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Fluorescent probes for the detection of catalytic Fe(II) ion

Iron (Fe) is the most abundant redox-active metal ion in the human body, and its redox-active inter-convertible multiple oxidation states contributes to numerous essential biological processes. Moreover, iron overload can potentially cause cellular damage and death, as wel as numerous diseases throu...

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Bibliographic Details
Published in:Free radical biology & medicine 2019-03, Vol.133, p.38-45
Main Author: Hirayama, Tasuku
Format: Article
Language:English
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Summary:Iron (Fe) is the most abundant redox-active metal ion in the human body, and its redox-active inter-convertible multiple oxidation states contributes to numerous essential biological processes. Moreover, iron overload can potentially cause cellular damage and death, as wel as numerous diseases through the aberrant production of highly reactive oxidative species (hROS). Protein-free or weakly-protein-bound Fe ions play a pivotal role as catalytic reactants of the Fenton reaction. In this reaction, hROS, such as hydroxyl radicals and high valent-iron-oxo species, are generated by a reaction between hydrogen peroxide and Fe(II), which is re-generated through reduction using abundant intracellular reductants, such as glutathione. This results in the catalytic evolution of hROS. Thus, selective detection of the catalytic Fe(II) in the living systems can explain both of the pathological and physiological functions of Fe(II). Written from the perspective of their modes of actions, this paper presents recent advances in the development of fluorescent and bioluminescent probes that can selectively detect catalytic Fe(II) together with their biological applications. [Display omitted] •Catalytic Fe(II) is highly important in oxidative stress.•Fluorescent probes for catalytic Fe(II) accelerate the understanding of iron-mediated oxidative stress as well as iron biology.•This review presents recent progress in the development of fluorescent probes for catalytic Fe(II).
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2018.07.004