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Decrease in mitochondrial levels of adenine nucleotides and concomitant mitochondrial dysfunction in ischemic rat

F Watanabe, W Kamiike, T Nishimura

    Journal of Biochemistry
    |August 1, 1983
    PubMed
    Summary
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    Mitochondrial dysfunction during liver ischemia involves adenine nucleotide loss, impairing oxidative phosphorylation. Preserving these nucleotides effectively maintains mitochondrial function.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Physiology

    Background:

    • Mitochondrial dysfunction is a key factor in ischemic liver injury.
    • Adenine nucleotides (ATP, ADP, AMP) are crucial for mitochondrial energy production via oxidative phosphorylation.

    Purpose of the Study:

    • To investigate the relationship between mitochondrial dysfunction and adenine nucleotide levels in ischemic rat liver.
    • To identify the mechanisms underlying adenine nucleotide loss and its impact on oxidative phosphorylation capacity.

    Main Methods:

    • Isolated rat liver mitochondria were subjected to anoxic incubation in vitro and in vivo.
    • Adenine nucleotide content and oxidative phosphorylation capacity were measured.
    • Effects of preservation methods and exogenous adenine nucleotides on mitochondrial function were assessed.

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    Main Results:

    • A significant decrease in mitochondrial adenine nucleotide content correlated with a loss of oxidative phosphorylation capacity.
    • Adenine nucleotide levels dropped from 15-20 nmol/mg protein to 1-2 nmol/mg protein after 120 minutes of ischemia.
    • Loss of adenine nucleotides was attributed to AMP degradation and subsequent adenosine leakage, not altered permeability or enzyme activity.
    • Conventional preservation methods and ATP/ADP addition effectively maintained adenine nucleotide levels and mitochondrial function.
    • Mitochondria with >5 nmol ATP+ADP/mg protein showed normal oxidative phosphorylation, while those with <2 nmol had no activity.

    Conclusions:

    • Adenine nucleotide depletion is a primary cause of impaired oxidative phosphorylation in ischemic rat liver.
    • Maintaining adequate intramitochondrial adenine nucleotide levels, particularly ATP and ADP, is essential for preserving mitochondrial function during ischemia.
    • Specific preservation strategies can mitigate adenine nucleotide loss and protect mitochondrial energy metabolism.