Siliprandi D, Toninello A, Zoccarato F, Rugolo M, Siliprandi N
J Bioenerg Biomembr. 1978 Apr;10(1-2):1-11. doi: 10.1007/BF00743223.
Addition to rat liver mitochondria of 2 mM inorganic phosphate or 0.15 mM diamide, a thiol-oxidizing agent, induced an efflux of endogenous Mg2+ linear with time and dependent on coupled respiration. No net Ca2+ release occurred under these conditions, while a concomitant release of K+ was observed. Mg2+ efflux mediated either by Pi or low concentration of diamide was completely prevented by EGTA, Ruthenium red, and NEM. These reagents also inhibited the increased rate of state 4 respiration induced both by Pi and diamide. At higher concentrations (0.4 mM), diamide induced an efflux of Mg2+ which was associated also with a release of endogenous Ca2+. Under these conditions EGTA completely prevented Mg2+ and K+ effluxes, while they were only partially inhibited by Ruthenium red and NEM. It is assumed that Mg2+ efflux, occurring at low diamide concentrations or in the presence of phosphate, is dependent on a cyclic in-and-out movement of Ca2+ across the inner mitochondrial membrane, in which the passive efflux is compensated by a continuous energy linked reuptake. This explains the dependence of Mg2+ efflux on coupled respiration, as well as the increased rate of state 4 respiration. The dependence of Mg2+ efflux on phosphate transport is explained by the phosphate requirement for Ca2+ movement.
向大鼠肝线粒体中添加2 mM无机磷酸盐或0.15 mM二酰胺(一种硫醇氧化剂)会诱导内源性Mg2+外流,其与时间呈线性关系且依赖于偶联呼吸作用。在这些条件下未发生净Ca2+释放,而观察到伴随有K+释放。由Pi或低浓度二酰胺介导的Mg2+外流被EGTA、钌红和NEM完全抑制。这些试剂也抑制了由Pi和二酰胺诱导的状态4呼吸速率的增加。在较高浓度(0.4 mM)时,二酰胺诱导Mg2+外流,这也与内源性Ca2+的释放有关。在这些条件下,EGTA完全阻止了Mg2+和K+外流,而它们仅被钌红和NEM部分抑制。据推测,在低浓度二酰胺或存在磷酸盐的情况下发生的Mg2+外流依赖于Ca离子跨线粒体内膜的循环进出运动,其中被动外流由连续的能量相关再摄取来补偿。这解释了Mg2+外流对偶联呼吸作用的依赖性以及状态4呼吸速率的增加。Mg2+外流对磷酸盐转运的依赖性由Ca2+移动对磷酸盐的需求来解释。