31P NMR studies of control of mitochondrial function in phosphofructokinase-deficient human skeletal muscle.
31P NMR studies of control of mitochondrial function in phosphofructokinase-deficient human skeletal muscle.
复制标题
磷酸果糖激酶缺陷的人类骨骼肌中线粒体功能控制的 31P NMR 研究。
DOI：
--
复制
发表时间：
1982
影响因子：
11.1
通讯作者：
R. Warnell
中科院分区：
文献类型：
--
作者：
B. Chance;S. Eleff;W. Bank;J. Leigh;R. Warnell
通过31P核磁共振测量正常运动的人骨骼组织中静息-活跃-静息转变过程中的PI水平，以及在这方面的贡献，在磷酸果糖激酶(PFK)缺乏的腿中，评价了PI和ADP对线粒体呼吸活动的代谢控制。后者的研究表明，在腿部最大运动后的恢复过程中，PI几乎是恒定的，而糖磷(SP)的变化与磷酸肌酸(PCr)的变化是相辅相成的。PFK缺乏允许在几乎恒定的PI和ATP的条件下观察到运动后恢复中的PCR重新合成--这一现象在正常运动肌肉中并不明显。游离PI的稳定性与其控制线粒体活性的作用不一致，使ADP成为关键的代谢控制元件。这些结果有助于澄清先前关于线粒体代谢活动控制性质的争论，扩展了ADP控制体内线粒体代谢状态的想法，此外，还为评估影响线粒体代谢的遗传缺陷提供了适当的运动方案。
Metabolic control of mitochondrial respiratory activity by Pi and ADP has been evaluated by 31P NMR measurements of the levels of Pi in normal exercising human skeletal tissues in the resting-active-resting transition and, in this contribution, in the phosphofructokinase (PFK)-deficient leg. The latter studies show near constancy of Pi in the recovery from maximal exercise of the leg, with large changes of sugar phosphate (SP) complementary to the changes of phosphocreatine (PCr). The PFK deficiency permits observation of PCr resynthesis in postexercise recovery under conditions of nearly constant Pi and ATP--a phenomenon not evident in normal exercising muscle. The constancy of free Pi is inconsistent with its role in control of mitochondrial activity, leaving ADP as a key metabolic control element. These results help clarify previous controversies on the nature of control of metabolic activity of mitochondria and extend the idea of ADP control of mitochondrial metabolic states in vivo and, in addition, provide an appropriate exercise protocol for the evaluation of a genetic deficiency affecting mitochondrial metabolism.