Redox state of glutathione in human plasma

Jones, Dean P.; Carlson, Joanne L; Mody, V.; Cai, Jiyang; Lynn, Michael; Sternberg, Paul

doi:10.1016/s0891-5849(99)00275-0

Cited by 533 publications

(430 citation statements)

References 26 publications

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“…One of the most unequivocal pieces of evidence is the disequilibrium of the cysteine/cystine (Cys/CySS) and GSH/GSSG couples in human plasma (84,87). Steady-state redox potential (E h ) values provide a convenient way to compare the tendency of redox couples to accept or donate electrons (83).…”

Section: Nonequilibrium Conditions Of Thiol-disulfide Couples In Biolmentioning

confidence: 99%

Radical-free biology of oxidative stress

Jones¹

2008

American Journal of Physiology-Cell Physiology

1,034

839

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Free radical-induced macromolecular damage has been studied extensively as a mechanism of oxidative stress, but large-scale intervention trials with free radical scavenging antioxidant supplements show little benefit in humans. The present review summarizes data supporting a complementary hypothesis for oxidative stress in disease that can occur without free radicals. This hypothesis, which is termed the "redox hypothesis," is that oxidative stress occurs as a consequence of disruption of thiol redox circuits, which normally function in cell signaling and physiological regulation. The redox states of thiol systems are sensitive to twoelectron oxidants and controlled by the thioredoxins (Trx), glutathione (GSH), and cysteine (Cys). Trx and GSH systems are maintained under stable, but nonequilibrium conditions, due to a continuous oxidation of cell thiols at a rate of about 0.5% of the total thiol pool per minute. Redox-sensitive thiols are critical for signal transduction (e.g., H-Ras, PTP-1B), transcription factor binding to DNA (e.g., Nrf-2, nuclear factor-B), receptor activation (e.g., ␣IIb␤3 integrin in platelet activation), and other processes. Nonradical oxidants, including peroxides, aldehydes, quinones, and epoxides, are generated enzymatically from both endogenous and exogenous precursors and do not require free radicals as intermediates to oxidize or modify these thiols. Because of the nonequilibrium conditions in the thiol pathways, aberrant generation of nonradical oxidants at rates comparable to normal oxidation may be sufficient to disrupt function. Considerable opportunity exists to elucidate specific thiol control pathways and develop interventional strategies to restore normal redox control and protect against oxidative stress in aging and age-related disease.thioredoxin; glutathione; cysteine; hydrogen peroxide; redox signaling; protein thiol ONE OF THE GREAT REDOX BIOLOGISTS of the past century, Howard S. Mason, professed that to advance science, a scientist must interpret observations at the limit of their meaning. The present review of the redox biology of thiol systems addresses the possibility that disruption of the function and homeostasis of thiol systems is the most central feature of oxidative stress that contributes to mechanisms of aging and age-related disease. I have termed this the "redox hypothesis" to facilitate distinction from free radical hypotheses.Many proteins contain redox-sensitive thiols, and reactions of thiol systems occur largely by nonradical two-electron transfers. Accumulating data show that central thiol-disulfide couples are maintained under nonequilibrium conditions in biological systems. This presents a condition wherein changes in abundance and distribution of redox catalysts and changes in rates of generation of relevant oxidants (e.g., peroxides) and precursors for NADPH supply can account for pathological effects of oxidative stress through altered functions of enzymes, receptors, transporters, transcription factors, and structural elements, without free ra...

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Section: Nonequilibrium Conditions Of Thiol-disulfide Couples In Biolmentioning

confidence: 99%

Radical-free biology of oxidative stress

Jones¹

2008

American Journal of Physiology-Cell Physiology

1,034

839

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“…Although the GSH levels and antioxidant enzyme activities could be measured in red blood cells, their measurement in plasma provides an approximation of the blood state, reflecting changes at the intracellular level (Jones et al, 2000;Tunez et al, 2007).…”

Section: Sample Collectionmentioning

confidence: 99%

Effects of an aerobic training program on oxidative stress biomarkers in bulls

Escribano¹,

Túnez²,

Requena³

et al. 2010

Vet. Med. - Czech

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ABSTRACT:The aim of this study was to evaluate the effect of aerobic training (16 weeks -T1 and 24 weeks -T2) on oxidative stress biomarkers. To this end, GSH, GSH-peroxidase (GSH-Px) and catalase (CAT) activity were analysed in plasma. Nine bulls (3-4 years), were included in this work. The exercise training protocol was performed in a track ("taurodromo") three days per week for 24 weeks and consisted of 400 m warming up, 1200 m to 4-5 m/s, two minutes' resting, 1200 m to 4-5 m/s and, finally, 400 m walking. The results reflected that GSH-Px activity was higher at T1 (6.18 ± 0.45) than at baseline (T0; 2.31 ± 0.08) while the GSH level (2.98 ± 0.37) was lower vs. T0 (14.59 ± 3.40). Moreover, there were significant increases in GSH-Px (18.23 ± 1.36) and CAT (2.52 ± 0.04) activities and the recovery of basal values in GSH (11.75 ± 2.84) in T2. In conclusion, the type of training carried out in this study involved two well-defined stages: (i) a period of perturbation, followed by (ii) adaptation. The former stage was characterised by the induction of oxidative stress manifested as a decrease in the GSH, and the latter (T2) by the recovery of this non-enzymatic antioxidant.

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“…Protein S-glutathionylation, the reversible binding of glutathione to protein thiols, is involved in protein redox regulation, storage of GSH, and protection of protein thiols from irreversible oxidation [26]. Protein S-glutathionylation levels increase under conditions of oxidative stress and are controlled by glutaredoxins (GRX) that, under physiological conditions, preferentially deglutathionylate cysteines and restore sulfhydryls [27].…”

Section: Discussionmentioning

confidence: 99%