Role of Free Radicals and Cellular Redox Status in Signal Transduction and Gene Expression

2013 ◽

Vol 2013 ◽

pp. 1-16 ◽

Cited By ~ 6

Author(s):

Teresa Anna Giancaspero ◽

Vittoria Locato ◽

Maria Barile

Keyword(s):

Saccharomyces Cerevisiae ◽

Nicotinamide Adenine Dinucleotide ◽

Flavin Adenine Dinucleotide ◽

Redox Balance ◽

Redox Status ◽

Cellular Redox ◽

Isolated Mitochondria ◽

Nudix Hydrolases ◽

Order Of Magnitude

Flavin adenine dinucleotide (FAD) and nicotinamide adenine dinucleotide (NAD) are two redox cofactors of pivotal importance for mitochondrial functionality and cellular redox balance. Despite their relevance, the mechanism by which intramitochondrial NAD(H) and FAD levels are maintained remains quite unclear inSaccharomyces cerevisiae. We investigated here the ability of isolated mitochondria to degrade externally added FAD and NAD (in both its reduced and oxidized forms). A set of kinetic experiments demonstrated that mitochondrial FAD and NAD(H) destroying enzymes are different from each other and from the already characterized NUDIX hydrolases. We studied here, in some detail, FAD pyrophosphatase (EC 3.6.1.18), which is inhibited by NAD+and NADH according to a noncompetitive inhibition, withKivalues that differ from each other by an order of magnitude. These findings, together with the ability of mitochondrial FAD pyrophosphatase to metabolize endogenous FAD, presumably deriving from mitochondrial holoflavoproteins destined to degradation, allow for proposing a novel possible role of mitochondrial NAD redox status in regulating FAD homeostasis and/or flavoprotein degradation inS. cerevisiae.

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Battle between plants as antioxidants with free radicals in human body

Journal of Herbmed Pharmacology ◽

10.34172/jhp.2020.25 ◽

2020 ◽

Vol 9 (3) ◽

pp. 191-199 ◽

Cited By ~ 3

Author(s):

Fatemeh Jamshidi-kia ◽

Joko Priyanto Wibowo ◽

Mostafa Elachouri ◽

Rohollah Masumi ◽

Alizamen Salehifard-Jouneghani ◽

...

Keyword(s):

Oxidative Stress ◽

Free Radicals ◽

Human Body ◽

Defense Mechanisms ◽

Natural Antioxidants ◽

Redox Status ◽

The Body ◽

Antioxidant Agents ◽

Endogenous Antioxidants

Free radicals are constructed by natural physiological activities in the human cells as well as in the environment. They may be produced as a result of diet, smoking, exercise, inflammation, exposure to sunlight, air pollutants, stress, alcohol and drugs. Imbalanced redox status may lead to cellular oxidative stress, which can damage the cells of the body, resulting in an incidence of various diseases. If the endogenous antioxidants do not stop the production of reactive metabolites, they will be needed to bring about a balance in redox status. Natural antioxidants, for example plants, play an important part in this context. This paper seeks to report the available evidence about oxidative stress and the application of plants as antioxidant agents to fight free radicals in the human body. For this purpose, to better understand oxidative stress, the principles of free radical production, the role of free radicals in diseases, antioxidant defense mechanisms, and the role of herbs and diet in oxidative stress are discussed.

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Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/6842568 ◽

2016 ◽

Vol 2016 ◽

pp. 1-13 ◽

Cited By ~ 23

Author(s):

Min Hee Choi ◽

Jin Rong Ow ◽

Nai-Di Yang ◽

Reshma Taneja

Keyword(s):

Oxidative Stress ◽

Molecular Level ◽

Redox Homeostasis ◽

Redox Status ◽

Muscle Degeneration ◽

Dystrophic Muscle ◽

Telomere Shortening ◽

Cellular Redox ◽

Pathological Conditions

Oxidative stress is a loss of balance between the production of reactive oxygen species during cellular metabolism and the mechanisms that clear these species to maintain cellular redox homeostasis. Increased oxidative stress has been associated with muscular dystrophy, and many studies have proposed mechanisms that bridge these two pathological conditions at the molecular level. In this review, the evidence indicating a causal role of oxidative stress in the pathogenesis of various muscular dystrophies is revisited. In particular, the mediation of cellular redox status in dystrophic muscle by NF-κB pathway, autophagy, telomere shortening, and epigenetic regulation are discussed. Lastly, the current stance of targeting these pathways using antioxidant therapies in preclinical and clinical trials is examined.

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Modification of Ca2+-handling in cardiomyocytes by redox sensitive mechanisms in response to ouabain

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2012-0215 ◽

2013 ◽

Vol 91 (1) ◽

pp. 45-55 ◽

Cited By ~ 1

Author(s):

Harjot K. Saini-Chohan ◽

Larry Hryshko ◽

Yan-Jun Xu ◽

Naranjan S. Dhalla

Keyword(s):

Signal Transduction ◽

Protein Kinase C ◽

Protein Kinase ◽

Protein Kinases ◽

Redox Status ◽

Rat Cardiomyocytes ◽

Adult Rat ◽

Kinase C ◽

Transduction Mechanisms

We examined the role of redox-sensitive signal transduction mechanisms in modifying the changes in [Ca2+]i produced by ouabain upon incubating adult rat cardiomyocytes with antioxidants or inhibitors of different protein kinases and monitoring alterations in fura-2 fluorescence. Ouabain increased basal [Ca2+]i, augmented the KCl-induced increase in [Ca2+]i, and promoted oxyradical production in cardiomyocytes. These actions of ouabain were attenuated by an oxyradical scavenging mixture (superoxide dismutase plus catalase), and the antioxidants (N-acetyl-l-cysteine and N-(2-mercaptoproprionyl)glycine). An inhibitor of MAP kinase (PD98059) depressed the ouabain-induced increase in [Ca2+], whereas inhibitors of tyrosine kinase (tyrphostin and genistein) and PI3 kinase (Wortmannin and LV294002) enhanced the ouabain-induced increase in [Ca2+]i. Inhibitors of protein kinase C (calphostin and bisindolylmalaimide) augmented the ouabain-induced increase in [Ca2+]i, whereas stimulation of protein kinase C by a phorbol ester (phorbol 12-myristate 13-acetate) depressed the action of ouabain. These results suggest that ouabain-induced inhibition of Na +–K+ ATPase may alter the redox status of cardiomyocytes through the production of oxyradicals, and increase the activities of various protein kinases. Thus, these redox-sensitive signal transduction mechanisms involving different protein kinases may modify Ca2+-handling sites in cardiomyocytes and determine the magnitude of net increase in [Ca2+]i in response to ouabain.

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The Emerging Role of TXNIP in Ischemic and Cardiovascular Diseases; A Novel Marker and Therapeutic Target

International Journal of Molecular Sciences ◽

10.3390/ijms22041693 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1693

Author(s):

Alison Domingues ◽

Julia Jolibois ◽

Perrine Marquet de Rougé ◽

Valérie Nivet-Antoine

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Therapeutic Target ◽

Redox Status ◽

Interacting Protein ◽

Cellular Redox ◽

Thioredoxin Interacting Protein ◽

Potential Biomarker ◽

Ischemic Diseases

Thioredoxin interacting protein (TXNIP) is a metabolism- oxidative- and inflammation-related marker induced in cardiovascular diseases and is believed to represent a possible link between metabolism and cellular redox status. TXNIP is a potential biomarker in cardiovascular and ischemic diseases but also a novel identified target for preventive and curative medicine. The goal of this review is to focus on the novelties concerning TXNIP. After an overview in TXNIP involvement in oxidative stress, inflammation and metabolism, the remainder of this review presents the clues used to define TXNIP as a new marker at the genetic, blood, or ischemic site level in the context of cardiovascular and ischemic diseases.

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Post-Translational S-Nitrosylation of Proteins in Regulating Cardiac Oxidative Stress

Antioxidants ◽

10.3390/antiox9111051 ◽

2020 ◽

Vol 9 (11) ◽

pp. 1051 ◽

Cited By ~ 1

Author(s):

Xiaomeng Shi ◽

Hongyu Qiu

Keyword(s):

Therapeutic Potential ◽

Heart Diseases ◽

Redox Homeostasis ◽

Redox Status ◽

Cardiac Protection ◽

Cellular Functions ◽

Post Translational Modifications ◽

Cellular Redox ◽

Novel Therapeutic Strategies

Like other post-translational modifications (PTMs) of proteins, S-nitrosylation has been considered a key regulatory mechanism of multiple cellular functions in many physiological and disease conditions. Emerging evidence has demonstrated that S-nitrosylation plays a crucial role in regulating redox homeostasis in the stressed heart, leading to discoveries in the mechanisms underlying the pathogenesis of heart diseases and cardiac protection. In this review, we summarize recent studies in understanding the molecular and biological basis of S-nitrosylation, including the formation, spatiotemporal specificity, homeostatic regulation, and association with cellular redox status. We also outline the currently available methods that have been applied to detect S-nitrosylation. Additionally, we synopsize the up-to-date studies of S-nitrosylation in various cardiac diseases in humans and animal models, and we discuss its therapeutic potential in cardiac protection. These pieces of information would bring new insights into understanding the role of S-nitrosylation in cardiac pathogenesis and provide novel avenues for developing novel therapeutic strategies for heart diseases.

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