Depletion of cytosolic GSH decreases the ATP levels and viability of synaptosomes from aged mice but not from young mice
References (16)
- et al.
Impairment of mitochondrial oxidative phosphorylation in the brain of aged mice
Brain Res.
(1994) - et al.
Mitochondrial role in cell aging
Exp. Gerontol.
(1980) - et al.
Depletion of ATP but not of GSH affects viability of rat hepatocytes
Eur. J. Pharmacol.
(1992) - et al.
Interaction with cellular ATP generating pathways mediates menadione-induced cytotoxicity in isolated rat hepatocytes
Arch. Biochem. Biophys.
(1990) Determination of pyridine nucleotides in cell extracts by high-performance liquid chromatography
J. Chromatogr.
(1981)- et al.
Protein measurement with the Folin phenol reagent
J. Biol. Chem.
(1951) - et al.
Alteration in energy status by menadione metabolism in hepatocytes isolated from fasted and fed rats
Arch. Biochem. Biophys.
(1989) - et al.
Blebbing, free Ca2+ and mitochondrial membrane potential preceding cell death in hepatocytes
Nature
(1987)
Cited by (27)
Proteomic Complexity in Parkinson's Disease: A Redox Signaling Perspective of the Pathophysiology and Progression
2021, NeuroscienceCitation Excerpt :It is the earliest indicator of dopaminergic neurodegeneration and the associated mitochondrial Complex I deficiency (Schapira et al., 1990; Swerdlow et al., 1996). Aging can also contribute to this process through the accumulation of oxidative damage, decreased antioxidant capacity, and the impairment of the mitochondrial bioenergetic ability in the brain by mechanisms that include protein oxidation (Bowling et al., 1993; Martinez-Banaclocha et al., 1994, 1995, 1996; Ferrandiz et al., 1994; Martinez-Banaclocha, 2001). The proportion of cysteine residues in proteins is only around 2%, but this amino acid is highly conserved within functional sites in proteins.
N-acetyl-cysteine in the treatment of Parkinson's disease. What are we waiting for?
2012, Medical HypothesesCitation Excerpt :As a consequence, compounds that can be metabolized to cysteine could be used as pro-drugs to increase neuronal GSH levels. NAC is the simplest cysteine pro-drug that can be systemically administered to deliver cysteine to the brain [8,34–37], acting as a precursor for glutathione synthesis as well as a stimulator of the cytosolic enzymes involved in glutathione regeneration. Increase in Complex I activities in vivo and in vitro in mitochondria isolated from pre-synaptic terminals of aged mice was proposed 10 years ago as evidence that NAC was able to cross the blood brain barrier having reparative effects on brain mitochondria and against age-associated memory decline [9,34,35].
Depletion of glutathione does not affect electron transport chain complex activity in brain mitochondria: Implications for Parkinson disease and postmortem studies
2011, Free Radical Biology and MedicineCitation Excerpt :The relative variations in levels of glutathione in different brain regions are cortex > cerebellum > hippocampus > striatum > substantia nigra [45–47]; however, glutathione profiles change throughout the life span, from high values during growth, dropping to a maturation plateau, and then decreasing 30% during aging [45]. After preparation of synaptosomes from mouse brain, depletion of glutathione in vitro decreased ATP levels and viability of synaptosomes from aged mice but not from young mice [48]. Nevertheless, after in vivo depletion of glutathione and a 24-h postmortem delay in which glutathione levels were decreased by 79%, approximately twofold more than in Parkinson disease, there was no effect on complex I activity or complex II–III and IV activity.
Glutathione, iron and Parkinson's disease
2002, Biochemical PharmacologyCitation Excerpt :Decreased GSH availability in the brain is believed to promote mitochondrial damage most likely via increases in levels of oxidative stress to this organelle. Depletion of brain GSH has been shown to result in decreases in mitochondrial enzyme activities in preweaning rats as well as losses in ATP production in the aging murine brain [65,66]. Previous studies have shown that complex I in bovine heart submitochondrial particles is particularly affected by oxidative stress [67,68].
The protective effect of vitamin E, idebenone and reduced glutathione on free radical mediated injury in rat brain synaptosomes
1998, Biochemical and Biophysical Research Communications