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Updated: May 23, 2026

Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells
Published on: May 16, 2019
Alterations in renal iron metabolism caused by a copper/zinc-superoxide dismutase deficiency
Daisaku Yoshihara1, Noriko Fujiwara, Shinsuke Kato
1Department of Biochemistry, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
Abstract:
Copper/zinc-superoxide dismutase knockout (SOD1 KO) mice have been extensively used as an experimental animal model of pathology associated with oxidative stress. The mice spontaneously develop mild chronic hemolytic anaemia (HA). We previously reported that the kidneys of these types of mice contain massive amounts of iron. In this study, to clarify the role of the kidney for iron metabolism under HA, changes in the levels of expression and functions of iron-related proteins were examined. In SOD1 KO mice kidneys, protein levels of iron transporters, the iron-responsive element (IRE)-binding activity of IRP1 and the levels of phosphorylation of IRP1 are all increased. These findings indicate that oxidative stress caused by a SOD1 deficiency probably enhances the phosphorylation of and the conversion of IRP1 to the IRE-binding form, which may accelerate the reabsorption of iron by renal tubular cells. Kidney could play an important role in iron homeostasis under conditions of HA.
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