 +稳态损失。

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