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在缺氧期间,线粒体基质的 pH 值会变酸,并由缺氧耐受的彩龟皮质神经元中的 FF-ATP 酶维持。

Mitochondrial matrix pH acidifies during anoxia and is maintained by the FF-ATPase in anoxia-tolerant painted turtle cortical neurons.

机构信息

Department of Cell and Systems Biology University of Toronto Canada.

Department of Ecology and Evolutionary Biology University of Toronto Canada.

出版信息

FEBS Open Bio. 2019 Mar 14;9(4):571-581. doi: 10.1002/2211-5463.12612. eCollection 2019 Apr.

DOI:10.1002/2211-5463.12612
PMID:30984533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6443863/
Abstract

The western painted turtle () can survive extended periods of anoxia via a series of mechanisms that serve to reduce its energetic needs. Central to these mechanisms is the response of mitochondria, which depolarize in response to anoxia in turtle pyramidal neurons due to an influx of K. It is currently unknown how mitochondrial matrix pH is affected by this response and we hypothesized that matrix pH acidifies during anoxia due to increased K/H exchanger activity. Inhibition of K/H exchange via quinine led to a collapse of mitochondrial membrane potential (Ψ) during oxygenated conditions in turtle cortical neurons, as indicated by rhodamine-123 fluorescence, and this occurred twice as quickly during anoxia which indicates an elevation in K conductance. Mitochondrial matrix pH acidified during anoxia, as indicated by SNARF-1 fluorescence imaged via confocal microscopy, and further acidification occurred during anoxia when the FF-ATPase was inhibited with oligomycin-A, indicating that ΔpH collapse is prevented during anoxic conditions. Collectively, these results indicate that the mitochondrial proton electrochemical gradient is actively preserved during anoxia to prevent a collapse of Ψ and ΔpH.

摘要

西部锦龟()可以通过一系列机制在缺氧环境中存活很长时间,这些机制可以降低其能量需求。这些机制的核心是线粒体的反应,由于 K 的流入,龟类锥体细胞的线粒体去极化对缺氧做出反应。目前尚不清楚线粒体基质 pH 值如何受到这种反应的影响,我们假设由于 K/H 交换器活性增加,基质 pH 值在缺氧期间酸化。奎宁通过抑制 K/H 交换,导致龟皮质神经元在充氧条件下的线粒体膜电位(Ψ)崩溃,如 rhodamine-123 荧光所示,在缺氧时发生的速度快两倍,这表明 K 电导率升高。线粒体基质在缺氧期间酸化,如通过共聚焦显微镜成像的 SNARF-1 荧光所示,当用寡霉素-A 抑制 FF-ATP 酶时,在缺氧期间进一步酸化,表明在缺氧条件下 ΔpH 值崩溃得到预防。总的来说,这些结果表明,在线粒体质子电化学梯度在缺氧期间被积极保存,以防止 Ψ 和 ΔpH 值崩溃。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/673720ddbc65/FEB4-9-571-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/3f3fdd9bb96c/FEB4-9-571-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/e14e6a078f29/FEB4-9-571-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/8a07ec1e4716/FEB4-9-571-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/6c92a25f69d2/FEB4-9-571-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/b5bbabe4d6a7/FEB4-9-571-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/673720ddbc65/FEB4-9-571-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/3f3fdd9bb96c/FEB4-9-571-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/e14e6a078f29/FEB4-9-571-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/8a07ec1e4716/FEB4-9-571-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/6c92a25f69d2/FEB4-9-571-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/b5bbabe4d6a7/FEB4-9-571-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107e/6443863/673720ddbc65/FEB4-9-571-g006.jpg

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