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Iron homeostasis and methionine-centred redox cycle in nasal polyposis.

机译:鼻息肉中的铁稳态和以蛋氨酸为中心的氧化还原循环。

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摘要

Nasal polyposis is a multifactorial disease with a strong inflammatory component. Its pathogenesis is often associated with ROS production catalysed by redox-active iron. This study aimed to characterize the roles of iron homeostasis and redox status in the pathogenesis of polyposis. Nasal polyps (NP) from asthmatics and non-asthmatics and turbinates from controls and NP-patients were analysed for ferritin, ferritin-bound iron (FBI) and levels of methionine-centred redox cycle proteins. The ferritin content in both NPs was significantly higher than in adjacent turbinates. No differences in FBI were observed between both NP groups and both turbinates groups, while in NPs it was significantly higher. In NP-turbinates the highest levels of redox proteins were observed. In conclusion, re-distribution of iron occurs upon the development of NP. While FBI is elevated in NPs, the adjacent turbinate remain iron-poor and low-inflammatory, suggesting the formation of virtual boundary between these tissues.
机译:鼻息肉病是具有强烈炎症成分的多因素疾病。其发病机理通常与氧化还原活性铁催化的ROS产生有关。这项研究旨在表征铁稳态和氧化还原状态在息肉病发病机制中的作用。分析了哮喘患者和非哮喘患者的鼻息肉(NP)以及对照组和NP患者的鼻甲的铁蛋白,铁蛋白结合铁(FBI)和蛋氨酸为中心的氧化还原循环蛋白的水平。两个NP中的铁蛋白含量均显着高于相邻鼻甲中的铁蛋白含量。在两个NP组和两个鼻甲组之间均未观察到FBI的差异,而在NP中则明显更高。在NP-涡轮中,观察到最高水平的氧化还原蛋白。总而言之,铁的重新分布会随着NP的发展而发生。尽管NPs中的FBI升高,但相邻的鼻甲仍然贫铁且低发炎,提示这些组织之间形成了虚拟边界。

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