scholarly journals Modulations of Cardiac Functions and Pathogenesis by Reactive Oxygen Species and Natural Antioxidants

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 760
Author(s):  
Sun-Hee Woo ◽  
Joon-Chul Kim ◽  
Nipa Eslenur ◽  
Tran-Nguyet Trinh ◽  
Long Nguyen Hoàng Do
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Myocytes ◽  
Cardiac Myocyte ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Natural Antioxidants ◽  
Oxygen Species ◽  
Membrane Conductivity ◽  
Cardiac Functions ◽  
Mitochondrial Functions

Homeostasis in the level of reactive oxygen species (ROS) in cardiac myocytes plays a critical role in regulating their physiological functions. Disturbance of balance between generation and removal of ROS is a major cause of cardiac myocyte remodeling, dysfunction, and failure. Cardiac myocytes possess several ROS-producing pathways, such as mitochondrial electron transport chain, NADPH oxidases, and nitric oxide synthases, and have endogenous antioxidation mechanisms. Cardiac Ca2+-signaling toolkit proteins, as well as mitochondrial functions, are largely modulated by ROS under physiological and pathological conditions, thereby producing alterations in contraction, membrane conductivity, cell metabolism and cell growth and death. Mechanical stresses under hypertension, post-myocardial infarction, heart failure, and valve diseases are the main causes for stress-induced cardiac remodeling and functional failure, which are associated with ROS-induced pathogenesis. Experimental evidence demonstrates that many cardioprotective natural antioxidants, enriched in foods or herbs, exert beneficial effects on cardiac functions (Ca2+ signal, contractility and rhythm), myocytes remodeling, inflammation and death in pathological hearts. The review may provide knowledge and insight into the modulation of cardiac pathogenesis by ROS and natural antioxidants.

scholarly journals Reactive Oxygen Species (ROS) Play a Critical Role in the cAMP-Induced Activation of Ras and the Phosphorylation of ERK1/2 in Leydig Cells

2011 ◽  
Vol 25 (5) ◽  
pp. 885-893 ◽  
Author(s):  
Ping Tai ◽  
Mario Ascoli
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Phosphorylation ◽  
Leydig Cells ◽  
Critical Role ◽  
Primary Cultures ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Mitochondrial Functions ◽  
Ros Scavenger

Abstract Activation of the LH receptor (LHR) in Leydig cells results in the phosphorylation of ERK1/2 by cAMP-dependent and cAMP-independent pathways. Here we examine the mechanisms by which cAMP stimulates ERK1/2 phosphorylation. We show that the stimulation of steroidogenesis is not necessary or sufficient to stimulate the phosphorylation of ERK1/2 but that other cAMP-dependent mitochondrial functions are involved. Using MA-10 cells as a model, we showed that cAMP analogs increase reactive oxygen species (ROS) formation and that an uncoupler of oxidative phosphorylation and a ROS scavenger prevent this increase. These two compounds also inhibit the increase in ERK1/2 phosphorylation provoked by cAMP analogs, thus suggesting that the cAMP-induced phosphorylation of ERK1/2 is mediated by mitochondrial ROS. In agreement with this hypothesis we also show that a reduction in glutathione levels, which alters the redox state of MA-10 cells, potentiates the effect of cAMP on ERK1/2 phosphorylation. Measurements of the dephosphorylation of ERK and the activation of Ras showed that the ROS scavenger prevents the cAMP-provoked activation of Ras and that cAMP, with or without a ROS scavenger, has little or no effect on the dephosphorylation of ERK. Lastly, we show that the uncoupler of oxidative phosphorylation and the ROS scavenger also prevent the ability of cAMP analogs to increase ERK1/2 phosphorylation in primary cultures of mouse Leydig cells. We conclude that, in Leydig cells, cAMP enhances the phosphorylation of ERK1/2 via a mitochondria-derived, ROS-dependent activation of Ras.

scholarly journals Role of Natural Antioxidants on Neuroprotection and Neuroinflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 608
Author(s):  
Domenico Nuzzo
Keyword(s):  
Reactive Oxygen Species ◽  
Energy Metabolism ◽  
Respiratory Chain ◽  
Reactive Oxygen ◽  
Natural Antioxidants ◽  
Oxygen Species

All cells continuously generate reactive oxygen species (ROS) through the respiratory chain during the energy metabolism process [...]

scholarly journals Reactive Oxygen Species: Beyond Their Reactive Behavior

2021 ◽  
Vol 46 (1) ◽  
pp. 77-87
Author(s):  
Arnaud Tauffenberger ◽  
Pierre J. Magistretti
Keyword(s):  
Reactive Oxygen Species ◽  
Second Messengers ◽  
Critical Role ◽  
Complex Function ◽  
Reactive Oxygen ◽  
High Reactivity ◽  
Oxygen Species ◽  
Health And Disease ◽  
Cellular Dysfunction ◽  
The Brain

AbstractCellular homeostasis plays a critical role in how an organism will develop and age. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. More recent research suggests more complex function of ROS, reaching far beyond the cellular dysfunction. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease.

scholarly journals Experimental Hepatic Carcinogenesis: Oxidative Stress and Natural Antioxidants

2017 ◽  
Vol 5 (5) ◽  
pp. 686-691 ◽  
Author(s):  
Velid Unsal ◽  
Ergül Belge-Kurutaş
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Natural Antioxidants ◽  
Toxic Substances ◽  
Oxygen Species ◽  
Leading Role ◽  
Hepatic Carcinogenesis ◽  
Key Factor ◽  
Tumour Promoters

Hepatocellular carcinoma is one of the most common cancers in the world, and it is influenced by agents such as DEN, 2-AAF, phenobarbital, alcohol, aflatoxin B1 metabolite or hepatitis viruses (B and C). Oxidative stress is becoming recognized as a key factor in the progression of hepatocarcinogenesis. Reactive oxygen species can play a leading role in initiation and promotion of hepatic carcinogenesis. The metabolites of DEN Diethylnitrosamine (DEN) mediate the binding of tumour promoters by covalently binding to the DNA with one or two oxidation-providing electrons. 2-AAF is the inducer of DEN, and it is involved in tumour formation in the bladder and liver. Reactive Oxygen species (ROS); carbohydrates, lipids, DNA and enzymes, such as affect all important structures. Additionally, an excessive amount of ROS is highly toxic to cells. Antioxidants are protects against ROS, toxic substances, carcinogens. This review focuses on the literature on studies of Hepatic Carcinogenesis, oxidative stress and antioxidant therapy.

scholarly journals Tomato SlIDA has a critical role in tomato fertilization by modifying reactive oxygen species homeostasis

2020 ◽  
Vol 103 (6) ◽  
pp. 2100-2118
Author(s):  
Rong Wang ◽  
ChunLin Shi ◽  
Xiaoyang Wang ◽  
Ruizhen Li ◽  
Yan Meng ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Glycated Proteins Stimulate Reactive Oxygen Species Production in Cardiac Myocytes

Circulation ◽  
2006 ◽  
Vol 113 (9) ◽  
pp. 1235-1243 ◽  
Author(s):  
Min Zhang ◽  
Ay Lin Kho ◽  
Narayana Anilkumar ◽  
Rakesh Chibber ◽  
Patrick J. Pagano ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Myocytes ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Glycated Proteins ◽  
Species Production

scholarly journals Mechanisms of Mitochondrial Damage in Keratinocytes by Pemphigus Vulgaris Antibodies

2013 ◽  
Vol 288 (23) ◽  
pp. 16916-16925 ◽  
Author(s):  
Mina Kalantari-Dehaghi ◽  
Yumay Chen ◽  
Wu Deng ◽  
Alex Chernyavsky ◽  
Steve Marchenko ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mouse Skin ◽  
Reactive Oxygen ◽  
Pemphigus Vulgaris ◽  
Mitochondrial Damage ◽  
Response To Treatment ◽  
Transfer Model ◽  
Clear Understanding ◽  
Oxygen Species ◽  
Mitochondrial Functions

The development of nonhormonal treatment of pemphigus vulgaris (PV) has been hampered by a lack of clear understanding of the mechanisms leading to keratinocyte (KC) detachment and death in pemphigus. In this study, we sought to identify changes in the vital mitochondrial functions in KCs treated with the sera from PV patients and healthy donors. PV sera significantly increased proton leakage from KCs, suggesting that PV IgGs increase production of reactive oxygen species. Indeed, measurement of intracellular reactive oxygen species production showed a drastic increase of cell staining in response to treatment by PV sera, which was confirmed by FACS analysis. Exposure of KCs to PV sera also caused dramatic changes in the mitochondrial membrane potential detected with the JC-1 dye. These changes can trigger the mitochondria-mediated intrinsic apoptosis. Although sera from different PV patients elicited unique patterns of mitochondrial damage, the mitochondria-protecting drugs nicotinamide (also called niacinamide), minocycline, and cyclosporine A exhibited a uniform protective effect. Their therapeutic activity was validated in the passive transfer model of PV in neonatal BALB/c mice. The highest efficacy of mitochondrial protection of the combination of these drugs found in mitochondrial assay was consistent with the ability of the same drug combination to abolish acantholysis in mouse skin. These findings provide a theoretical background for clinical reports of the efficacy of mitochondria-protecting drugs in PV patients. Pharmacological protection of mitochondria and/or compensation of an altered mitochondrial function may therefore become a novel approach to development of personalized nonhormonal therapies of patients with this potentially lethal autoimmune blistering disease.

Strain-stimulated hypertrophy in cardiac myocytes is mediated by reactive oxygen species-dependent Ras S-glutathiolation

2006 ◽  
Vol 41 (4) ◽  
pp. 613-622 ◽  
Author(s):  
David R. Pimentel ◽  
Takeshi Adachi ◽  
Yasuo Ido ◽  
Tyler Heibeck ◽  
Bingbing Jiang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Myocytes ◽  
Reactive Oxygen ◽  
Oxygen Species
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