Masini A, Trenti T, Ceccarelli-Stanzani D, Ventura E
Biochim Biophys Acta. 1985 Oct 29;810(1):27-32. doi: 10.1016/0005-2728(85)90203-8.
It has been found that addition of iron(III)-gluconate complex to rat liver mitochondria disturbed the mitochondrial Ca2+ transport. Indirect evidence when the changes in the membrane potential during the transport of Ca2+ were followed, as well as direct evidence, when the fluxes of Ca2+ were monitored by a Ca2+-selective electrode, indicated that this iron complex induced an efflux of Ca2+ from liver mitochondria. The mechanisms by which iron induced Ca2+ release appeared to be linked to the induction of lipoperoxidation of mitochondrial membrane. The mitochondrial membrane, however, did not become irreversibly damaged under these conditions, as indicated by its complete repolarization. It was also shown that the induction by iron of lipoperoxidation brought about an efflux of K+ from mitochondria.
已发现向大鼠肝线粒体中添加葡萄糖酸铁（III）络合物会干扰线粒体的Ca2+转运。当追踪Ca2+转运过程中膜电位的变化时得到的间接证据，以及当用Ca2+选择性电极监测Ca2+通量时得到的直接证据，均表明这种铁络合物会诱导Ca2+从肝线粒体中流出。铁诱导Ca2+释放的机制似乎与线粒体膜脂质过氧化的诱导有关。然而，如线粒体膜完全复极化所示，在这些条件下线粒体膜并未受到不可逆转的损伤。还表明铁诱导的脂质过氧化会导致K+从线粒体中流出。
