Masini A, Trenti T, Ceccarelli D, Muscatello U
Biochim Biophys Acta. 1987 Apr 15;891(2):150-6. doi: 10.1016/0005-2728(87)90007-7.
Addition of iron(III)-gluconate complex to isolated rat liver mitochondria induced a net efflux of Ca2+ which was not inhibited by ruthenium red. This process resulted in the enhancement of Ca2+ cycling and a consequent membrane potential drop. Under these experimental conditions the content of mitochondrial glutathione did not appear to be critically modified, whereas an extensive oxidation of mitochondrial pyridine nucleotides was parallelly detected. Iron failed to induce appreciable changes in the oxidation level of pyridine nucleotides in mitochondria isolated from rats fed a selenium deficient diet, a condition in which mitochondrial glutathione peroxidase resulted inhibited by 80%. The iron-induced Ca2+ release in Se-deficient mitochondria appeared largely delayed and the membrane potential of these mitochondrial did not present gross alterations. Iron was also found to induce a transient increase in the mitochondrial cyanide-insensitive oxygen consumption. This effect was largely prevented by the addition of the hydrogen peroxide scavenger catalase. It was concluded that iron induced the activation of a specific Ca2+ efflux pathway via the oxidation of pyridine nucleotides due to the hydrogen peroxide metabolism by glutathione enzyme system.
向分离的大鼠肝线粒体中添加葡萄糖酸铁（III）复合物会诱导Ca2+的净流出，这种流出不受钌红抑制。该过程导致Ca2+循环增强，进而导致膜电位下降。在这些实验条件下，线粒体谷胱甘肽的含量似乎没有受到严重影响，而同时检测到线粒体吡啶核苷酸发生了广泛氧化。在喂食缺硒饮食的大鼠分离的线粒体中，铁未能诱导吡啶核苷酸氧化水平发生明显变化，在这种情况下，线粒体谷胱甘肽过氧化物酶受到80%的抑制。缺硒线粒体中铁诱导的Ca2+释放似乎大大延迟，这些线粒体的膜电位没有出现明显改变。还发现铁会诱导线粒体对氰化物不敏感的氧消耗短暂增加。添加过氧化氢清除剂过氧化氢酶可在很大程度上阻止这种效应。得出的结论是，由于谷胱甘肽酶系统参与过氧化氢代谢，铁通过吡啶核苷酸的氧化诱导了特定Ca2+流出途径的激活。
