Estimation of H<sub>2</sub>O<sub>2</sub> gradients across biomembranes

Antunes, Fernando; Cadenas, Enrique

doi:10.1016/s0014-5793(00)01638-0

Cited by 463 publications

(337 citation statements)

References 22 publications

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“…Furthermore, it appears that cells become more oxidized during the progression of the life cycle from the proliferative state (−230 to 260 mV), through cell cycle arrest and differentiation (−200 mV) to apoptosis (−150 mV). The latter trend is paralleled by a progressive increase in the cellular quasi steady-state level of H 2 O 2 , with expected changes in the subcellular H 2 O 2 gradients across membranebound organelles [8,9]: a proliferative state can be observed in Jurkat T cells at [2] ss < 0.7 M; at slightly higher levels (1-3 M) cells enter the apoptotic process and, at even higher levels (>3 M) cells undergo necrosis (Fig. 1).…”

Section: Oxidative/nitrosative Stressmentioning

confidence: 84%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

310

178

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Oxidative and nitrosative stress is increasingly associated with the pathology of neurodegeneration and aging. The molecular mechanisms underlying oxidative/nitrosative stress-induced neuronal damage are emerging and appear to involve a mode of death in which mitogen-activated protein kinase (MAPK) signaling pathways are strongly implicated. Thus, attention is turning towards the modulation of intracellular signaling as a therapeutic approach against neurodegeneration. Both endogenous and dietary agents have been suggested as potent modulators of intracellular signal transduction, e.g. nitric oxide and flavonoids, respectively. This review addresses recent findings on the biological effects of flavonoids and nitric oxide in neurodegeneration and aims to elucidate the rationale for their prospective use as modulators of cellular signal transduction. © 2002 Elsevier Science Inc. All rights reserved.Keywords: Apoptosis; Oxidative stress; Neuron; Flavonoids; MAP kinase; JNK; ERK; Epicatechin; Nitric oxide; Mitochondria; Redox status; Polyphenols Abbreviations: AKT, serine/threonine kinase (also known as protein kinase B); AP-1, activator protein-1; Apaf-1, apoptosis protease activating factor-1; ASK1, apoptosis signal-regulating kinase-1; Bad, Bcl-2/BclX Lassociated death promoting protein; Bax, pro-apoptotic protein of the Bcl-2 family; Bcl-2, B-cell lymphoma 2: protein with anti-apoptotic properties; BclX L , long form of Bclx: anti-apoptotic protein of the Bcl-2 family; Caspase, cysteinyl aspartic acid-protease; c-Jun, mammalian equivalent of Jun: part of the AP-1 transcription complex; CREB, cAMP response element binding protein; DIABLO/smac, mitochondria-related pro-apoptotic protein: inhibits XIAP; ERK1/2, extracellular signal-related kinase; Fas, CD95: member of the TNF receptor family; GSHST, glutathione Stransferase; JNK, c-Jun amino-terminal kinase; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; MAPKKK, MAPKK kinase; MEK1/2, ERK1/2-specific MAPKK; MKK4/7, JNK-specific MAPKK; MSK1, mitogen-and stress-activated kinase-1; NF-B, nuclear factor of immunoglobulin k locus in B-cells; ONOO − , peroxynitrite anion; p53, pro-apoptotic tumor suppressor gene product; PI3-kinase, phosphoinositol 3-kinase; Ras, small G-protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; RSK, pp90 ribosomal S6 kinase; SAPK, stressactivated protein kinase; XIAP, X-linked inhibitor of apoptosis: inhibits the activation of caspase-9

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Section: Oxidative/nitrosative Stressmentioning

confidence: 84%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

310

178

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“…As a consequence, a rapid equilibrium is established in which the intracellular concentration of these oxidants is ~10-fold less than their applied extracellular concentration. 70,71 Hence, the intracellular concentration of H 2 O 2 or t-BOOH in these experiments is estimated to be 2-20 μM.…”

Section: Incorporation Of Daz-1 Into Proteins In Cultured Human Cellsmentioning

confidence: 85%

A chemical approach for detecting sulfenic acid-modified proteins in living cells

et al. 2008

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Oxidation of the thiol functional group in cysteine (Cys-SH) to sulfenic (Cys-SOH), sulfinic (Cys-SO 2 H) and sulfonic acids (Cys-SO 3 H) is emerging as an important post-translational modification that can activate or deactivate the function of many proteins. Changes in thiol oxidation state have been implicated in a wide variety of cellular processes and correlate with disease states but are difficult to monitor in a physiological setting because of a lack of experimental tools. Here, we describe a method that enables live cell labeling of sulfenic acidmodified proteins. For this approach, we have synthesized the probe DAz-1, which is chemically selective for sulfenic acids and cell permeable. In addition, DAz-1 contains an azide chemical handle that can be selectively detected with phosphine reagents via the Staudinger ligation for identification, enrichment and visualization of modified proteins. Through a combination of biochemical, mass spectrometry and immunoblot approaches we characterize the reactivity of DAz-1 and highlight its utility for detecting protein sulfenic acids directly in mammalian cells. This novel method to isolate and identify sulfenic acid-modified proteins should be of widespread utility for elucidating signaling pathways and regulatory mechanisms that involve oxidation of cysteine residues.

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“…It is generally accepted that following its generation in the inner mitochondrial membrane, at the level of the respiratory chain, superoxide ions are vectorially released into the mitochondrial matrix and subsequently dismutated in hydrogen peroxide by the high-level matrix enzyme Mn SOD. Conversely to the low diffusion capacity of the charged superoxide anion, hydrogen peroxide can easily cross the mitochondrial membrane towards cytoplasm [11,12]. It should be added that a direct release of superoxide anion into the intermembrane space has been recently proposed [13].…”

Section: How When and Why Are Ros Produced In Mitochondria?mentioning

confidence: 99%

Determination of mitochondrial reactive oxygen species: methodological aspects

Batandier

Fontaine

Kériel

et al. 2002

J Cellular Molecular Medi

139

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The generation of Reactive Oxygen Species (ROS) as by-products in mitochondria Electron Transport Chain (ETC) has long been admitted as the cost of aerobic energy metabolism with oxidative damages as consequence. The purpose of this methodological review is to present some of the most widespread methods of ROS generation and to underline the limitations as well as some problems, identified with some experiments as examples, in the interpretation of such results. There is now no doubt that besides their pejorative role, ROS are involved in a variety of cellular processes for the continuous adaptation of the cell to its environment. Because ROS metabolism is a complex area (low production, instability of species, efficient antioxidant defense system, several places of production…) bias, variances and limitations in ROS measurements must be recognized in order to avoid artefactual conclusions, and especially to improve our understanding of physiological and pathophysiological mechanisms of such phenomenon.

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Estimation of H₂O₂ gradients across biomembranes

Cited by 463 publications

References 22 publications

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

A chemical approach for detecting sulfenic acid-modified proteins in living cells

Determination of mitochondrial reactive oxygen species: methodological aspects

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Estimation of H2O2 gradients across biomembranes

Cited by 463 publications

References 22 publications

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

A chemical approach for detecting sulfenic acid-modified proteins in living cells

Determination of mitochondrial reactive oxygen species: methodological aspects

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Estimation of H₂O₂ gradients across biomembranes