Terminal oxidation and the effects of zinc in prostate versus liver mitochondria
Terminal oxidation and the effects of zinc in prostate versus liver mitochondria
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DOI：
10.1016/j.mito.2004.07.031
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发表时间：
2004-08-01
期刊：
影响因子：
4.4
通讯作者：
Franklin, RB
中科院分区：
文献类型：
--
作者：
Costello, LC;Guan, ZX;Franklin, RB
虽然细胞的总锌含量通常接近0.2 mM，但胞质游离锌离子浓度可忽略不计（亚纳摩尔浓度）。然而，所有报道的锌对细胞呼吸和末端氧化的影响的研究都涉及μ M-mM水平的游离锌离子。前列腺细胞和它们的线粒体积累的锌比其他哺乳动物细胞多3-10倍。我们认为，细胞溶质池的移动的反应性低分子量锌配体可以抑制呼吸和终端氧化。用前列腺和肝线粒体研究了Zn配体，特别是柠檬酸锌，与游离Zn + +离子对呼吸和末端氧化的影响。ZnLigands在抑制前列腺和肝脏线粒体的呼吸和末端氧化方面与游离Zn + +离子同样有效，这支持了我们的概念，即锌可以从胞质供体ZnLigands直接转移到末端氧化组分的锌结合位点。此外，前列腺线粒体的呼吸和末端氧化组分的比活性是肝线粒体的20-50%。锌抑制和固有的低水平的电子传递成分可能是导致前列腺细胞低呼吸的主要因素。(C)2004年Elsevier B. V.和线粒体研究学会。All rights reserved.
Although the total zinc content of cells generally approximates 0.2 mM, the cytosolic free zinc ion concentration is negligible (subnanomolar concentrtations). However, all reported studies of effects of zinc on cellular respiration and terminal oxidation involved muM-mM levels of free zinc ions. Prostate cells and their mitochondria accumulate 3-10 fold more zinc than other mammalian cells. We considered that a cytosolic pool of mobile reactive low molecular weight zinc ligands could inhibit respiration and terminal oxidation. The effects of ZnLigands, especially ZnCitrate, versus free Zn + + ions on respiration and terminal oxidation were studied with prostate and liver mitochondria. ZnLigands were equally as effective as free Zn + + ions in the inhibition of respiration and terminal oxidation of both prostate and liver mitochondria, which supports our concept that zinc can be transferred from cytosolic donor ZnLigands directly to zinc-binding sites of terminal oxidation components. Also, the respiration and specific activities of terminal oxidation components of prostate mitochondria are 20-50% of liver mitochondria. Zinc inhibition and inherently low levels of electron transport components are likely major factors responsible for the low respiration that characterizes prostate cells. (C) 2004 Elsevier B.V. and Mitochondria Research Society. All rights reserved.