Review articleSuperoxide dependent iron release from ferritin in inflammatory diseases
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2016, Applied Catalysis B: EnvironmentalCitation Excerpt :The ROS production, as described in the previous chapter can play the role of the intermediate, which “unlocks” the structures and releases iron into the cell. More specifically, the superoxide anion can extract iron from the iron-storage proteins [158–161], through oxidation of dehydratases, for instance. As described before, the critical iron atom is bound and the cluster is left in an unstable state [125]; the [4Fe-4S]2+ form is univalently oxidizing the cluster to [4Fe-4S]3+, resulting into released ferrous iron and [3Fe-4S]+ cluster [161,162].
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2016, Seminars in NephrologyCitation Excerpt :In 1993, Baliga et al45 reported that the excess iron that accumulated in the kidney after AKI may originate from degraded red blood cells. Some researchers have pointed to ferritin as the culprit responsible for iron release,53–55 whereas others have suggested the iron may originate from mitochondria rich in heme and nonheme iron.56,57 In a model of AKI initiated by administration of the antibiotic gentamycin, only catalase was protective despite the use of a superoxide anion scavenger, hydroxyl scavengers, and iron chelators.56
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G. Swaak, M.D., Rheumatologist. Henk G. van Eijk, Ph.D., Professor of Chemical Pathology. Johan F. Koster, Ph.D., Professor of Medical Enzymology.