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Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
09:27

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue

Published on: March 23, 2015

Haemodialysis induces mitochondrial dysfunction and apoptosis

D S C Raj1, M A Boivin, E A Dominic

  • 1University of New Mexico Health Sciences Center, Division of Nephrology and Epidemiology, Department of Medicine, Albuquerque, New Mexico 87131-5271, USA. draj@salud.unm.edu

European Journal of Clinical Investigation
|November 27, 2007
PubMed
Abstract

Insights

Hemodialysis increases oxidative stress and apoptosis in patients with end-stage renal disease by impairing mitochondrial function and activating inflammatory pathways. The body attempts to counteract this cell stress and apoptosis during the procedure.

Area of Science:

  • Cell Biology
  • Nephrology
  • Biochemistry

Background:

  • Mitochondria are key regulators of apoptosis induced by oxidative stress.
  • Nuclear factor-kappaB (NF-kappaB) integrates pro-inflammatory signals and oxidative stress.

Purpose of the Study:

  • To investigate the impact of hemodialysis on mitochondrial function, reactive oxygen species (ROS) generation, and peripheral blood mononuclear cell (PBMC) apoptosis in end-stage renal disease (ESRD) patients.

Main Methods:

  • PBMCs were isolated from eight ESRD patients before and during hemodialysis (HD).
  • Flow cytometry was used to assess intracellular ROS, mitochondrial membrane potential (Δψm), and PBMC apoptosis.
  • Levels of IL-6, IL-6 soluble receptor, IL-6 gp130, NF-kappaB, B-cell lymphoma protein-2, and heat shock protein-70 were measured.

Main Results:

  • Hemodialysis significantly increased plasma and PBMC-secreted IL-6 levels.
  • A higher percentage of lymphocytes showed mitochondrial membrane potential collapse, apoptosis, and increased ROS generation (superoxide and hydrogen peroxide) during HD.
  • NF-kappaB activation and expression of anti-apoptotic proteins (Bcl-2, HSP70) were elevated during HD.

Conclusions:

  • Intra-dialytic cytokine activation and impaired mitochondrial function during hemodialysis contribute to increased ROS and PBMC apoptosis.
  • The body activates compensatory pathways to mitigate cell stress and apoptosis during hemodialysis.

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