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Inhibitory effects of adenine nucleotides on brain mitochondrial permeability transition

Angela Saito1, Roger F Castilho

  • 1Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil.

Neurochemical Research
|July 24, 2010
PubMed

Insights

Adenosine diphosphate (ADP) potently inhibits the mitochondrial permeability transition (MPT) in the brain, protecting against tissue damage. Adenosine triphosphate (ATP) is a weaker inhibitor, with its effects largely attributed to conversion to ADP.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Neuroscience

Background:

  • The mitochondrial permeability transition (MPT) is a critical process implicated in cell death.
  • Adenine nucleotides, adenosine diphosphate (ADP) and adenosine triphosphate (ATP), are known endogenous regulators of MPT.

Purpose of the Study:

  • To investigate the inhibitory effects of ADP and ATP on brain MPT.
  • To determine the relative potencies of ADP and ATP as MPT inhibitors.
  • To elucidate the role of ADP and ATP in protecting brain tissue against MPT-mediated damage.

Main Methods:

  • Measurement of mitochondrial swelling, calcium (Ca2+) uptake, and cytochrome c release in brain mitochondria.
  • Assessment of nucleotide effects under various conditions, including ATP-regenerating systems, anoxia/reoxygenation, and oxidative phosphorylation.

Main Results:

  • Both ADP and ATP inhibited Ca2+-induced MPT, preventing mitochondrial swelling and cytochrome c release.
  • ATP's inhibitory effect diminished in the presence of ATP-regenerating systems, suggesting hydrolysis to ADP.
  • ADP demonstrated a significantly higher inhibitory potency (Ki = 4.5 μM) compared to ATP (Ki = 98 μM).
  • ADP's inhibitory effect was robust against anoxia/reoxygenation but reduced by oxidative phosphorylation.

Conclusions:

  • ADP is a potent endogenous inhibitor of brain MPT.
  • ATP acts as a weaker inhibitor, primarily through its conversion to ADP.
  • ADP may play a crucial protective role against MPT-related brain damage during ischemia and hypoglycemia.

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