Quantification of Iron Release from Native Ferritin and Magnetoferritin Induced by Vitamins B<sub>2</sub> and C
Various pathological processes in humans are associated with biogenic iron accumulation and the mineralization of iron oxide nanoparticles, especially magnetite. Ferritin has been proposed as a precursor to pathological magnetite mineralization. This study quantifies spectroscopically the release of...
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2020-08-01
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author | Oliver Strbak Lucia Balejcikova Martina Kmetova Jan Gombos Alzbeta Trancikova Michal Pokusa Peter Kopcansky |
author_facet | Oliver Strbak Lucia Balejcikova Martina Kmetova Jan Gombos Alzbeta Trancikova Michal Pokusa Peter Kopcansky |
author_sort | Oliver Strbak |
collection | DOAJ |
description | Various pathological processes in humans are associated with biogenic iron accumulation and the mineralization of iron oxide nanoparticles, especially magnetite. Ferritin has been proposed as a precursor to pathological magnetite mineralization. This study quantifies spectroscopically the release of ferrous ions from native ferritin and magnetoferritin as a model system for pathological ferritin in the presence of potent natural reducing agents (vitamins C and B<sub>2</sub>) over time. Ferrous cations are required for the transformation of ferrihydrite (physiological) into a magnetite (pathological) mineral core and are considered toxic at elevated levels. The study shows a significant difference in the reduction and iron release from native ferritin compared to magnetoferritin for both vitamins. The amount of reduced iron formed from a magnetoferritin mineral core is two to five times higher than from native ferritin. Surprisingly, increasing the concentration of the reducing agent affects only iron release from native ferritin. Magnetoferritin cores with different loading factors seem to be insensitive to different concentrations of vitamins. An alternative hypothesis of human tissue magnetite mineralization and the process of iron-induced pathology is proposed. The results could contribute to evidence of the molecular mechanisms of various iron-related pathologies, including neurodegeneration. |
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spelling | doaj.art-c3fac8da71f54e90b1bca401e949f76c2023-11-20T12:04:35ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-08-012117633210.3390/ijms21176332Quantification of Iron Release from Native Ferritin and Magnetoferritin Induced by Vitamins B<sub>2</sub> and COliver Strbak0Lucia Balejcikova1Martina Kmetova2Jan Gombos3Alzbeta Trancikova4Michal Pokusa5Peter Kopcansky6Biomedical Center Martin, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora 4, 036 01 Martin, SlovakiaInstitute of Hydrology, Slovak Academy of Sciences, Dubravska cesta 9, 841 04 Bratislava, SlovakiaDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Mala Hora 4, 036 01 Martin, SlovakiaDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Mala Hora 4, 036 01 Martin, SlovakiaBiomedical Center Martin, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora 4, 036 01 Martin, SlovakiaBiomedical Center Martin, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora 4, 036 01 Martin, SlovakiaInstitute of Experimental Physics, Slovak Academy of Sciences, Watsonova 47, 040 01 Kosice, SlovakiaVarious pathological processes in humans are associated with biogenic iron accumulation and the mineralization of iron oxide nanoparticles, especially magnetite. Ferritin has been proposed as a precursor to pathological magnetite mineralization. This study quantifies spectroscopically the release of ferrous ions from native ferritin and magnetoferritin as a model system for pathological ferritin in the presence of potent natural reducing agents (vitamins C and B<sub>2</sub>) over time. Ferrous cations are required for the transformation of ferrihydrite (physiological) into a magnetite (pathological) mineral core and are considered toxic at elevated levels. The study shows a significant difference in the reduction and iron release from native ferritin compared to magnetoferritin for both vitamins. The amount of reduced iron formed from a magnetoferritin mineral core is two to five times higher than from native ferritin. Surprisingly, increasing the concentration of the reducing agent affects only iron release from native ferritin. Magnetoferritin cores with different loading factors seem to be insensitive to different concentrations of vitamins. An alternative hypothesis of human tissue magnetite mineralization and the process of iron-induced pathology is proposed. The results could contribute to evidence of the molecular mechanisms of various iron-related pathologies, including neurodegeneration.https://www.mdpi.com/1422-0067/21/17/6332ferritinmagnetoferritinmineral corereductionascorbic acidriboflavin |
spellingShingle | Oliver Strbak Lucia Balejcikova Martina Kmetova Jan Gombos Alzbeta Trancikova Michal Pokusa Peter Kopcansky Quantification of Iron Release from Native Ferritin and Magnetoferritin Induced by Vitamins B<sub>2</sub> and C International Journal of Molecular Sciences ferritin magnetoferritin mineral core reduction ascorbic acid riboflavin |
title | Quantification of Iron Release from Native Ferritin and Magnetoferritin Induced by Vitamins B<sub>2</sub> and C |
title_full | Quantification of Iron Release from Native Ferritin and Magnetoferritin Induced by Vitamins B<sub>2</sub> and C |
title_fullStr | Quantification of Iron Release from Native Ferritin and Magnetoferritin Induced by Vitamins B<sub>2</sub> and C |
title_full_unstemmed | Quantification of Iron Release from Native Ferritin and Magnetoferritin Induced by Vitamins B<sub>2</sub> and C |
title_short | Quantification of Iron Release from Native Ferritin and Magnetoferritin Induced by Vitamins B<sub>2</sub> and C |
title_sort | quantification of iron release from native ferritin and magnetoferritin induced by vitamins b sub 2 sub and c |
topic | ferritin magnetoferritin mineral core reduction ascorbic acid riboflavin |
url | https://www.mdpi.com/1422-0067/21/17/6332 |
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