Sheftel Alex D, Lill Roland
Institut fur Zytobiologie, Philipps Universitat Marburg, Germany.
Ann Med. 2009;41(2):82-99. doi: 10.1080/07853890802322229.
Iron is required for a barrage of essential biochemical functions in virtually every species of life. Perturbation of the availability or utilization of iron in these functions or disruption of other components along iron-requiring pathways can not only lead to cellular/organismal insufficiency of respective biochemical end-products but also result in a broad derangement of iron homeostasis. This is largely because of the elaborate regulatory mechanisms that connect cellular iron utilization with uptake and distribution. Such mechanisms are necessitated by the 'double-edged' nature of the metal, whose very property as a useful biological catalyst also makes it able to generate highly toxic compounds. Since the majority of iron is dispatched onto a functional course by mitochondria-localized pathways, these organelles are in an ideal position within the cellular iron anabolic pathways to be a central site for regulation of iron homeostasis. The goal of this article is to provide an overview of how mitochondria acquire and use iron and examine the ramifications of disturbances in these processes on overall cellular iron homeostasis.
事实上,几乎每一种生命形式都需要铁来进行一系列重要的生化功能。这些功能中铁的可用性或利用率受到干扰,或者沿铁需求途径的其他成分受到破坏,不仅会导致相应生化终产物的细胞/机体不足,还会导致铁稳态的广泛紊乱。这主要是因为存在将细胞铁利用与摄取和分布联系起来的精细调节机制。这种机制是由金属的“双刃剑”性质所必需的,金属作为一种有用的生物催化剂的特性也使其能够产生剧毒化合物。由于大多数铁是通过线粒体定位途径进入功能过程的,这些细胞器在细胞铁合成代谢途径中处于理想位置,成为调节铁稳态的中心位点。本文的目的是概述线粒体如何获取和利用铁,并探讨这些过程中的干扰对整体细胞铁稳态的影响。