Literature DB >> 25152357

A comparison of ceruloplasmin to biological polyanions in promoting the oxidation of Fe(2+) under physiologically relevant conditions.

Bruce X Wong1, Scott Ayton1, Linh Q Lam1, Peng Lei1, Paul A Adlard1, Ashley I Bush2, James A Duce3.   

Abstract

BACKGROUND: Iron oxidation is thought to be predominantly handled enzymatically in the body, to minimize spontaneous combustion with oxygen and to facilitate cellular iron export by loading transferrin. This process may be impaired in disease, and requires more accurate analytical assays to interrogate enzymatic- and auto-oxidation within a physiologically relevant environment.
METHOD: A new triplex ferroxidase activity assay has been developed that overcomes the previous assay limitations of measuring iron oxidation at a physiologically relevant pH and salinity.
RESULTS: Revised enzymatic kinetics for ceruloplasmin (Vmax≈35μMFe(3+)/min/μM; Km≈15μM) are provided under physiological conditions, and inhibition by sodium azide (Ki for Ferric Gain 78.3μM, Ki for transferrin loading 8.1×10(4)μM) is quantified. We also used this assay to characterize the non-enzymatic oxidation of iron that proceeded linearly under physiological conditions. CONCLUSIONS AND GENERAL SIGNIFICANCE: These findings indicate that the requirement of an enzyme to oxidize iron may only be necessary under conditions of adverse pH or anionic strength, for example from hypoxia. In a normal physiological environment, Fe(3+) incorporation into transferrin would be sufficiently enabled by the biological polyanions that are prevalent within extracellular fluids.
Copyright © 2014. Published by Elsevier B.V.

Entities:  

Keywords:  Ceruloplasmin; Ferroxidase; Iron; Oxidation; Transferrin

Year:  2014        PMID: 25152357     DOI: 10.1016/j.bbagen.2014.08.006

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


  4 in total

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Journal:  Neurotherapeutics       Date:  2015-01       Impact factor: 7.620

2.  CuII (atsm) inhibits ferroptosis: Implications for treatment of neurodegenerative disease.

Authors:  Adam Southon; Kathryn Szostak; Karla M Acevedo; Krista A Dent; Irene Volitakis; Abdel A Belaidi; Kevin J Barnham; Peter J Crouch; Scott Ayton; Paul S Donnelly; Ashley I Bush
Journal:  Br J Pharmacol       Date:  2020-01-14       Impact factor: 8.739

3.  β-Amyloid precursor protein does not possess ferroxidase activity but does stabilize the cell surface ferrous iron exporter ferroportin.

Authors:  Bruce X Wong; Andrew Tsatsanis; Linh Q Lim; Paul A Adlard; Ashley I Bush; James A Duce
Journal:  PLoS One       Date:  2014-12-02       Impact factor: 3.240

Review 4.  Iron Dyshomeostasis and Ferroptosis: A New Alzheimer's Disease Hypothesis?

Authors:  Feixue Wang; Jiandong Wang; Ying Shen; Hao Li; Wolf-Dieter Rausch; Xiaobo Huang
Journal:  Front Aging Neurosci       Date:  2022-03-22       Impact factor: 5.750

  4 in total

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