Reduced and oxidized glutathione in human and monkey brain
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Cited by (152)
Functions and dysfunctions of nitric oxide in brain
2019, Biochimica et Biophysica Acta - Molecular Basis of DiseaseOverview and recent advances in electrochemical sensing of glutathione – A review
2019, Analytica Chimica ActaCitation Excerpt :GSH is the major nonprotein thiol in living cells, with cellular concentrations ranging from 0.5 to 10 mM [2] and is found in physiological fluids at concentrations of approximately 2–12 μM for healthy individuals [3]. In healthy cells and tissues, more than 90% of the total glutathione pool exists in the reduced form (GSH), and less than 10% exists in the disulfide form (GSSH) [4]. GSH is also an essential cofactor in many biological processes, such as catabolism, transportation and detoxification of drugs, aids in maintaining communication between cells through gap junctions and generally prevents protein-SH groups from oxidizing and cross-linking [5].
Normal glutathione levels in autopsied brain of chronic users of heroin and of cocaine
2018, Drug and Alcohol DependenceGlutathione in the human brain: Review of its roles and measurement by magnetic resonance spectroscopy
2017, Analytical BiochemistryCitation Excerpt :This contrasts with values recorded from cells in culture with levels in human neurons reported at 93 ± 13 μmol/g protein and 177 ± 10 μmol/g protein in astrocytes [12]. Careful study of the relative amounts of reduced vs oxidized glutathione has shown levels of GSSG in rat and monkey brain to be 1.2% [13], or less [14], of total glutathione indicating that previous reports of levels as high as 40% GSSG in brain are likely erroneous. Induction of ischemia in rat brain has been shown to decrease GSH without any concomitant increase in GSSG [15], while induction of oxidative stress by lipid peroxidation did result in accumulation of GSSG [14] showing different mechanisms at work in these conditions.
Do glutathione levels decline in aging human brain?
2016, Free Radical Biology and MedicineCitation Excerpt :Further, in a positive “neurological control” investigation [12], we detected, using our assay procedure, the expected loss of GSH in postmortem substantia nigra of patients with Parkinson’s disease [9–11]. Nevertheless, given the low abundance of GSSG as compared to GSH and its (expected) variability [10,11,19,28,35–37], interpretation of the data on GSSG concentrations and the ratios of GSH/GSSG should be made cautiously. A generic limitation of our study is the possibility that postmortem breakdown of GSH and GSSG [38] might have somehow skewed our results, particularly in view of our previous report of markedly lower levels of GSH and GSSG in autopsied versus biopsied human brain [12] and by our observation of significant negative correlations between postmortem interval and levels of GSH or GSSG in several brain regions.