Dietary iron loading negatively affects liver mitochondrial function
Abstract
Iron is an essential co-factor for several metabolic processes, including mitochondrial respiration, and mitochondria are the major sites of iron-utilization. Cellular iron homeostasis must be tightly regulated, as intracellular iron deficiency can lead to insufficient energy production, whereas iron overload triggers ROS (reactive oxygen species) formation via the Fenton reaction. So far little is known on how iron imbalances affect mitochondrial function in vivo and the impact of the genotype on that, we studied the effects of dietary iron loading on mitochondrial respiratory capacity in liver by comparing two genetically divergent mouse strains, namely C57BL/6N and FVB mice. Both mouse strains differed in their basal iron levels and their metabolic responses to iron loading as determined by expression of iron trafficking proteins (ferritin was increased in livers of animals receiving high iron diet) as well as tissue iron content (2-fold increase, FVB p = 0.0013; C57BL/6N p = 0.0022). Dietary iron exposure caused a significant impairment of mitochondrial oxidative phosphorylation, especially regarding OXPHOS capacity (FVB p = 0.0006; C57BL/6N p = 0.0087) and S-ETS capacity (FVB p = 0.0281; C57BL/6N p = 0.0159). These effects were more pronounced in C57BL/6N than in FVB mice and were paralleled by an iron mediated induction of oxidative stress in mitochondria. The increased susceptibility of C57BL6/N mice to iron loading may be due to reduced expression of anti-oxidant defense mechanisms and altered iron trafficking upon dietary challenge pointing to a role of genetic modifiers for cellular and mitochondrial iron trafficking. Finally, iron-mediated induction of mitochondrial oxidative stress and reduction of oxidative phosphorylation may underlie fatigue in subjects with iron loading diseases.
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Imbalanced iron levels in the cell can lead to dysfunctional mitochondria, increased oxidative damage, and increased toxicity.
“Imbalanced iron levels in the cell can lead to dysfunctional mitochondria, increased oxidative damage and increased toxicity (Richardson et al., 2010; Volani et al., 2017).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Volani et al., 2017
A general decrease in Fe3+ reduction resulting in scarcity of Fe2+ and increase of Fe3+ would affect many aspects of cellular metabolism, contributing to reduced T cell proliferation observed with BH4-deficiency.
“A general decrease in Fe3+ reduction resulting in a scarcity of Fe2+ and increase of Fe3+ would affect many aspects of cellular metabolism (Volani et al., 2017) which contribute to the reduced T cell proliferation observed with BH4-deficiency.”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Volani et al., 2017
Cellular iron availability controls mitochondrial respiration and affects citric acid cycle enzymes.
“In addition, cellular iron availability not only controls mitochondrial respiration, but also affects citric acid cycle enzymes [8,9].”
From Iron as a central player and promising target in cancer progression (2019) · cites this paper as [9]
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- Authors
- Volani, C., Doerrier, C., Demetz, E., Haschka, D., Paglia, G., Lavdas, A. A., Gnaiger, E., & Weiss, G.
- Affiliations
- Eurac Research (IT)
- Oroboros Instruments (Austria) (AT)
- Innsbruck Medical University (AT)
- Institute for Biomedicine, Eurac Research
- Department of Internal Medicine II (Infectious Diseases, Immunology, Rheumatology and Pneumology), Medical University of Innsbruck
- ORCID
- Venue
- Metallomics
- Publisher
- Oxford University Press (OUP)
- Published
- 2017
- Volume
- 9
- Issue
- 11
- Pages
- 1634-1644
- ISSN
- 1756-5901 (ISSN-L)
- 1756-591X
- OpenAlex
- W2762656910
- Cited by
- 59
- References
- 45
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 10 · 2023: 3 · 2022: 8 · 2021: 8 · 2020: 5 · 2019: 9 · 2018: 9 · 2017: 1
- FWCI
- 5.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Metallomics (publishedVersion)
- PubMed (publishedVersion)
- BOA (University of Milano-Bicocca) (submittedVersion)
- Open Research (University of Surrey) (submittedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- iron overload, liver mitochondria, mitochondrial respiration, oxidative phosphorylation, superoxide dismutase, ferritin, iron trafficking, oxidative stress, genetic strain differences, C57BL/6N mice, FVB mice, fatigue, iron metabolism
- MeSH terms
- Animals, Cells, Cultured, Ferritins, Humans, Iron, Male, Mice, Inbred C57BL, Mitochondria, Liver, Oxidative Phosphorylation, Oxygen Consumption, Species Specificity, Gene Expression, Oxidative Stress, Iron, Dietary, Hep G2 Cells
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