The generation and subsequent fate of glutathionyl radicals in biological systems.

Ross, David; Norbeck, Kajsa; Moldéus, Peter

doi:10.1016/s0021-9258(18)95697-8

Cited by 136 publications

(14 citation statements)

References 16 publications

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“…GSH itself is not efficiently transported into most animal cells. GSH in excess may be a source of thiol or thionyl radicals under oxidative conditions (215). Thus intracellular GSH concentrations are not easily manipulated by extracellular GSH.…”

Section: Supplementation Of Gsh or Its Precursorsmentioning

confidence: 99%

Lung glutathione and oxidative stress: implications in cigarette smoke-induced airway disease

Rahman

MacNee

1999

American Journal of Physiology-Lung Cellular and Molecular Phys

288

271

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Glutathione (GSH), a ubiquitous tripeptide thiol, is a vital intra- and extracellular protective antioxidant in the lungs. The rate-limiting enzyme in GSH synthesis is gamma-glutamylcysteine synthetase (gamma-GCS). The promoter (5'-flanking) region of the human gamma-GCS heavy and light subunits are regulated by activator protein-1 and antioxidant response elements. Both GSH and gamma-GCS expression are modulated by oxidants, phenolic antioxidants, and inflammatory and anti-inflammatory agents in lung cells. gamma-GCS is regulated at both the transcriptional and posttranscriptional levels. GSH plays a key role in maintaining oxidant-induced lung epithelial cell function and also in the control of proinflammatory processes. Alterations in alveolar and lung GSH metabolism are widely recognized as a central feature of many inflammatory lung diseases including chronic obstructive pulmonary disease (COPD). Cigarette smoking, the major factor in the pathogenesis of COPD, increases GSH in the lung epithelial lining fluid of chronic smokers, whereas in acute smoking, the levels are depleted. These changes in GSH may result from altered gene expression of gamma-GCS in the lungs. The mechanism of regulation of GSH in the epithelial lining fluid in the lungs of smokers and patients with COPD is not known. Knowledge of the mechanisms of GSH regulation in the lungs could lead to the development of novel therapies based on the pharmacological or genetic manipulation of the production of this important antioxidant in lung inflammation and injury. This review outlines 1) the regulation of cellular GSH levels and gamma-GCS expression under oxidative stress and 2) the evidence for lung oxidant stress and the potential role of GSH in the pathogenesis of COPD.

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Section: Supplementation Of Gsh or Its Precursorsmentioning

confidence: 99%

Lung glutathione and oxidative stress: implications in cigarette smoke-induced airway disease

Rahman

MacNee

1999

American Journal of Physiology-Lung Cellular and Molecular Phys

288

271

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“…However, upon illumination at 546 ± 10 nm, the expected triplet of doublets splitting was observed for both compounds with identical hyperfine couplings (Figure b,c; a N = 16.2 G, a H = 3.8 G). For comparison purposes, we generated and trapped an N -acetylcysteine thiyl radical produced by horseradish peroxidase catalyzed oxidation (100 mM TRIS buffer, 1 mM EDTA, pH ∼ 8.0) . This procedure furnishes a thiyl radical with very similar hyperfines (Figure d, a N = 15.7 G, a H = 3.8 G).…”

Section: Resultsmentioning

confidence: 90%

“…(2) Peroxidase generated thiyl radicals . NAcSH radicals were generated from horseradish peroxidase catalyzed oxidation according to a literature procedure . Briefly, NAcSH (5 mM), PBN (100 mM), p -phentidine (500 μM), and horseradish peroxidase (2 μg/mL, ∼2 units/mL) were mixed in phosphate buffered saline (100 μL, 100 mM, 1 mM EDTA, pH 8.0) and then purged with N 2 for 10 min.…”

Section: Methodsmentioning

confidence: 99%

“…NAcSH radicals were generated from horseradish peroxidase catalyzed oxidation according to a literature procedure. 33 Briefly, NAcSH (5 mM), PBN (100 mM), p-phentidine (500 μM), and horseradish peroxidase (2 μg/mL, ∼2 units/mL) were mixed in phosphate buffered saline (100 μL, 100 mM, 1 mM EDTA, pH 8.0) and then purged with N 2 for 10 min. Hydrogen peroxide (250 μM) was quickly added to initiate oxidation, and the solution was loaded into a quartz capillary and scanned immediately since the thiol-PBN adduct signal decays with time.…”

Section: ■ Experimental Sectionmentioning

confidence: 99%

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Fluorophore Assisted Photolysis of Thiolato-Cob(III)alamins

et al. 2016

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Cobalamins are known to react with thiols to yield stable β-axial CoIII–S bonded thiolato-cobalamin complexes. However, in stark contrast to the Co–C bond in alkylcobalamins, the photolability of the Co–S bond in thiolato-cobalamins remains undetermined. We have investigated the photolysis of N-acetylcysteinyl cob(III)alamin at several wavelengths within the ultraviolet and visible spectrum. To aid in photolysis, we show that attaching fluorophore “antennae” to the cobalamin scaffold can improve photolytic efficiency by up to an order of magnitude. Additionally, electron paramagnetic resonance confirms previous conjectures that the photolysis of thiolato-cobalamins at wavelengths as long as 546 nm produces thiyl radicals.

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“…CAT and GPX share the function of controlling the concentrations of H 2 O 2 and are the most outstanding cellular mechanisms for the neutralization of ROS [58]. Whenever the concentrations of H 2 O 2 are in a high level, CAT becomes more effective than GPX and vice versa [59]. Nevertheless, GPX is capable of removing organic peroxides, such as those derived from lipid peroxidation [60].…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress and Histopathological Evaluation of Rat Lung Tissue during Hypobaric Hypoxia

Pasha¹

2015

J Proteomics Bioinform

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The generation and subsequent fate of glutathionyl radicals in biological systems.

Cited by 136 publications

References 16 publications

Lung glutathione and oxidative stress: implications in cigarette smoke-induced airway disease

Lung glutathione and oxidative stress: implications in cigarette smoke-induced airway disease

Fluorophore Assisted Photolysis of Thiolato-Cob(III)alamins

Oxidative Stress and Histopathological Evaluation of Rat Lung Tissue during Hypobaric Hypoxia

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