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1. Full Text Nitric oxide/reactive oxygen species generation and nitroso/redox imbalance in heart failure: From molecular mechanisms to therapeutic implications
by Nediani, Chiara and Raimondi, Laura and Borchi, Elisabetta and Cerbai, Elisabetta
Antioxidants and Redox Signaling, ISSN 1523-0864, 01/2011, Volume 14, Issue 2, pp. 289 - 331
Adaptation of the heart to intrinsic and external stress involves complex modifications at the molecular and cellular levels that lead to tissue remodeling,... 
ISCHEMIA-REPERFUSION INJURY | OXIDASE-DERIVED SUPEROXIDE | MITOCHONDRIAL PERMEABILITY TRANSITION | ACTIVATED PROTEIN-KINASE | FATTY-ACID OXIDATION | RENIN-ANGIOTENSIN SYSTEM | HUMAN FAILING MYOCARDIUM | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOCRINOLOGY & METABOLISM | SMOOTH-MUSCLE-CELLS | INDUCED CARDIAC-HYPERTROPHY | CANINE VENTRICULAR MYOCYTES | Heart Failure - therapy | Nitric Oxide - biosynthesis | Animals | Nitroso Compounds - metabolism | Reactive Oxygen Species - metabolism | Oxidation-Reduction | Oxidative Stress | Signal Transduction | Humans | Heart Failure - physiopathology | Heart Failure - metabolism | Nitric Oxide - metabolism | Heart failure | Care and treatment | Nitric oxide | Heart cells | Physiological aspects | Research | Free radicals (Chemistry) | Health aspects | Risk factors
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2. Full Text Brain and muscle redox imbalance elicited by acute ethylmalonic acid administration
by Schuck, Patrícia Fernanda and Milanez, Ana Paula and Felisberto, Francine and Galant, Leticia Selinger and Machado, Jéssica Luca and Furlanetto, Camila Brulezi and Petronilho, Fabricia and Al-Pizzol, Felipe and Streck, Emilio Luiz and Ferreira, Gustavo Costa
PLoS ONE, ISSN 1932-6203, 05/2015, Volume 10, Issue 5, p. e0126606
Ethylmalonic acid (EMA) accumulates in tissues and biological fluids of patients affected by short-chain acyl-CoA dehydrogenase deficiency (SCADD) and... 
ELECTRON-TRANSPORT CHAIN | INHIBITION | LIPID-PEROXIDATION | OXIDATIVE DAMAGE | MULTIDISCIPLINARY SCIENCES | MITOCHONDRIA | STRESS | CREATINE-KINASE ACTIVITY | Cerebral Cortex - enzymology | Muscle, Skeletal - enzymology | Oxidation-Reduction | Rats, Wistar | Glutathione - metabolism | Fluoresceins - metabolism | Male | Muscle, Skeletal - metabolism | Thiobarbituric Acid Reactive Substances - metabolism | Mitochondria - metabolism | Mitochondria - drug effects | Malonates - administration & dosage | Protein Carbonylation - drug effects | Malonates - adverse effects | Brain - drug effects | Brain - metabolism | Sulfhydryl Compounds - metabolism | Animals | Electron Transport Chain Complex Proteins - metabolism | Muscle Proteins - metabolism | Superoxides - metabolism | Cerebral Cortex - drug effects | Muscles | Physiological aspects | Brain | Research | Health aspects | Malonates | Oxidative stress | Cerebral cortex | Disease | Lipid peroxidation | Lipids | Acyl-CoA dehydrogenase | Electron transport chain | Mitochondria | Illnesses | Metabolites | Bioaccumulation | Rodents | Animal tissues | Encephalopathy | Fibroblasts | Oxidation | Peroxidase | Thiobarbituric acid | Glutathione | Carbonyls | Peroxidation | Glutathione peroxidase | Neuromuscular diseases | Cortex | Rats | Superoxide | Metabolism | Patients | Skeletal muscle | Musculoskeletal system | Acids | Brain damage | Electron transport | Laboratory animals | Brain injury
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3. Full Text Hydralazine and organic nitrates restore impaired excitation-contraction coupling by reducing calcium leak associated with nitroso-redox imbalance
by Dulce, Raul A and Yiginer, Omer and Gonzalez, Daniel R and Goss, Garrett and Feng, Ning and Zheng, Meizi and Hare, Joshua M
Journal of Biological Chemistry, ISSN 0021-9258, 03/2013, Volume 288, Issue 9, pp. 6522 - 6533
Although the combined use of hydralazine and isosorbide dinitrate confers important clinical benefits in patients with heart failure, the underlying mechanism... 
PHOSPHOLAMBAN PHOSPHORYLATION | S-NITROSYLATION | XANTHINE-OXIDASE | OXIDATIVE STRESS | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | MYOCARDIAL OXYGEN-CONSUMPTION | ISOSORBIDE DINITRATE | RABBIT AORTA | SARCOPLASMIC-RETICULUM | Calcium - metabolism | Hydralazine - pharmacology | Myocardial Contraction - drug effects | Rats, Inbred WKY | Male | Nitroglycerin - pharmacology | Dose-Response Relationship, Drug | Myocardial Contraction - genetics | Muscle Proteins - metabolism | Oxidation-Reduction - drug effects | Sarcoplasmic Reticulum - metabolism | Excitation Contraction Coupling - drug effects | Vasodilator Agents - pharmacology | Cells, Cultured | Rats | Excitation Contraction Coupling - genetics | Mice, Knockout | Muscle Proteins - genetics | Myocytes, Cardiac - pathology | Animals | Nitric Oxide Synthase Type I - metabolism | Myocytes, Cardiac - metabolism | Sarcoplasmic Reticulum - pathology | Mice | Nitric Oxide Synthase Type I - genetics | Nitroso-Redox Imbalance | Molecular Bases of Disease | Oxidative Stress | Sarcoplasmic Reticulum (SR) | Heart Failure | Nitric-oxide Synthase | Redox Regulation | Cardiomyocytes | SR Calcium Leak | Hydralazine | Organic Nitrates
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4. Full Text Skeletal muscle specific overexpression of the mitochondrial H.sub.2O.sub.2 scavenger, peroxiredoxin 3, rescues mitochondrial dysfunction and sarcopenia phenotypes elicited by redox imbalance
by Ahn, Bumsoo and Ranjit, Rojina and Piekarz, Katarzyna and Poopal, Ashiwini and Bian, Jan and Sataranatarajan, Kavithalakshmi and Ran, Qitao and Van Remmen, Holly
Free Radical Biology and Medicine, ISSN 0891-5849, 11/2018, Volume 128, p. S123
Reactive oxygen species (ROS) are known to impair contractile function and contribute to muscle atrophy, and one of the primary sources of ROS is mitochondria.... 
Sarcopenia | Hydrogen peroxide | Codon | Actin | Analysis | Muscles | Genetic engineering | Genetic aspects | Muscle proteins
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5. Full Text Alpha B-crystallin induction in skeletal muscle cells under redox imbalance is mediated by a JNK-dependent regulatory mechanism
by Fittipaldi, Simona and Mercatelli, Neri and Dimauro, Ivan and Jackson, Malcolm J and Paronetto, Maria Paola and Caporossi, Daniela
Free Radical Biology and Medicine, ISSN 0891-5849, 09/2015, Volume 86, pp. 331 - 342
The small heat shock protein α-B-crystallin (CRYAB) is critically involved in stress-related cellular processes such as differentiation, apoptosis, and redox... 
c-Jun | p38 | Sodium arsenite | Nrf2 | Myoblasts | OXIDATIVE STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CARDIAC MYOCYTES | MAP KINASES | KAPPA-B | HEAT-SHOCK-PROTEIN | GLUTATHIONE DISULFIDE | ENDOCRINOLOGY & METABOLISM | HEME OXYGENASE-1 | EXPRESSION | alpha-Crystallin B Chain - genetics | Cell Line | Oxidation-Reduction | Transcriptional Activation | Molecular Sequence Data | alpha-Crystallin B Chain - metabolism | Antioxidant Response Elements | Muscle Fibers, Skeletal - metabolism | MAP Kinase Signaling System | Animals | Proto-Oncogene Proteins c-jun - metabolism | Base Sequence | NF-E2-Related Factor 2 - metabolism | Transcription Initiation Site | Protein Binding | Transcription, Genetic | Mice | Myoblasts, Skeletal - metabolism | Antioxidants | Analysis | Chronic diseases | Genetic research | Muscles | Heat shock proteins | Cell differentiation | Phosphotransferases | Arsenic compounds
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6. Full Text Sources and implications of NADH/NAD+ redox imbalance in diabetes and its complications
by Wu, Jinzi and Jin, Zhen and Zheng, Hong and Yan, Liang-Jun
Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, ISSN 1178-7007, 05/2016, Volume 9, pp. 145 - 153
NAD(+) is a fundamental molecule in metabolism and redox signaling. In diabetes and its complications, the balance between NADH and NAD(+) can be severely... 
Sirtuins | Oxidative stress | Mitochondria | Reactive oxygen species | Oxidative damage | Poly ADP ribosylation | Complex I | Polyol pathway | polyol pathway | POLY(ADP-RIBOSE) POLYMERASE INHIBITORS | OXYGEN SPECIES PRODUCTION | ACTIVATED PROTEIN-KINASE | LIPID-PEROXIDATION | mitochondria | sirtuins | BETA-CELL FAILURE | oxidative damage | ALDOSE REDUCTASE INHIBITOR | GLUTAMATE-DEHYDROGENASE | MITOCHONDRIAL COMPLEX-I | INSULIN-RESISTANCE | reactive oxygen species | poly ADP ribosylation | ENDOCRINOLOGY & METABOLISM | complex I | oxidative stress | Enzymes | Liver diseases | Dehydrogenases | Pathogenesis | Smooth muscle | Glucose | Metabolism | Fatty acids | Proteins | Hyperglycemia | Chinese medicine | Rodents | Insulin resistance | Oxidation | Diabetes | Apoptosis
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7. Full Text Long-term intermittent feeding, but not caloric restriction, leads to redox imbalance, insulin receptor nitration, and glucose intolerance
by Cerqueira, Fernanda M and da Cunha, Fernanda M and Caldeira da Silva, Camille C and Chausse, Bruno and Romano, Renato L and Garcia, Camila C.M and Colepicolo, Pio and Medeiros, Marisa H.G and Kowaltowski, Alicia J
Free Radical Biology and Medicine, ISSN 0891-5849, 10/2011, Volume 51, Issue 7, pp. 1454 - 1460
Calorie restriction is a dietary intervention known to improve redox state, glucose tolerance, and animal life span. Other interventions have been adopted as... 
Glucose tolerance | Nitration | Nitric oxide synthase | Free radicals | Insulin receptor | Calorie restriction | LIFE-SPAN | OXIDATIVE STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIAL-FUNCTION | MECHANISMS | DIETARY RESTRICTION | HYPOTHESIS | ENDOCRINOLOGY & METABOLISM | NITRIC-OXIDE | RESISTANCE | MICE | TYROSINE NITRATION | Glucose Intolerance - metabolism | Obesity - diet therapy | Body Weight | Humans | Male | Muscle, Skeletal - metabolism | Adiposity | Insulin Receptor Substrate Proteins - biosynthesis | Nitric Oxide Synthase - biosynthesis | Insulin Receptor Substrate Proteins - analysis | Nitric Oxide Synthase - analysis | Oxidation-Reduction | Rats | Caloric Restriction - methods | Intra-Abdominal Fat - metabolism | Receptor, Insulin - antagonists & inhibitors | Rats, Sprague-Dawley | Blotting, Western | Obesity - metabolism | Insulin - metabolism | Animals | Nitro Compounds | Diet, Reducing - methods | Glucose - metabolism | Receptor, Insulin - metabolism | Glucose intolerance | Analysis | Nitric oxide | Glucose | Free radicals (Chemistry) | Insulin | Dextrose
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8. Full Text Redox imbalance in peripheral blood of type 1 myotonic dystrophy patients
by Nikolić-Kokić, Aleksandra and Marinković, Dragan and Perić, Stojan and Stević, Zorica and Spasić, Mihajlo B and Blagojević, Duško and Rakocˇević-Stojanović, Vidosava
Redox Report, ISSN 1351-0002, 09/2016, Volume 21, Issue 5, pp. 232 - 237
Objectives: The aim of our study was to determine if redox imbalance caused by the activities of antioxidant enzymes existed in erythrocytes of type 1 myotonic... 
Superoxide dismutase | Catalase | Glutatione peroxidase | Type 1 myotonic dystrophy | Glutathione reductase | Erythrocytes | SKELETAL-MUSCLE | OXIDATIVE STRESS | PRODUCTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | SUPEROXIDE-DISMUTASE | FREE-RADICALS | Glutathione Peroxidase - metabolism | Myotonic Dystrophy - metabolism | Oxidation-Reduction | Glutathione Reductase - metabolism | Humans | Oxidative Stress - physiology | Male | Catalase - metabolism | Myotonic Dystrophy - pathology | Erythrocytes - metabolism | Adult | Female | Superoxide Dismutase - metabolism
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9. Full Text Redox imbalance influence in the myocardial Akt activation in aged rats treated with DHEA
by Jacob, Maria Helena Vianna Metello and Janner, Daiane da Rocha and Araújo, Alex Sander da Rosa and Jahn, Matheus Parmegiani and Kucharski, Luiz Carlos Rios and Moraes, Tarsila Barros and Filho, Carlos Severo Dutra and Ribeiro, Maria Flavia Marques and Belló-Klein, Adriane
Experimental Gerontology, ISSN 0531-5565, 2010, Volume 45, Issue 12, pp. 957 - 963
This study examined, in young and old (3 and 24 month-old, respectively) healthy Wistar rats, the in vivo effect of DHEA (10 mg/kg body weight) administered... 
DHEA | Heart | Aging | Hydrogen peroxide | Akt | GSH | OXIDATIVE STRESS | ANTIOXIDANT ENZYMES | MUSCLE | CELL-SURVIVAL | GLUTATHIONE REDOX | DEHYDROEPIANDROSTERONE | DAMAGE | GERIATRICS & GERONTOLOGY | PATHWAY | DISEASE | HYDROGEN-PEROXIDE | Glutathione Peroxidase - metabolism | Rats, Wistar | Dehydroepiandrosterone - pharmacology | Glutathione Transferase - metabolism | Rats | Male | Glutathione Disulfide - metabolism | Animals | Myocardium - metabolism | NF-E2-Related Factor 2 - metabolism | Oxidation-Reduction - drug effects | Heart - drug effects | Models, Animal | Proto-Oncogene Proteins c-akt - metabolism | Aging - metabolism
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10. Full Text Astaxanthin supplementation delays physical exhaustion and prevents redox imbalances in plasma and soleus muscles of wistar rats
by Polotow, Tatiana G and Vardaris, Cristina V and Mihaliuc, Andrea R and Gonçalves, Marina S and Pereira, Benedito and Ganini, Douglas and Barros, Marcelo P
Nutrients, ISSN 2072-6643, 12/2014, Volume 6, Issue 12, pp. 5819 - 5838
Astaxanthin (ASTA) is a pinkish-orange carotenoid commonly found in marine organisms, especially salmon. ASTA is a powerful antioxidant and suggested to... 
Oxidative stress | Mitochondria | Iron | Exercise | Uric acid | Carotenoid | LIPID-METABOLISM | ANTIOXIDANTS | mitochondria | exercise | carotenoid | DAMAGE | FREE-RADICALS | SKELETAL-MUSCLE | NUTRITION & DIETETICS | GLUTATHIONE | TISSUE DISTRIBUTION | iron | uric acid | oxidative stress | URIC-ACID | Rats, Wistar | Cholesterol - blood | Male | Muscle, Skeletal - metabolism | Muscle, Skeletal - drug effects | Uric Acid - blood | Physical Conditioning, Animal | Superoxide Dismutase - metabolism | Iron - blood | Glutathione Peroxidase - metabolism | Oxidation-Reduction | Fatigue - blood | Hemoglobins - metabolism | Rats | Mitochondria - metabolism | Antioxidants - pharmacology | Biomarkers - blood | Mitochondria - drug effects | Catalase - metabolism | Animals | Triglycerides - blood | Xanthophylls - pharmacology | Oxidative Stress - drug effects | Blood Glucose - metabolism | Dietary Supplements | Glutathione - blood
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11. Full Text Vascular redox imbalance in rats submitted to chronic exercise
by da Rocha, Ricardo Fagundes and de Oliveira, Marcos Roberto and de Bittencourt Pasquali, Matheus Augusto and Andrades, Michael Éverton and Oliveira, Max William Soares and Behr, Guilherme Antônio and Moreira, José Cláudio Fonseca
Cell Biochemistry and Function, ISSN 0263-6484, 04/2010, Volume 28, Issue 3, pp. 190 - 196
Exercise training has been used for treatment/prevention of many cardiovascular diseases, but the mechanisms need to be clarified. Thus, our aim was to compare... 
aorta artery | heart | oxidative stress | exercise training | reactive oxygen species | Heart | Oxidative stress | Reactive oxygen species | Exercise training | Aorta artery | LIPID-PEROXIDATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | PHYSICAL-EXERCISE | ANTIOXIDANT CAPACITY | CELL BIOLOGY | SKELETAL-MUSCLE | INDUCED OXIDATIVE STRESS | NITRIC-OXIDE | HYDROGEN-PEROXIDE | AEROBIC EXERCISE | SUPEROXIDE-DISMUTASE | TYROSINE NITRATION | Protein Carbonylation | Oxidation-Reduction | Oxidative Stress | Antioxidants - metabolism | Humans | Thiobarbiturates - metabolism | Rats | Male | Aorta - metabolism | Physical Conditioning, Animal - physiology | Catalase - metabolism | Animals | Myocardium - metabolism | Adolescent | Adult | Female | Child | Superoxide Dismutase - metabolism
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12. Full Text Cystathionine gamma-lyase-deficient smooth muscle cells exhibit redox imbalance and apoptosis under hypoxic stress conditions
by Bryan, Sean and Yang, Guangdong and Wang, Rui and Khaper, Neelam
Experimental and Clinical Cardiology, ISSN 1205-6626, 12/2011, Volume 16, Issue 4, pp. e36 - e41
BACKGROUND: Hydrogen sulphide (H2S) has recently emerged as a novel and important gasotransmitter in the cardiovascular system, where it is generated mainly by... 
Hydrogen sulphide | Oxidative stress | Vascular smooth muscle cell | Cystathionine gamma-lyase | Apoptosis | CARDIAC & CARDIOVASCULAR SYSTEMS | MECHANISM | HEART-FAILURE | H2S | INJURY | HYDROGEN-SULFIDE | PROTECTS | ANIMATION-LIKE STATE | MICE | HYPERTENSION | Original
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13. Full Text Creatine prevents the imbalance of redox homeostasis caused by homocysteine in skeletal muscle of rats
by Kolling, Janaína and Scherer, Emilene B.S and Siebert, Cassiana and Marques, Eduardo Peil and dos Santos, Tiago Marcom and Wyse, Angela T.S
Gene, ISSN 0378-1119, 07/2014, Volume 545, Issue 1, pp. 72 - 79
Homocystinuria is a neurometabolic disease caused by severe deficiency of cystathionine beta-synthase activity, resulting in severe hyperhomocysteinemia.... 
Oxidative stress | Soleus skeletal muscle | Creatine | Severe hyperhomocysteinemia | HYPERHOMOCYSTEINEMIA | ANTIOXIDANTS | NITRIC-OXIDE SYNTHASE | SUPPLEMENTATION | OXYGEN | GLUTATHIONE | GENETICS & HEREDITY | HEALTH | ENERGY-METABOLISM | EXPRESSION | Creatine - pharmacology | Glutathione Peroxidase - metabolism | Oxidation-Reduction | Rats, Wistar | Glutathione - metabolism | Fluoresceins - metabolism | Hyperhomocysteinemia - metabolism | Nitrites - metabolism | Rats | Male | Muscle, Skeletal - metabolism | Thiobarbituric Acid Reactive Substances - metabolism | Hyperhomocysteinemia - drug therapy | Catalase - metabolism | Animals | Homocysteine - pharmacology | Muscle, Skeletal - drug effects | Creatine - metabolism | Female | Homeostasis - drug effects | Superoxide Dismutase - metabolism | Antioxidants | Muscles | Enzymes | Homocysteine
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