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Related Experiment Videos

Possible mechanism for the decrease of mitochondrial aspartate aminotransferase activity in ischemic and hypoxic rat

S Endo1, S Ishiguro, M Tamai

  • 1Department of Ophthalmology, Tohoku University School of Medicine, 1-1 Seiryou-machi, Aoba-ku, Sendai 980-8574, Japan. satoko@oph.med.tohoku.ac.jp

Biochimica Et Biophysica Acta
|July 9, 1999
PubMed
Summary

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Ischemia and hypoxia decrease mitochondrial aspartate aminotransferase (AAT) activity in rat retinas. This decrease is mediated by calpain, a calcium-dependent protease, suggesting calpain inhibitors may protect retinal cells.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Ophthalmology

Background:

  • Glutamate is a key excitatory neurotransmitter in the retina, with its metabolism involving several enzymes, including aspartate aminotransferase (AAT).
  • Mitochondrial enzymes are susceptible to damage from increased intracellular calcium during ischemia, potentially through calpain activation.
  • Mitochondrial AAT (mAAT) constitutes a significant portion of total AAT activity in the rat retina.

Purpose of the Study:

  • To investigate the changes in AAT activity in rat retinas under ischemic and hypoxic conditions.
  • To explore the role of intracellular calcium and calpain in the degradation of mAAT.
  • To evaluate the protective effects of calpain inhibitors against AAT activity loss.

Main Methods:

  • Induction of retinal ischemia in vivo by optic nerve clamping and in vitro by incubating eye cups in hypoxic conditions.

Related Experiment Videos

  • Measurement of cytosolic AAT (cAAT) and mitochondrial AAT (mAAT) activity.
  • Utilized calcium modulators (EGTA, ryanodine, thapsigargin) and various protease inhibitors, including calpain inhibitors (calpeptin, calpain inhibitor peptide).

    • Main Results:

    • Ninety minutes of ischemia or hypoxia significantly decreased mAAT activity by 20%, while cAAT activity remained unaffected.
    • Thapsigargin, but not ryanodine, prevented AAT degradation in Ca2+-free solutions, indicating a role for Ca2+-ATPase.
    • Calpain inhibitors, including calpeptin and calpain inhibitor peptide, effectively prevented AAT degradation, while other protease inhibitors did not.

    Conclusions:

    • Decreased mitochondrial AAT activity in ischemic and hypoxic retinas is likely due to calpain-catalyzed proteolysis within mitochondria.
    • Calpain activation, potentially triggered by calcium influx during ischemia, plays a crucial role in mAAT degradation.
    • Calpain inhibitors show promise in protecting retinal AAT activity against ischemic/hypoxic damage.