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Metabolic depression and increased reactive oxygen species production by isolated mitochondria at moderately lower temperatures

Academic Article
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Overview

authors

  • Ali, S. S.
  • Marcondes, Maria Cecilia
  • Bajova, H.
  • Dugan, L. L.
  • Conti, Bruno

publication date

  • 2010

journal

  • Journal of Biological Chemistry  Journal

abstract

  • Temperature (T) reduction increases lifespan, but the mechanisms are not understood. Because reactive oxygen species (ROS) contribute to aging, we hypothesized that lowering T might decrease mitochondrial ROS production. We measured respiratory response and ROS production in isolated mitochondria at 32, 35, and 37 °C. Lowering T decreased the rates of resting (state 4) and phosphorylating (state 3) respiration phases. Surprisingly, this respiratory slowdown was associated with an increase of ROS production and hydrogen peroxide release and with elevation of the mitochondrial membrane potential, ΔΨ(m). We also found that at lower T mitochondria produced more carbon-centered lipid radicals, a species known to activate uncoupling proteins. These data indicate that reduced mitochondrial ROS production is not one of the mechanisms mediating lifespan extension at lower T. They suggest instead that increased ROS leakage may mediate mitochondrial responses to hypothermia.
  • Temperature (T) reduction increases lifespan, but the mechanisms are not understood. Because reactive oxygen species (ROS) contribute to aging, we hypothesized that lowering T might decrease mitochondrial ROS production. We measured respiratory response and ROS production in isolated mitochondria at 32, 35, and 37 �C. Lowering T decreased the rates of resting (state 4) and phosphorylating (state 3) respiration phases. Surprisingly, this respiratory slowdown was associated with an increase of ROS production and hydrogen peroxide release and with elevation of the mitochondrial membrane potential, ??(m). We also found that at lower T mitochondria produced more carbon-centered lipid radicals, a species known to activate uncoupling proteins. These data indicate that reduced mitochondrial ROS production is not one of the mechanisms mediating lifespan extension at lower T. They suggest instead that increased ROS leakage may mediate mitochondrial responses to hypothermia.

subject areas

  • Animals
  • Cell Respiration
  • Cold Temperature
  • Energy Metabolism
  • Life Expectancy
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria
  • Reactive Oxygen Species
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Identity

PubMed Central ID

  • PMC2952254

International Standard Serial Number (ISSN)

  • 0021-9258

Digital Object Identifier (DOI)

  • 10.1074/jbc.M110.155432

PubMed ID

  • 20716522
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Additional Document Info

start page

  • 32522

end page

  • 32528

volume

  • 285

issue

  • 42

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