Altered mitochondrial function and oxidative stress in leukocytes of anorexia nervosa patients

PLoS One. 2014 Sep 25;9(9):e106463. doi: 10.1371/journal.pone.0106463. eCollection 2014.

Abstract

Context: Anorexia nervosa is a common illness among adolescents and is characterised by oxidative stress.

Objective: The effects of anorexia on mitochondrial function and redox state in leukocytes from anorexic subjects were evaluated.

Design and setting: A multi-centre, cross-sectional case-control study was performed.

Patients: Our study population consisted of 20 anorexic patients and 20 age-matched controls, all of which were Caucasian women.

Main outcome measures: Anthropometric and metabolic parameters were evaluated in the study population. To assess whether anorexia nervosa affects mitochondrial function and redox state in leukocytes of anorexic patients, we measured mitochondrial oxygen consumption, membrane potential, reactive oxygen species production, glutathione levels, mitochondrial mass, and complex I and III activity in polymorphonuclear cells.

Results: Mitochondrial function was impaired in the leukocytes of the anorexic patients. This was evident in a decrease in mitochondrial O2 consumption (P<0.05), mitochondrial membrane potential (P<0.01) and GSH levels (P<0.05), and an increase in ROS production (P<0.05) with respect to control subjects. Furthermore, a reduction of mitochondrial mass was detected in leukocytes of the anorexic patients (P<0.05), while the activity of mitochondrial complex I (P<0.001), but not that of complex III, was found to be inhibited in the same population.

Conclusions: Oxidative stress is produced in the leukocytes of anorexic patients and is closely related to mitochondrial dysfunction. Our results lead us to propose that the oxidative stress that occurs in anorexia takes place at mitochondrial complex I. Future research concerning mitochondrial dysfunction and oxidative stress should aim to determine the physiological mechanism involved in this effect and the physiological impact of anorexia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Anorexia Nervosa / metabolism*
  • Anorexia Nervosa / pathology*
  • Electron Transport Complex I / metabolism
  • Electron Transport Complex III / metabolism
  • Female
  • Glutathione / metabolism
  • Humans
  • Leukocytes / metabolism*
  • Membrane Potential, Mitochondrial
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Mitochondrial Size
  • Oxidative Stress*
  • Oxygen Consumption
  • Reactive Oxygen Species / metabolism
  • Young Adult

Substances

  • Reactive Oxygen Species
  • Electron Transport Complex I
  • Electron Transport Complex III
  • Glutathione

Grants and funding

This study was financed by grants PI12/1984, PI13/1025 and PI13/073 from FIS and co-funded by the European Regional Development Fund of the European Union (FEDER), CIBERehd CB06/04/0071 and PROMETEO 2010/060. V.M.V. and M.R. are recipients of contracts from the Ministry of Health of the Valencian Regional Government and Carlos III Health Institute (CES10/030 and CP10/0360, respectively). S.R. is recipient of a predoctoral fellowship from Carlos III Health Institute (FI11/00637). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.