Heaton F W, Elie J P
Magnesium. 1984;3(1):21-8.
Comparisons were made between the metabolic activities of whole mitochondria and intact mitochondrial inner membrane preparations from magnesium-deficient and control rats in a basic medium without exogenous magnesium. Magnesium deficiency partially uncoupled oxidative phosphorylation in whole mitochondria and completely uncoupled it with inner membrane preparations. Addition of 1 mM MgCl2 to the medium prevented the total uncoupling of inner membranes and gave ADP:O values similar to those obtained with whole mitochondria from magnesium-deficient rats. No impairment in proton extrusion by intact inner membranes or in ATPase activity by either intact or fragmented inner membranes was detected during magnesium deficiency, but there was evidence of increased membrane permeability to the inward movement of protons. It is concluded that magnesium deficiency probably increases the permeability of the mitochondrial inner membrane and this weakens the coupling between oxidation and phosphorylation.
在无外源镁的基础培养基中，对缺镁大鼠和对照大鼠的完整线粒体及完整线粒体内膜制剂的代谢活性进行了比较。缺镁使完整线粒体中的氧化磷酸化部分解偶联，而使内膜制剂中的氧化磷酸化完全解偶联。向培养基中添加1 mM MgCl2可防止内膜完全解偶联，并使ADP:O值与缺镁大鼠完整线粒体所获得的值相似。在缺镁期间，未检测到完整内膜质子外排受损或完整或破碎内膜的ATP酶活性受损，但有证据表明膜对质子向内移动的通透性增加。得出的结论是，缺镁可能会增加线粒体内膜的通透性，从而削弱氧化与磷酸化之间的偶联。
