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Dietary iron loading negatively affects liver mitochondrial function.

Chiara Volani¹, Carolina Doerrier, Egon Demetz

¹Department of Internal Medicine II (Infectious Diseases, Immunology, Rheumatology and Pneumology), Medical University of Innsbruck, Anichstr. 35, A-6020 Innsbruck, Austria. guenter.weiss@i-med.ac.at.

Metallomics : Integrated Biometal Science

|October 14, 2017

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Dietary iron overload impairs mitochondrial function and oxidative phosphorylation in mice. Genetic background influences susceptibility, with C57BL/6N mice showing greater impairment due to altered iron handling and oxidative stress.

Area of Science:

Mitochondrial Biology
Nutritional Biochemistry
Genetics

Background:

Iron is vital for mitochondrial respiration, but imbalances disrupt cellular homeostasis.
Iron overload can cause reactive oxygen species (ROS) formation and mitochondrial dysfunction.
Limited knowledge exists on in vivo effects of iron imbalance on mitochondrial function and genotype impact.

Purpose of the Study:

To investigate the impact of dietary iron loading on liver mitochondrial respiratory capacity.
To compare these effects in two genetically divergent mouse strains: C57BL/6N and FVB.
To explore the role of genetic background in cellular and mitochondrial iron trafficking and response to iron overload.

Main Methods:

Dietary iron loading was administered to C57BL/6N and FVB mice.

Related Experiment Videos

Liver tissue was analyzed for iron content and expression of iron trafficking proteins (e.g., ferritin).

Mitochondrial respiratory capacity, specifically oxidative phosphorylation (OXPHOS) and substrate-ETS capacity, was measured.

Main Results:

Both mouse strains showed increased liver iron content and ferritin expression upon high-iron diet.
Dietary iron loading significantly impaired mitochondrial OXPHOS and S-ETS capacity in both strains.
C57BL/6N mice exhibited more pronounced mitochondrial dysfunction compared to FVB mice.
Iron overload induced oxidative stress in mitochondria, more so in C57BL/6N mice.
Genetic differences in antioxidant defenses and iron trafficking were observed.

Conclusions:

Dietary iron loading impairs mitochondrial function and induces oxidative stress in mice.
Genetic factors significantly influence susceptibility to iron-induced mitochondrial dysfunction.
Altered iron trafficking and reduced antioxidant defenses may explain increased susceptibility in C57BL/6N mice.
Iron-mediated mitochondrial dysfunction could contribute to fatigue in iron-loading diseases.