离体大鼠肝脏线粒体蛋白质合成的铁需求
Iron requirement for isolated rat liver mitochondrial protein synthesis.
作者信息
Marcus D L, Ibrahim N G, Gruenspecht N, Freedman M L
出版信息
Biochim Biophys Acta. 1980 Mar 28;607(1):136-44. doi: 10.1016/0005-2787(80)90227-0.
Isolated rat liver mitochondrial protein synthesis was severly inhibited by alpha, alpha-dipyridyl (a ferrous iron-chelating agent), chloramphenicol and hemin (10(-7) M or greater). In contrast, gamma, gamma-dipyridyl (a non-iron-chelating analogue of alpha, alpha-dipyridyl), cycloheximide and lower concentrations of hemin were non-inhibitory. The inhibitory action of alpha, alpha-dipyridyl was reversed by addition of Fe(NH4)2(SO4)2 while ZnCl2, CuCl2 and CoCl2 were ineffective. Hemin, however, did not protect against the alpha, alpha-dipyridyl inhibition of mitochondrial protein synthesis. These results indicate that ferrous iron is required for mitochondrial protein synthesis and suggests that it is through a mechanism independent of hemin concentration.
α,α-联吡啶（一种亚铁离子螯合剂）、氯霉素和血红素（10⁻⁷M或更高浓度）能严重抑制离体大鼠肝线粒体蛋白质合成。相比之下，γ,γ-联吡啶（α,α-联吡啶的一种非铁螯合类似物）、环己酰亚胺和较低浓度的血红素则无抑制作用。添加硫酸亚铁铵可逆转α,α-联吡啶的抑制作用，而氯化锌、氯化铜和氯化钴则无效。然而，血红素并不能防止α,α-联吡啶对线粒体蛋白质合成的抑制。这些结果表明，线粒体蛋白质合成需要亚铁离子，且提示其作用机制与血红素浓度无关。
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