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Mitochondrial changes associated with glutathione deficiency

A Meister1

  • 1Department of Biochemistry, Cornell University Medical College, New York, NY 10021, USA.

Biochimica Et Biophysica Acta
|May 24, 1995
PubMed
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Glutathione deficiency causes lethal mitochondrial damage. Supplementing with glutathione esters or ascorbate protects against this damage, revealing their synergistic roles in cellular protection.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Toxicology

Background:

  • Mitochondria generate reactive oxygen species, necessitating antioxidant defense.
  • Cellular glutathione (GSH) plays a crucial role in mitigating oxidative stress.
  • Mitochondria lack endogenous GSH synthesis, relying on cytosolic transport.

Purpose of the Study:

  • To investigate the consequences of GSH deficiency on mitochondrial function and integrity.
  • To explore the protective effects of GSH esters and ascorbate against GSH depletion-induced toxicity.
  • To elucidate the interrelationship between GSH and ascorbate in mitochondrial protection.

Main Methods:

  • Induction of GSH deficiency using buthionine sulfoximine in animal models.
  • Assessment of GSH levels in cellular compartments, particularly mitochondria.

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  • Evaluation of mitochondrial damage and animal survival rates.
  • Administration of GSH esters and ascorbate to assess protective effects.

    • Main Results:

    • Buthionine sulfoximine treatment induced a biphasic decline in GSH levels and mitochondrial sequestration.
    • GSH deficiency led to significant mitochondrial damage, proving lethal in newborn rats and guinea pigs.
    • Both GSH esters and ascorbate demonstrated protective effects against GSH depletion.
    • Ascorbate increased mitochondrial GSH levels in GSH-deficient animals, sparing GSH.
    • GSH esters delayed scurvy in ascorbate-deficient guinea pigs, indicating GSH spares ascorbate.

    Conclusions:

    • GSH and ascorbate exhibit a reciprocal sparing relationship, functioning synergistically.
    • Combined GSH and ascorbate offer robust protection against mitochondrial oxidative damage.
    • Maintaining adequate GSH and ascorbate levels is vital for preventing severe oxidative stress and cellular damage.