Ironing out neurodegeneration: iron chelation for neuroprotection.
Ironing out neurodegeneration: iron chelation for neuroprotection.
复制标题
消除神经退行性变：用于神经保护的铁螯合。
DOI：
10.1016/j.freeradbiomed.2011.05.009
复制
发表时间：
2011
影响因子：
7.4
通讯作者：
Dunaief,JoshuaL
中科院分区：
文献类型：
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作者：
Dunaief,JoshuaL
铁是谚语“好东西多了反而不好”所适用的物质之一。铁易于改变其氧化还原状态的能力有助于细胞呼吸，但当铁的水平或位置不合适时，也可以催化有害羟基自由基的产生。在这一期的《自由基生物学与医学》中，Obolensky等人的论文强调了铁螯合的神经保护潜力，即使铁的失调不是变性的主要原因。他们仔细执行的研究表明，用铁螯合剂锌-去铁胺（Zn-DFO）治疗可以改善rd10小鼠的视网膜变性。Rd10小鼠光转导所需的杆状光感受器磷酸二酯酶发生突变，导致杆状和锥状光感受器在大约6周龄时几乎完全丧失。从出生后第4天开始通过ip注射锌- dfo的小鼠在几个年龄阶段的视网膜结构和功能相对保留，氧化应激减轻。在接受治疗的小鼠中，视杆细胞和视锥细胞的数量更高。视网膜电图显示，锌- dfo治疗改善了视杆和视锥功能。免疫染色和生化分析显示，锌- dfo处理小鼠的氧化应激减轻。
Iron is one of the substances for which the adage “Too much of a good thing is not better” holds true. Iron's ability to readily shift its redox state facilitates cellular respiration but can also catalyze the production of harmful hydroxyl radical when iron's level or location is inappropriate. In this issue of Free Radical Biology & Medicine, the paper by Obolensky et al. highlights the neuroprotective potential of iron chelation, even when iron dysregulation is not the primary cause of the degeneration.Their carefully executed study shows that retinal degeneration in rd10 mice can be ameliorated by treatment with the iron chelator zinc–deferoxamine (Zn-DFO). Rd10 mice have a mutation in the rod photoreceptor phosphodiesterase, required for phototransduction, resulting in a nearly complete loss of both rod and cone photoreceptors by about 6 weeks of age. Mice given Zn-DFO by ip injection beginning at postnatal day 4 have relatively preserved retinal structure and function at several ages, as well as diminished oxidative stress. The number of rods and cones is higher in the treated mice. Electroretinography reveals improved rod and cone function with the Zn-DFO treatment. Both immunostaining and biochemical assays reveal diminished oxidative stress in the Zn-DFO-treated mice.