Myoglobin-mediated oxygen delivery to mitochondria of isolated cardiac myocytes.

Myoglobin-mediated oxygen delivery to mitochondria of isolated cardiac myocytes.
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DOI:
10.1073/pnas.84.21.7503
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发表时间:
1987-11
影响因子:
11.1
通讯作者:
B. Wittenberg;J. Wittenberg
B. Wittenberg;J. Wittenberg
中科院分区:
综合性期刊1区
文献类型:
--
作者:
B. Wittenberg;J. Wittenberg

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肌红蛋白介导的氧输送到细胞内线粒体证明在心肌细胞分离的成熟大鼠的心脏。将肌细胞保持在高环境氧压下,40-340 kPa(5-45 kPa);肌浆肌红蛋白完全氧化。在这种情况下,氧的可用性不限制呼吸速率;肌红蛋白促进的扩散不贡献额外的氧通量,并且由于在稳定状态下测量氧消耗,肌红蛋白的储存功能消失。逐步引入的一氧化碳从细胞内氧合肌红蛋白中置换氧,而不改变大量氧化的细胞内线粒体的光谱。一氧化碳阻断肌红蛋白的氧合作用可使大部分(约三分之一)的稳态氧摄取消失。肌红蛋白依赖性组分的氧摄取随细胞内氧合肌红蛋白分数的降低而线性降低,斜率接近1。使用线粒体电子传递抑制剂的研究表明,肌红蛋白递送的氧摄取依赖于通过线粒体电子传递链的电子流。我们的结论是,心脏线粒体接受两个附加的同时流动的氧:溶解氧的细胞色素氧化酶和肌红蛋白结合的氧的线粒体末端的流量。肌红蛋白介导的氧输送支持心脏细胞在生理环境氧压下产生ATP。
Myoglobin-mediated oxygen delivery to intracellular mitochondria is demonstrated in cardiac myocytes isolated from the hearts of mature rats. Myocytes are held at high ambient oxygen pressure, 40-340 torr (5-45 kPa); sarcoplasmic myoglobin is fully oxygenated. In this condition oxygen availability does not limit respiratory rate; myoglobin-facilitated diffusion contributes no additional oxygen flux and, since oxygen consumption is measured in steady states, the storage function of myoglobin vanishes. Carbon monoxide, introduced stepwise, displaces oxygen from intracellular oxymyoglobin without altering the optical spectrum of the largely oxidized intracellular mitochondria. A large part, about one-third, of the steady-state oxygen uptake is abolished by carbon monoxide blockade of myoglobin oxygenation. The myoglobin-dependent component of the oxygen uptake decreases linearly with decreasing fraction of intracellular oxymyoglobin, with a slope near unity. Studies using inhibitors of mitochondrial electron transport indicate that myoglobin-delivered oxygen uptake depends on electron flow through the mitochondrial electron transport chain. We conclude that cardiac mitochondria accept two additive simultaneous flows of oxygen: a flow of dissolved oxygen to cytochrome oxidase and a flow of myoglobin-bound oxygen to a mitochondrial terminus. Myoglobin-mediated oxygen delivery supports ATP generation by heart cells at physiological ambient oxygen pressure.