Volani 2016 Abstract Mito Xmas Meeting Innsbruck

From Bioblast
Effects of systemic iron perturbations on mitochondrial activity and on cellular metabolism in vivo.


Volani C, Demetz E, Doerrier C, Gnaiger, E, Paglia G, Weiss G (2016)

Event: Mito Xmas Meeting 2016 Innsbruck AT

Mitochondria are dynamic organelles, involved in different cellular functions, including oxidative phosphorylation, where iron is a fundamental co-factor [1]. Besides being central part of mitochondrial I-IV complexes in the electron transport system, iron also regulates the TCA (tricarboxylic acid cycle) by modulating mitochondrial aconitase [2,3]. Hence, imbalances of iron homeostasis could affect mitochondrial activity and cellular metabolism [4]. Nevertheless, little is known on that. Therefore, we aimed at investigating the impact of alterations of iron homeostasis on mitochondrial function, and on peripheral blood metabolites, in order to potentially identify distinctive signatures. Mitochondrial respiration was studied in liver samples of 10-week old FVB mice and C57BL/6N mice, receiving either normal- or high iron (25 g/kg)-diet two weeks before being sacrificed. Livers were homogenized and mitochondrial respiration was assessed by means of high resolution respirometry (Oroboros Instruments, Austria). Peripheral blood was collected, and metabolomics analysis was performed by using liquid chromatography-mass spectrometry (LC-MS). Our ongoing experiments indicate that dietary iron supplementation affects the phosphorylation system in the mouse liver of both FVB and C57BL/6N mice. The analysis of peripheral blood metabolites is currently under investigation, and might provide useful information on changes in the overall metabolism.

β€’ O2k-Network Lab: AT Innsbruck Oroboros

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, mt-Medicine  Pathology: Other  Stress:Oxidative stress;RONS  Organism: Mouse  Tissue;cell: Liver  Preparation: Homogenate  Enzyme: Complex IV;cytochrome c oxidase  Regulation: Coupling efficiency;uncoupling, Cyt c, Flux control  Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: N, S  HRR: Oxygraph-2k, O2k-Protocol  Event: B2, Oral  Labelled by author 


Volani C(1), Demetz E(1), Doerrier C(2), Gnaiger, E(2), Paglia G(2), Weiss G(1)
  1. Dept Internal Medicine VI, Medical Univ Innsbruck, Austria
  2. Oroboros Instruments, Innsbruck, Austria
  3. EURAC, Center Biomedicine, Bolzano, Italy


  1. Martelli A et al. (2015) Iron regulatory protein 1 sustains mitochondrial iron loading and function in frataxin deficiency. Cell Metab 21:311-22.
  2. Oexle H et al. (1999) Iron-dependent changes in cellular energy metabolism: influence on citric acid cycle and oxidative phosphorylation. Biochim Biophys Acta 1413:99-107.
  3. Rouault TA (2016) Mitochondrial iron overload: causes and consequences. Curr Opin Genet Dev 38:31-7.
  4. Lakhal-Littleton S et al. (2015) Cardiac ferroportin regulates cellular iron homeostasis and is important for cardiac function. PNAS 112:3164-9.
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