Barnard P A, Cockrell R S
Biochim Biophys Acta. 1982 Jan 20;679(1):68-74. doi: 10.1016/0005-2728(82)90256-0.
The Na+ and K+ conductances of rat brain mitochondria were estimated from rates of metabolically dependent swelling and uncoupling of respiration. These were maximal in the presence of EDTA plus Pi. Pi could not be replaced with acetate. Na+ conductance was greater than that of K+ and was therefore examined in greater detail. According to the influences of N-ethylmaleimide, internal Pi (exogenous and perhaps endogenous) promoted Na+ permeability. Treatment with the ionophore A23187 obviated the Pi requirement although EDTA was still necessary. The stimulation by EDTA with Pi or A23187 and inhibition by exogenous Mg2+ suggested endogenous polyvalent cations could also regulate Na+ conductance. The influence of these substances upon endogenous Mg2+ (and Ca2+) levels is consistent with such a role of membrane-bound Mg2+. Low levels of ruthenium red (150 pmol/mg) inhibit Na+ permeation, indicating that the number of 'sites' or 'channels' involved may be small. The Ca2+ uniport is not directly involved in Na+ flow according to its greater sensitivity to inhibition by ruthenium red.
通过代谢依赖性肿胀速率和呼吸解偶联来估算大鼠脑线粒体的Na⁺和K⁺电导率。在存在乙二胺四乙酸（EDTA）和无机磷酸盐（Pi）的情况下，这些电导率达到最大值。Pi不能被乙酸盐替代。Na⁺电导率大于K⁺电导率，因此对其进行了更详细的研究。根据N - 乙基马来酰亚胺的影响，线粒体内的Pi（外源性的，可能还有内源性的）促进了Na⁺通透性。用离子载体A23187处理消除了对Pi的需求，不过EDTA仍然是必需的。EDTA与Pi或A23187共同作用产生的刺激以及外源性Mg²⁺的抑制作用表明，内源性多价阳离子也可能调节Na⁺电导率。这些物质对内源性Mg²⁺（和Ca²⁺）水平的影响与膜结合Mg²⁺的这种作用是一致的。低水平的钌红（150 pmol/mg）抑制Na⁺通透，这表明所涉及的“位点”或“通道”数量可能很少。根据其对钌红抑制的更高敏感性，Ca²⁺单向转运体不直接参与Na⁺流动。
