Department of Genetic Engineering, Cheongju University, Korea.
BMB Rep. 2011 Mar;44(3):165-9. doi: 10.5483/BMBRep.2011.44.3.165.
Excess free iron generates oxidative stress that may contribute to the pathogenesis of various causes of neurodegenerative diseases. In this study, we assessed the modification of ferritin induced by H(2)O(2). When ferritin was incubated with H(2)O(2), the degradation of ferritin L-chain increased with the H(2)O(2) concentration whereas ferritin H-chain was remained. Free radical scavengers, azide, thiourea, and N-acetyl-(L)-cysteine suppressed the H(2)O(2)-mediated ferritin modification. The iron specific chelator, deferoxamine, effectively prevented H(2)O(2)-mediated ferritin degradation in modified ferritin. The release of iron ions from ferritin was increased in H(2)O(2) concentration-dependent manner. The present results suggest that free radicals may play a role in the modification and iron releasing of ferritin by H(2)O(2). It is assumed that oxidative damage of ferritin by H(2)O(2) may induce the increase of iron content in cells and subsequently lead to the deleterious condition.
过量的游离铁会产生氧化应激,这可能导致各种神经退行性疾病的发病机制。在这项研究中,我们评估了 H(2)O(2)对铁蛋白的修饰。当铁蛋白与 H(2)O(2)孵育时,铁蛋白 L 链的降解随着 H(2)O(2)浓度的增加而增加,而铁蛋白 H 链则保持不变。自由基清除剂叠氮化物、硫脲和 N-乙酰-L-半胱氨酸抑制了 H(2)O(2)介导的铁蛋白修饰。铁特异性螯合剂去铁胺有效地防止了 H(2)O(2)介导的铁蛋白降解。铁蛋白从铁蛋白中释放的铁离子数量呈 H(2)O(2)浓度依赖性增加。这些结果表明,自由基可能在 H(2)O(2)对铁蛋白的修饰和铁释放中起作用。据推测,H(2)O(2)对铁蛋白的氧化损伤可能导致细胞内铁含量增加,进而导致有害状态。