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Hyperthermia impairs liver mitochondrial function in vitro.

W T Willis1, M R Jackman, M E Bizeau

  • 1Exercise and Sport Research Institute, Arizona State University, Tempe, Arizona 85287-0404, USA. waynewillis@asu.edu

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|May 9, 2000
PubMed
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Hyperthermia increases proton leak in liver mitochondria, reducing energy production. This offsets temperature-stimulated pyruvate carboxylase activity in intact mitochondria, preventing a Q(10) effect.

Area of Science:

  • Mitochondrial Physiology
  • Biochemistry
  • Cellular Respiration

Background:

  • Temperature significantly influences cellular metabolic processes.
  • Mitochondria are key regulators of cellular energy production and are sensitive to thermal stress.
  • Pyruvate carboxylation is a critical anaplerotic pathway in hepatic mitochondria.

Purpose of the Study:

  • To investigate the impact of elevated temperatures on mitochondrial respiration and ATP hydrolysis.
  • To determine how temperature affects pyruvate carboxylation rates in intact versus disrupted mitochondria.
  • To elucidate the relationship between mitochondrial membrane properties and energy transduction under hyperthermia.

Main Methods:

  • Isolated rat liver mitochondria were used to assess pyruvate carboxylation, oxygen consumption (J(o)), and oxidative phosphorylation (J(p)).

Related Experiment Videos

  • Experiments were conducted at physiological (37°C) and hyperthermic (40°C, 43°C) temperatures.
  • Fluorescent probes measured mitochondrial membrane phospholipid polarization to assess membrane order and proton conductance.

    • Main Results:

    • In disrupted mitochondria, pyruvate carboxylase activity showed a Q(10) of 2.25, increasing with temperature.
    • In intact mitochondria, hyperthermia did not enhance pyruvate carboxylation but increased J(o) and decreased the free energy of ATP hydrolysis (G(p)).
    • Hyperthermia (43°C) reduced the J(p)/J(o) ratio and increased membrane proton conductance, indicating increased proton leak.

    Conclusions:

    • Hyperthermia enhances proton leak across the inner mitochondrial membrane.
    • This increased proton leak degrades the mitochondrial energy state, counteracting the direct temperature stimulation of pyruvate carboxylase.
    • Consequently, intact liver mitochondria may not exhibit a Q(10) effect on pyruvate carboxylation at temperatures near 43°C.