2019-01-15
Mitochondrial changes associated with glutathione deficiency. [1995]; Meister, Cornell University;_WJD_2019-0115_V001R01_IR94_
Source (資訊來源):
https://www.ncbi.nlm.nih.gov/pubmed/7599223
Info cited on 2019-01-15-WD2 (資訊引用於 中華民國108年1月15日) by 湯偉晉 (WeiJin Tang)
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Biochim Biophys Acta. 1995 May 24;1271(1):35-42.
Mitochondrial changes associated with glutathione deficiency.
Mitochondrial changes associated with glutathione deficiency.
Mitochondrial changes associated with glutathione deficiency.
Meister A1.
Author information
1
Department of Biochemistry, Cornell University Medical College, New York, NY 10021, USA.
Abstract
Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of gamma-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 Kms of approx. 60 microM 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.
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