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肺中的铁稳态

Iron homeostasis in the lung.

作者信息

Ghio Andrew J, Turi Jennifer L, Yang Funmei, Garrick Laura M, Garrick Michael D

机构信息

National Health and Environmental Effects Research Laboratory, Office of Research and Development, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.

出版信息

Biol Res. 2006;39(1):67-77. doi: 10.4067/s0716-97602006000100008.

Abstract

Iron is essential for many aspects of cellular function. However, it also can generate oxygen-based free radicals that result in injury to biological molecules. For this reason, iron acquisition and distribution are tightly regulated. Constant exposure to the atmosphere results in significant exposure of the lungs to catalytically active iron. The lungs have a mechanism for detoxification to prevent associated generation of oxidative stress. Those same proteins that participate in iron uptake in the gut are also employed in the lung, to transport iron intracellularly and sequester it in an inactive form within ferritin. The release of metal is expedited (as transferrin and ferritin) from lung tissue to the respiratory lining fluid for clearance by the mucocilliary pathway or to the reticuloendothelial system for long-term storage. This pathway is likely to be the major method for the control of oxidative stress presented to the respiratory tract.

摘要

铁对于细胞功能的多个方面至关重要。然而,它也会产生基于氧的自由基,从而导致生物分子受损。因此,铁的获取和分布受到严格调控。持续暴露于大气中会使肺部大量接触具有催化活性的铁。肺部有一种解毒机制来防止相关氧化应激的产生。那些参与肠道铁摄取的相同蛋白质也在肺部发挥作用,将铁转运到细胞内并以无活性形式螯合在铁蛋白中。金属(以转铁蛋白和铁蛋白的形式)从肺组织快速释放到呼吸道内衬液中,通过黏液纤毛途径清除,或释放到网状内皮系统进行长期储存。这条途径可能是控制呼吸道氧化应激的主要方法。

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