Alterations in iron metabolism or oxidative damage in response to hypoxic incidents have been examined following re-oxygenation of the hypoxic tissue. To understand the consequences of decreased tissue oxygen on iron load, metal-catalyzed redox activity and oxidative modifications in isolation from re-oxygenation, the present study exposed mice to either normoxia, or mild hypoxia (380 Torr; approximately 10% normobaric oxygen) where the tissue was not allowed to re-oxygenate prior to examination. Brain, liver and skeletal muscle were examined for Fe3+ load, metal-catalyzed redox activity and oxidative modifications to proteins (N(epsilon)-(carboxymethyl)lysine), lipids (4-hydroxynonenal pyrrole) and nucleic acids (8-hydroxyguanosine). Hypoxia induced a 43% increase in the iron content of the liver (P < 0.001) as determined by ICP-MS and a 3.8-fold increase in Fe3+ load (P < 0.001) as determined by Perl's stain. There was a corresponding 2-fold increase in metal-catalyzed redox activity (P < 0.01) in the liver, but no change in the expression of oxidative markers. In contrast, non-significant increases in Fe3+ and metal-catalyzed redox activity were observed in the cerebral cortex, and molecular and granular layers of the hippocampus and cerebellum. Interestingly, hypoxia significantly decreased oxidative modifications to proteins and lipids, but not nucleic acids in most brain regions examined. In addition, hypoxia did not alter the Fe content of skeletal muscle, or the contents of Zn, Cu, Ni or Mn in liver, skeletal muscle, cerebral cortex or hippocampus. Together, these results indicate that there is a tighter regulation of iron metabolism in the brain than the liver, which limits the redistribution of Fe3+ following hypoxia.

中文翻译：

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轻度缺氧后，铁体内平衡维持在大脑中，而不是肝脏中。

在低氧组织再充氧后，已经检查了因缺氧事件而引起的铁代谢或氧化损伤的变化。为了了解组织氧减少对铁负荷，金属催化的氧化还原活性以及与再氧化隔离的氧化修饰的后果，本研究将小鼠暴露于常氧或轻度低氧（380托；约10％的常压氧）下，检查前不允许组​​织再充氧。检查脑，肝和骨骼肌的Fe3 +负载，金属催化的氧化还原活性以及对蛋白质（N（ε）-（羧甲基）赖氨酸），脂质（4-羟基壬烯吡咯）和核酸（8-羟基鸟苷）的氧化修饰。根据ICP-MS的测定，低氧诱导肝脏铁含量增加43％（P <0.001），而铁含量为3。通过Perl染色确定，Fe3 +负载增加8倍（P <0.001）。肝脏中金属催化的氧化还原活性相应增加了2倍（P <0.01），但氧化标记的表达没有变化。相反，在大脑皮层，海马和小脑的分子和颗粒层中，Fe3 +和金属催化的氧化还原活性没有明显增加。有趣的是，低氧显着降低了对蛋白质和脂质的氧化修饰，但并未降低大多数受检大脑区域的核酸。另外，低氧不会改变骨骼肌中的铁含量，或肝脏，骨骼肌，大脑皮层或海马中锌，铜，镍或锰的含量。总之，这些结果表明，与肝脏相比，大脑中铁代谢的调控更加严格，