Interaction of reactive oxygen species  with ion transport mechanisms

Kourie, Joseph I.

doi:10.1152/ajpcell.1998.275.1.c1

Cited by 569 publications

(428 citation statements)

References 156 publications

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“…Consistent with previous reports (5,6,20), the current data indicate that MV results in significant atrophy of the costal diaphragm. Furthermore, atrophy of MHC type I and MHC type IIa fibers corresponds with previous data demonstrating deficits in force production after 12 h of MV (4).…”

Section: Mv-induced Myonuclear Apoptosissupporting

confidence: 93%

“…Numerous cellular mechanisms lead to caspase-3 activation, including mitochondrial-dependent (cytochrome c release) and mitochondrial-independent (e.g., Ca 2ϩ activation of calpain) pathways resulting in the stimulation of DNases responsible for cellular DNA fragmentation and protein degradation (19). Oxidative stress occurs rapidly in the diaphragm during mechanical ventilation (18), and oxidant stress can promote cytochrome c release and cellular Ca 2ϩ overload in cells (10,20). This fact suggests a potential role for caspase-3 activation in the regulation of myonuclear number during the rapid atrophy that occurs in the diaphragm after prolonged MV.…”

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confidence: 99%

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Caspase-3 Regulation of Diaphragm Myonuclear Domain during Mechanical Ventilation–induced Atrophy

McClung

Kavazis

DeRuisseau

et al. 2007

Am J Respir Crit Care Med

161

178

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Rationale: Unloading the diaphragm via mechanical ventilation (MV) results in rapid diaphragmatic fiber atrophy. It is unknown whether the myonuclear domain (cytoplasmic myofiber volume/ myonucleus) of diaphragm myofibers is altered during MV. Objective: We tested the hypothesis that MV-induced diaphragmatic atrophy is associated with a loss of myonuclei via a caspase-3-mediated, apoptotic-like mechanism resulting in a constant myonuclear domain. Methods: To test this postulate, Sprague-Dawley rats were randomly assigned to a control group or to experimental groups exposed to 6 or 12 h of MV with or without administration of a caspase-3 inhibitor. Measurements and Main Results:After 12 h of MV, type I and type IIa diaphragm myofiber areas were decreased by 17 and 23%, respectively, and caspase-3 inhibition attenuated this decrease. Diaphragmatic myonuclear content decreased after 12 h of MV and resulted in the maintenance of a constant myonuclear domain in all fiber types. Both 6 and 12 h of MV resulted in caspase-3-dependent increases in apoptotic markers in the diaphragm (e.g., number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling positive nuclei and DNA fragmentation). Caspase-3-dependent increases in apoptotic markers occurred after 6 h of MV, before the onset of myofiber atrophy. Conclusions: Collectively, these data support the hypothesis that the myonuclear domain of diaphragm myofibers is maintained during prolonged MV and that caspase-3-mediated myonuclear apoptosis contributes to this process. Keywords: muscle atrophy; respiratory muscle; apoptosis; ventilatory weaning Mechanical ventilation (MV) is a clinical intervention for patients who are unable to maintain adequate alveolar ventilation. Recent evidence reveals that controlled MV results in a swift progression of diaphragmatic atrophy and weakness (1-6). It seems that this diaphragmatic atrophy and weakness contributes to difficulty in weaning patients from the ventilator (7). The mechanism(s) responsible for the rapid onset of diaphragmatic atrophy and weakness are not fully understood. Therefore, delineating these mechanisms is a prerequisite for the development of therapeutic strategies to circumvent weaning difficulties. Although mechanical ventilation-induced diaphragm inactivity results in fiber atrophy, it is unknown if prolonged mechanical ventilation is associated with alterations in myonuclear domain via apoptotic mechanisms. What This Study Adds to the FieldOur results reveal that inhibiting caspase-3 activation and myonuclear loss during mechanical ventilation attenuates diaphragmatic muscle atrophy.Mechanical ventilation-induced diaphragmatic atrophy and contractile dysfunction is characterized by oxidative stress and stress-related gene expression in myofibers that occurs within a matter of hours (7,8). In addition to myofibrillar protein loss, extracellular matrix expansion, and metabolic enzyme alterations (9-11), prolonged disuse of skeletal muscle results in the selective loss of myonuclei (12-16). Myonu...

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Section: Mv-induced Myonuclear Apoptosissupporting

confidence: 93%

mentioning

confidence: 99%

Caspase-3 Regulation of Diaphragm Myonuclear Domain during Mechanical Ventilation–induced Atrophy

McClung

Kavazis

DeRuisseau

et al. 2007

Am J Respir Crit Care Med

161

178

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“…The present study was designed to determine mechanisms responsible for differences between renal PTE cells from hypertensive and normotensive rats on their sensitivity to [20] which is line with observations on the role of ROS in the regulation of ion transport in some cells [23,24]. In fact, H 2 O 2 has been demonstrated to stimulate the activity of other transporters, namely NHE and Na/K/2Cl.…”

Section: Discussionsupporting

confidence: 59%

Increased responsiveness to JNK1/2 mediates the enhanced H2O2-induced stimulation of Cl−/HCO3− exchanger activity in immortalized renal proximal tubular epithelial cells from the SHR

Simão¹,

Gomes²,

José³

et al. 2010

Biochemical Pharmacology

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. Increased responsiveness to JNK1/2 mediates the enhanced HO-induced stimulation of Cl/HCO exchanger activity in immortalized renal proximal tubular epithelial cells from the SHR. Biochemical Pharmacology, Elsevier, 2010, 80 (6) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Aldehyde products, such as MDA and 4-HNE, react with amine and thiol groups of membrane protein, causing several damages, including inactivation of enzymes. Conformational changes of membrane molecules also include lipid-lipid cross-links and lipid-protein cross-links [91,92].Moreover, lipid peroxidation modifies the global biophysical properties of the memb r a n e s .T h i sp r o c e s sa f f e c t st h ep a c k i n go flipids and the permeability to solutes, which in turn, changes its function, including the membrane potential. Furthermore, the process Novel Prospects in Oxidative and Nitrosative Stress 6 of peroxidation can inhibit the activity of protein transporters and ion channels [89,91].…”

mentioning

confidence: 99%

“…Conformational changes of membrane molecules also include lipid-lipid cross-links and lipid-protein cross-links [91,92].…”

mentioning

confidence: 99%

Oxidative Stress: Noxious but Also Vital

Bagatini¹,

Jaques²,

Oliveira³

et al. 2018

Novel Prospects in Oxidative and Nitrosative Stress

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The imbalance between reactive oxygen species (ROS) production and antioxidant defenses determines the condition called oxidative stress. When there is an increase in ROS production or a decrease in the antioxidant defenses, this systemic antioxidant/pro-oxidant imbalance may lead to the accumulation of oxidative damage, which, in turn, may lead to a modification of biomolecules. These consist of reactions resulting in protein adducts, DNA oxidation, and formation of lipid peroxides, which, in turn, reduce the cellular functional capacity and increase the risk of disease development. The body has natural scavenging systems against free radicals and other reactive species. However, sometimes the endogenous antioxidant capacity is exceeded by the production of ROS. When this occurs, exogenous antioxidants exert important function for the human health. These bioactive compounds act preventing and neutralizing the formation of new reactive species and free radical s .I ns o m ec a s e s ,a n increase of ROS can help the host to resolve an infection or even to control the tumor growth. Finally, the levels of ROS can be perceived by signal transduction pathways involving known targets(i.e.,p53,Ras,andNF-κB) and regulate physiopathological events such as the cellular cycle, apoptosis, and inflammation.Keywords: reactive species, cellular oxidation, antioxidant system, health, disease © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cellular respiration and generation of reactive species in the mitochondria: implications in cell viability and agingOxidative phosphorylation is the center of energy metabolism in plants, animals and several microbial life forms [1]. In eukaryotes, this process occurs in mitochondria. The mitochondria is a cytoplasmic organelle surrounded by two membranes, outer and inner membrane, which main function is the production of most of the phosphate compounds necessary for the energetic balance of the cell. In addition, other functions such as the regulation of the body'sheatgeneration [2][3][4] programmed cell death [5][6][7], reactive oxygen species (ROS) generation and cell signaling [8] is also associated with mitochondria. Cellular vitality is directly related to mitochondria, and mitochondrial dysfunctions are frequent causes of accidental cell death [5,[9][10][11], cancer [12, 13], diabetes [14][15][16] and neurodegenerative diseases [17][18][19], among others.The characterization of the respiratory electron chain could be performed in studies using the fractionation of its components by certain detergents that at low concentrations break the interactions between proteins and lipids in the membranes, leaving associations between proteins intact [20]. In electron transport chain, through this process, four protein complexes were found....

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Interaction of reactive oxygen species with ion transport mechanisms

Cited by 569 publications

References 156 publications

Caspase-3 Regulation of Diaphragm Myonuclear Domain during Mechanical Ventilation–induced Atrophy

Caspase-3 Regulation of Diaphragm Myonuclear Domain during Mechanical Ventilation–induced Atrophy

Increased responsiveness to JNK1/2 mediates the enhanced H2O2-induced stimulation of Cl−/HCO3− exchanger activity in immortalized renal proximal tubular epithelial cells from the SHR

Oxidative Stress: Noxious but Also Vital

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