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在预处理过程中在线粒体基质中形成的磷酸钙缓冲液支持 ΔpH 的形成和缺血时的 ATP 生成,并延长细胞存活-一个假说。

Calcium phosphate buffer formed in the mitochondrial matrix during preconditioning supports ΔpH formation and ischemic ATP production and prolongs cell survival -A hypothesis.

机构信息

Department of Biophysics, Warsaw University of Life Sciences - SGGW, Nowoursynowska 159, Warszawa 02-776, Poland.

出版信息

Mitochondrion. 2019 Jul;47:210-217. doi: 10.1016/j.mito.2018.11.007. Epub 2018 Nov 15.

DOI:10.1016/j.mito.2018.11.007
PMID:30448366
Abstract

Ischemic preconditioning makes cells less sensitive to oxygen deprivation. A similar effect can be achieved by increasing the calcium concentration and applying potassium channel openers. A hypothetical mechanism of preconditioning is presented. In the mitochondrial matrix, there is a calcium hydroxide buffer consisting of a few insoluble calcium phosphate minerals. During ischemia, calcium ions stored in the matrix buffer start to leak out, forming an electric potential difference, while hydroxyl ions remain in the matrix, maintaining its pH and the matrix volume. Preconditioning factors increase the matrix buffer capacity. Production of ATP during ischemia might be the relic of a pre-endosymbiotic past.

摘要

缺血预处理使细胞对缺氧变得不那么敏感。通过增加钙离子浓度和应用钾通道开放剂可以达到类似的效果。提出了预处理的一个假设机制。在线粒体基质中,存在由几种不溶性磷酸钙矿物质组成的氢氧化钙缓冲液。在缺血期间,储存在基质缓冲液中的钙离子开始泄漏,形成电势差,而羟基离子留在基质中,维持其 pH 值和基质体积。预处理因素增加了基质缓冲能力。缺血期间产生的 ATP 可能是前内共生期的遗留物。

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