Mitochondrial changes associated with glutathione deficiency

Mitochondrial changes associated with glutathione deficiency Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) to animals, leads to biphasic decline in cellular glutathione levels associated with sequestration of glutathione in mitochondria. Liver mitochondria lack the enzymes needed for glutathione synthesis. Mitochondrial glutathione arises from the cytosol. Rat liver mitochondria have a multicomponent system (with K s of approx. 60 μM and 5.4 mM) that underlies their remarkable ability to transport and retain glutathione. Mitochondria produce substantial quantities of reactive oxygen species; this is opposed by reactions involving glutathione. Glutathione deficiency leads to widespread mitochondrial damage which is lethal in newborn rats and guinea pigs, animals that do not synthesize ascorbate. Glutathione esters and ascorbate protect against the lethal and other effects of glutathione deficiency. Ascorbate spares glutathione; it increases mitochondrial glutathione in glutathione-deficient animals. Glutathione esters delay onset of scurvy in ascorbate-deficient guinea pigs; thus, glutathione spares ascorbate. Glutathione and ascorbate function together in protecting mitochondria from oxidative damage. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease Elsevier

Mitochondrial changes associated with glutathione deficiency

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Publisher
Elsevier
Copyright
Copyright © 1995 Elsevier Ltd
ISSN
0925-4439
D.O.I.
10.1016/0925-4439(95)00007-Q
Publisher site
See Article on Publisher Site

Abstract

Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) to animals, leads to biphasic decline in cellular glutathione levels associated with sequestration of glutathione in mitochondria. Liver mitochondria lack the enzymes needed for glutathione synthesis. Mitochondrial glutathione arises from the cytosol. Rat liver mitochondria have a multicomponent system (with K s of approx. 60 μM and 5.4 mM) that underlies their remarkable ability to transport and retain glutathione. Mitochondria produce substantial quantities of reactive oxygen species; this is opposed by reactions involving glutathione. Glutathione deficiency leads to widespread mitochondrial damage which is lethal in newborn rats and guinea pigs, animals that do not synthesize ascorbate. Glutathione esters and ascorbate protect against the lethal and other effects of glutathione deficiency. Ascorbate spares glutathione; it increases mitochondrial glutathione in glutathione-deficient animals. Glutathione esters delay onset of scurvy in ascorbate-deficient guinea pigs; thus, glutathione spares ascorbate. Glutathione and ascorbate function together in protecting mitochondria from oxidative damage.

Journal

Biochimica et Biophysica Acta (BBA) - Molecular Basis of DiseaseElsevier

Published: May 24, 1995

References

  • Glutathione Chemical, Biochemical and Medical Aspects, Parts A and B
  • Biochem. J.
    Harris, E.J.; Baum, H.
  • Biochem. Biophys. Res. Commun.
    Romero, F.J.; Sies, H.

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