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Oxidative Stress in Cardiac Disease

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A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (10 April 2022) | Viewed by 38857

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Special Issue Editors

Dr. Nicola King

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Guest Editor

School of Biomedical Sciences, Faculty of Health, University of Plymouth, Plymouth PL4 8AA, UK
Interests: myocardial protection; amino acids; meta-analysis; glutathione; anti-oxidant enzymes

Prof. Dr. M.-Saadeh Suleiman

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Guest Editor

Bristol Medical School, University of Bristol, Bristol Royal Infirmary, Bristol BS2 8HW, UK
Interests: cardioprotection; cardioplegia; cardiac remodeling post-acute infarction; molecular changes in diseased heart; ischemia; mitochondria; calcium
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Dear Colleagues,

Oxidative stress is a key mediator/trigger of organ impairment and injury during the progression of disease states. In the heart, oxidative stress plays a major role in the pathogenesis of various pathologic conditions such as coronary artery and valve diseases, cardiac infarction, and remodelling to heart failure. Oxidative stress may also occur during therapeutic interventions including open heart surgery and percutaneous coronary interventions. The deleterious effects on cardiomyocytes are largely due to opening of the mitochondrial permeability transition pore triggered by calcium loading and oxidiative stress. Understanding triggers and mediators of reactive oxygen species in diseased hearts and during treatement will help in identifying targets for therpeutic interventions.

As guest editors, we invite you to contribute to this Special Issue, whose focus will be the role of oxidative stress in cardiac disease progression and during therpeutic interventions.

Dr. Nicola King
Prof. Dr. M.-Saadeh Suleiman
Guest Editors

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Keywords

Ischemia
Oxidative stress
Coronary artery disease
Cardiac valve disease
Reperfusion injury
Antioxidants
Heart failure
Mitochondria

Published Papers (14 papers)

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22 pages, 6224 KiB

Open AccessArticle

Effect of Extracellular Matrix Stiffness on Candesartan Efficacy in Anti-Fibrosis and Antioxidation

by Tong Zhu, Jingjing Song, Bin Gao, Junjie Zhang, Yabei Li, Zhaoyang Ye, Yuxiang Zhao, Xiaogang Guo, Feng Xu and Fei Li

Antioxidants 2023, 12(3), 679; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12030679 - 09 Mar 2023

Cited by 1 | Viewed by 1689

Abstract

Myocardial fibrosis progression and imbalanced redox state are closely associated with increased extracellular matrix (ECM) stiffness. Candesartan (CAN), an angiotensin II (Ang II) receptor inhibitor, has shown promising anti-fibrosis and antioxidant efficacy in previous cardiovascular disease studies. However, the effect of ECM stiffness on CAN efficacy remains elusive. In this study, we constructed rat models with three different degrees of myocardial fibrosis and treated them with CAN, and then characterized the stiffness, cardiac function, and NADPH oxidase-2 (NOX2) expression of the myocardial tissues. Based on the obtained stiffness of myocardial tissues, we used polyacrylamide (PA) gels with three different stiffness to mimic the ECM stiffness of cardiac fibroblasts (CFs) at the early, middle, and late stages of myocardial fibrosis as the cell culture substrates and then constructed CFs mechanical microenvironment models. We studied the effects of PA gel stiffness on the migration, proliferation, and activation of CFs without and with CAN treatment, and characterized the reactive oxygen species (ROS) and glutathione (GSH) levels of CFs using fluorometry and scanning electrochemical microscopy (SECM). We found that CAN has the best amelioration efficacy in the cardiac function and NOX2 levels in rats with medium-stiffness myocardial tissue, and the most obvious anti-fibrosis and antioxidant efficacy in CFs on the medium-stiffness PA gels. Our work proves the effect of ECM stiffness on CAN efficacy in myocardial anti-fibrosis and antioxidants for the first time, and the results demonstrate that the effect of ECM stiffness on drug efficacy should also be considered in the treatment of cardiovascular diseases. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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13 pages, 2426 KiB

Open AccessArticle

Cardioprotective Antioxidant and Anti-Inflammatory Mechanisms Induced by Intermittent Hypobaric Hypoxia

by Alejandro González-Candia, Alejandro A. Candia, Adolfo Paz, Fuad Mobarec, Rodrigo Urbina-Varela, Andrea del Campo, Emilio A. Herrera and Rodrigo L. Castillo

Antioxidants 2022, 11(6), 1043; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061043 - 25 May 2022

Cited by 7 | Viewed by 2250

Abstract

More than 80 million people live and work (in a chronic or intermittent form) above 2500 masl, and 35 million live in the Andean Mountains. Furthermore, in Chile, it is estimated that 100,000 people work in high-altitude shifts, where stays in the lowlands are interspersed with working visits in the highlands. Acute exposure to high altitude has been shown to induce oxidative stress in healthy human lowlanders due to increased free radical formation and decreased antioxidant capacity. However, intermittent hypoxia (IH) induces preconditioning in animal models, generating cardioprotection. Here, we aim to describe the responses of a cardiac function to four cycles of intermittent hypobaric hypoxia (IHH) in a rat model. The twelve adult Wistar rats were randomly divided into two equal groups, a four-cycle of IHH and a normobaric hypoxic control. Intermittent hypoxia was induced in a hypobaric chamber in four continuous cycles (1 cycle = 4 days of hypoxia + 4 days of normoxia), reaching a barometric pressure equivalent to 4600 m of altitude (428 Torr). At the end of the fourth cycle, cardiac structural and functional variables were also determined by echocardiography; furthermore, cardiac oxidative stress biomarkers (4-Hydroxynonenal, HNE; nitrotyrosine, NT), antioxidant enzymes, and NLRP3 inflammasome panel expression are also determined. Our results show a higher ejection and a shortening fraction of the left ventricle function by the end of the fourth cycle. Furthermore, cardiac tissue presented a decreased expression of antioxidant proteins. However, a decrease in IL-1β, TNF-αn, and oxidative stress markers is observed in IHH compared to normobaric hypoxic controls. Non-significant differences were found in protein levels of NLRP3 and caspase-1. IHH exposure determines structural and functional heart changes. These findings suggest that initial states of IHH are beneficial for cardiovascular function and protection. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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15 pages, 2354 KiB

Open AccessArticle

Cardiac NF-κB Acetylation Increases While Nrf2-Related Gene Expression and Mitochondrial Activity Are Impaired during the Progression of Diabetes in UCD-T2DM Rats

by Max A. Thorwald, Jose A. Godoy-Lugo, Ruben Rodriguez, Kimber L. Stanhope, James L. Graham, Peter J. Havel, Henry Jay Forman and Rudy M. Ortiz

Antioxidants 2022, 11(5), 927; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11050927 - 09 May 2022

Cited by 4 | Viewed by 1769

Abstract

The onset of type II diabetes increases the heart’s susceptibility to oxidative damage because of the associated inflammation and diminished antioxidant response. Transcription factor NF-κB initiates inflammation while Nrf2 controls antioxidant defense. Current evidence suggests crosstalk between these transcription factors that may become dysregulated during type II diabetes mellitus (T2DM) manifestation. The objective of this study was to examine the dynamic changes that occur in both transcription factors and target genes during the progression of T2DM in the heart. Novel UC Davis T2DM (UCD-T2DM) rats at the following states were utilized: (1) lean, control Sprague-Dawley (SD; n = 7), (2) insulin-resistant pre-diabetic UCD-T2DM (Pre; n = 9), (3) 2-week recently diabetic UCD-T2DM (2Wk; n = 9), (4) 3-month diabetic UCD-T2DM (3Mo; n = 14), and (5) 6-month diabetic UCD-T2DM (6Mo; n = 9). NF-κB acetylation increased 2-fold in 3Mo and 6Mo diabetic animals compared to SD and Pre animals. Nox4 protein increased 4-fold by 6Mo compared to SD. Nrf2 translocation increased 82% in Pre compared to SD but fell 47% in 6Mo animals. GCLM protein fell 35% in 6Mo animals compared to Pre. Hmox1 mRNA decreased 45% in 6Mo animals compared to SD. These data suggest that during the progression of T2DM, NF-κB related genes increase while Nrf2 genes are suppressed or unchanged, perpetuating inflammation and a lesser ability to handle an oxidant burden altering the heart’s redox state. Collectively, these changes likely contribute to the diabetes-associated cardiovascular complications. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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11 pages, 1594 KiB

Open AccessArticle

Oxidative Stress and Indicators of Brain Damage Following Pediatric Heart Surgery

by Débora Cañizo Vázquez, Stephanie M. Hadley, Marta Pérez Ordóñez, Miriam Lopez-Abad, Anna Valls, Marta López Viñals, Bosco A. Moscoso, Sergio Benito Fernandez, Marta Camprubí-Camprubí and Joan Sanchez-de-Toledo

Antioxidants 2022, 11(3), 489; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11030489 - 28 Feb 2022

Cited by 4 | Viewed by 2094

Abstract

Pediatric cardiac surgery induces an increased oxidative stress (OS) response. Increased OS is associated with poor neurologic outcomes in neonatal populations with similar patterns of brain injury. We investigated OS and brain injury in infants undergoing heart surgery. Patients 6 months or younger, undergoing cardiac surgery with or without cardiopulmonary bypass (CPB), were included in this prospective, observational study. Patients were divided into infant (30 days–6 months) and neonatal (<30 days) groups for analysis. Urine OS biomarker 8-iso-prostaglandin F2α (8-iso-PGF2α) was quantified pre-surgery and at 0 and 24 h post-surgery. A serum brain damage biomarker S100B protein was also measured pre-surgery and at 0 and 72 h post-surgery. Amplitude-integrated electroencephalography during surgery was analyzed. Neuropsychological evaluation using the Bayley III or Vineland test was performed in all patients at 24 months of age. Sixty-two patients were included, 44 of whom underwent follow-up neurologic evaluation. 8-iso-PGF2α and S100B levels were increased after surgery. Postoperative levels of S100B were positively correlated with 8-iso-PGF2α levels 24 h after surgery (rho = 0.5224; p = 0.0261). There was also a correlation between immediate post-surgery levels of 8-iso-PGF2α and intra-surgery seizure burden (rho = 0.4285, p = 0.0205). Patients with an abnormal neurological evaluation had increased levels of S100B 72 h after surgery (p = 0.048). 8-iso-PGF2α levels 24 h after surgery were also related to abnormal neurologic outcomes. Levels of 8-iso-PGF2α following pediatric cardiac surgery are associated with several indicators of brain injury including brain damage biomarkers, intra-operative seizures, and abnormal neurological evaluation at follow-up, suggesting the importance of oxidative stress response in the origin of brain damage in this population. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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13 pages, 2367 KiB

Open AccessArticle

Brain Oxygen Perfusion and Oxidative Stress Biomarkers in Fetuses with Congenital Heart Disease—A Retrospective, Case-Control Pilot Study

by Maria C. Escobar-Diaz, Miriam Pérez-Cruz, Miguel Arráez, Mari-Merce Cascant-Vilaplana, Abel Albiach-Delgado, Julia Kuligowski, Máximo Vento, Narcis Masoller, Maria Dolores Gómez-Roig, Olga Gómez, Joan Sanchez-de-Toledo and Marta Camprubí-Camprubí

Antioxidants 2022, 11(2), 299; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020299 - 31 Jan 2022

Cited by 2 | Viewed by 2403

Abstract

Fetuses with congenital heart disease (CHD) have circulatory changes that may lead to predictable blood flow disturbances that may affect normal brain development. Hypoxemia and hypoperfusion may alter the redox balance leading to oxidative stress (OS), that can be assessed measuring stable end-products. OS biomarkers (OSB) were measured in amniotic fluid in fetuses with (n = 41) and without CHD (n = 44) and analyzed according to aortic flow, expected cyanosis after birth, and a CHD classification derived from this. Birth head circumference (HC) was used as a neurodevelopment biomarker. CHD fetuses had higher levels of ortho-Tyrosine (o-Tyr) than controls (p = 0.0003). There were no differences in o-Tyr levels considering aortic flow obstruction (p = 0.617). Fetuses with expected extreme cyanosis presented the highest levels of o-Tyr (p = 0.003). Among groups of CHD, fetuses without aortic obstruction and extreme cyanosis had the highest levels of o-Tyr (p = 0.005). CHD patients had lower HC than controls (p = 0.023), without correlation with OSB. Patients with HC < 10th percentile, presented high levels of o-Tyr (p = 0.024). Fetuses with CHD showed increased OSB and lower HC when compared to controls, especially those with expected extreme cyanosis. Our results suggest that increased levels of OSB are more influenced by the effect of low oxygenation than by aortic flow obstruction. Future studies with larger sample size are needed to further investigate the role of OSB as an early predictor of neurodevelopmental problems in CHD survivors. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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16 pages, 1946 KiB

Open AccessArticle

Effects of Ferroptosis on the Metabolome in Cardiac Cells: The Role of Glutaminolysis

by Keishla M. Rodríguez-Graciani, Xavier R. Chapa-Dubocq, Esteban J. Ayala-Arroyo, Ivana Chaves-Negrón, Sehwan Jang, Nataliya Chorna, Taber S. Maskrey, Peter Wipf and Sabzali Javadov

Antioxidants 2022, 11(2), 278; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020278 - 29 Jan 2022

Cited by 16 | Viewed by 3391

Abstract

Ferroptosis is a novel iron-dependent regulated cell death mechanism that affects cell metabolism; however, a detailed metabolomic analysis of ferroptotic cells is not yet available. Here, we elucidated the metabolome of H9c2 cardioblasts by gas chromatography-mass spectrometry during ferroptosis induced by RSL3, a GPX4 inhibitor, in the presence of ferrostatin-1 (a ferroptosis inhibitor), XJB-5-131 (a mitochondrial-targeted ROS scavenger), or TSM-1005-44 (a newly developed cellular ROS scavenger). Results demonstrated that RSL3 decreased the levels of amino acids involved in glutathione synthesis more than two-fold. In contrast, saturated fatty acids levels were markedly increased in RSL3-challenged cells, with no effects on unsaturated fatty acids. RSL3 significantly altered the levels of mitochondrial tricarboxylic acid cycle intermediates; isocitrate and 2-oxoglutarate were found to increase, whereas succinate was significantly decreased in RSL3-challenged cells. Ferrostatin-1, XJB-5-131, and TSM-1005-44 prevented RSL3-induced cell death and conserved the metabolomic profile of the cells. Since 2-oxoglutarate is involved in the regulation of ferroptosis, particularly through glutamine metabolism, we further assessed the role of glutaminolysis in ferroptosis in H9c2 cardioblasts. Genetic silencing of GLS1, which encodes the K-type mitochondrial glutaminase (glutaminase C), protected against ferroptosis in the early stage. In conclusion, our study demonstrates that RSL3-induced ferroptosis impairs the metabolome of H9c2 cardioblasts. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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11 pages, 1217 KiB

Open AccessArticle

Jaboticaba (Myrciaria jaboticaba) Attenuates Ventricular Remodeling after Myocardial Infarction in Rats

by Renata Candido da Silva, Bertha Furlan Polegato, Paula Shmidt Azevedo, Ana Angélica Fernandes, Katashi Okoshi, Sergio Alberto Rupp de Paiva, Marcos Ferreira Minicucci and Leonardo Antônio Mamede Zornoff

Antioxidants 2022, 11(2), 249; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020249 - 27 Jan 2022

Cited by 3 | Viewed by 1516

Abstract

The cardiac remodeling after myocardial infarction is characterized by inflammation and oxidative stress. Thus, this study aimed to test the hypothesis that jaboticaba, due to its anti-inflammatory and antioxidants properties, attenuates cardiac remodeling after myocardial infarction. Wistar rats were submitted to myocardial infarction due to coronary artery occlusion, and divided into four experimental groups: C, sham control animals; I, animals submitted to myocardial infarction, received a standard diet; IJ2, animals submitted to myocardial infarction, received a standard diet plus 2% jaboticaba; and IJ4, animals submitted to myocardial infarction, received a standard diet plus 4% jaboticaba. After a three-month follow-up, echocardiography, histology, oxidative stress, and cardiac energy metabolism were analyzed. There was no difference in infarct size or mortality among the infarcted groups. The IJ4 group displayed improved diastolic function, as assessed by isovolumetric relaxation time normalized to the heart rate. As expected, the percentage of collagen was higher in all infarcted groups than in the C group. However, the IJ2 group had less collagen than groups I and IJ4. The IJ4 group presented lower PFK activity than I and IJ2, and lower pyruvate dehydrogenase activity than controls, whereas the IJ2 group showed no differences compared to the control group in both LDH and ATP synthase activity. The 2% and 4% doses attenuated lipid peroxidation and increased the activity of glutathione peroxidase compared with the I group. In conclusion, jaboticaba attenuated the remodeling process after myocardial infarction, which was associated with decreased oxidative stress and improved energy metabolism. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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13 pages, 2964 KiB

Open AccessArticle

Effects of Colchicine in a Rat Model of Diet-Induced Hyperlipidemia

by Denisa-Mădălina Zălar, Cristina Pop, Elena Buzdugan, Bela Kiss, Maria-Georgia Ştefan, Steliana Ghibu, Doiniţa Crişan, Alexandra Buruiană-Simic, Adriana Grozav, Ileana Monica Borda and Cristina Ionela Mogoșan

Antioxidants 2022, 11(2), 230; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020230 - 25 Jan 2022

Cited by 10 | Viewed by 3442

Abstract

Inflammation and hyperlipidemia play an essential role in the pathophysiology of endothelial dysfunction as well as atherosclerotic plaque formation, progression and rupture. Colchicine has direct anti-inflammatory effects by inhibiting multiple inflammatory signaling pathways. The purpose of our study was to evaluate colchicine activity in an animal model of hyperlipidemia induced by diet. A total of 24 male rats (wild type, WT) were divided into three groups: group one fed with a basic diet (BD) (WT + BD, n = 8), group two fed with a high-fat diet (HFD) (WT + HFD, n = 8)), and group three which received HFD plus drug treatment (colchicine, 0.5 mg/kg, i.p., daily administration). Total cholesterol, LDL-, HDL-cholesterol and triglycerides were determined. In addition, plasma transaminases, inflammation of oxidative stress markers, were measured. Tissue samples were evaluated using hematoxylin-eosin and red oil stain. At the end of the study, rats presented increased serum lipid levels, high oxidative stress and pro-inflammatory markers. The aortic histopathological section revealed that HFD induced signs of endothelial dysfunction. Colchicine treatment significantly resolved and normalized these alterations. Moreover, colchicine did not influence NAFLD activity score but significantly increased ALT and AST levels, suggesting that colchicine amplified the hepatocellular injury produced by the diet. Colchicine reduces plasma lipid levels, oxidative stress and inflammation markers and leads to more favorable histopathologic vascular and cardiac results. However, the adverse effects of colchicine could represent an obstacle to its safe use. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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14 pages, 1042 KiB

Open AccessArticle

Overexpression of NOX2 Exacerbates AngII-Mediated Cardiac Dysfunction and Metabolic Remodelling

by Synne S. Hansen, Tina M. Pedersen, Julie Marin, Neoma T. Boardman, Ajay M. Shah, Ellen Aasum and Anne D. Hafstad

Antioxidants 2022, 11(1), 143; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11010143 - 10 Jan 2022

Cited by 2 | Viewed by 1952

Abstract

The present study aimed to examine the effects of low doses of angiotensin II (AngII) on cardiac function, myocardial substrate utilization, energetics, and mitochondrial function in C57Bl/6J mice and in a transgenic mouse model with cardiomyocyte specific upregulation of NOX2 (csNOX2 TG). Mice were treated with saline (sham), 50 or 400 ng/kg/min of AngII (AngII₅₀ and AngII₄₀₀) for two weeks. In vivo blood pressure and cardiac function were measured using plethysmography and echocardiography, respectively. Ex vivo cardiac function, mechanical efficiency, and myocardial substrate utilization were assessed in isolated perfused working hearts, and mitochondrial function was measured in left ventricular homogenates. AngII₅₀ caused reduced mechanical efficiency despite having no effect on cardiac hypertrophy, function, or substrate utilization. AngII₄₀₀ slightly increased systemic blood pressure and induced cardiac hypertrophy with no effect on cardiac function, efficiency, or substrate utilization. In csNOX2 TG mice, AngII₄₀₀ induced cardiac hypertrophy and in vivo cardiac dysfunction. This was associated with a switch towards increased myocardial glucose oxidation and impaired mitochondrial oxygen consumption rates. Low doses of AngII may transiently impair cardiac efficiency, preceding the development of hypertrophy induced at higher doses. NOX2 overexpression exacerbates the AngII -induced pathology, with cardiac dysfunction and myocardial metabolic remodelling. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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13 pages, 944 KiB

Open AccessArticle

Serum Zinc and Selenium Concentrations in Patients with Hypertrophy and Remodelling of the Left Ventricle Secondary to Arterial Hypertension

by Paweł Gać, Karolina Czerwińska, Małgorzata Poręba, Adam Prokopowicz, Helena Martynowicz, Grzegorz Mazur and Rafał Poręba

Antioxidants 2021, 10(11), 1803; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10111803 - 12 Nov 2021

Cited by 2 | Viewed by 1826

Abstract

The aim of the study was to assess the relationship between serum selenium and zinc concentrations (Se-S and Zn-S) and the left ventricle geometry in patients suffering from arterial hypertension. A total of 78 people with arterial hypertension (mean age: 53.72 ± 12.74 years) participated in the study. Se-S and Zn-S were determined in all patients. The type of left ventricular remodelling and hypertrophy was determined by the left ventricular mass index (LVMI) and relative wall thickness (RWT) measured by echocardiography. Se-S and Zn-S in the whole group were 89.84 ± 18.75 µg/L and 0.86 ± 0.13 mg/L. Normal left ventricular geometry was found in 28.2% of patients; left ventricular hypertrophy (LVH) in 71.8%, including concentric remodelling in 28.2%, concentric hypertrophy in 29.5%, and eccentric hypertrophy in 14.1%. LVH was statistically significantly more frequent in patients with Se-S < median compared to patients with Se-S ≥ median (87.2% vs. 56.4%, p < 0.05), as well as in patients with Zn-S < median compared to patients with Zn-S ≥ median (83.8% vs. 60.9%, p < 0.05). In hypertensive patients, older age, higher LDL cholesterol, higher fasting glucose, lower Se-S, and lower Zn-S were independently associated with LVH. In conclusion, in hypertensive patients, left ventricular hypertrophy may be associated with low levels of selenium and zinc in the serum. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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11 pages, 1228 KiB

Open AccessArticle

Oxysterols and Retinal Microvascular Dysfunction as Early Risk Markers for Cardiovascular Disease in Normal, Ageing Individuals

by Hala Shokr, Irundika HK Dias and Doina Gherghel

Antioxidants 2021, 10(11), 1756; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10111756 - 03 Nov 2021

Cited by 10 | Viewed by 1669

Abstract

The aim of the present paper is to assess the relationship between oxysterol levels and retinal microvascular function in individuals of various age groups, free of clinically evident diseases. Forty-two apparently healthy individuals were included in the present study (group 1: 19–30 years, group 2: 31–50 years, and group 3: 51–70 years). Retinal microvascular function was assessed using the dynamic retinal vessel analyzer (DVA, IMEDOS GmbH, Jena, Germany). Fasting plasma was obtained from all subjects and quantification of monohydroxy and dihydroxy oxysterols assessment was performed using LC-MS/MS following reverse phase chromatography. A Griess assay was used to evaluate the Nitric Oxide (NO) concentration in all individuals. The glutathione redox ratio was also analyzed by means of whole blood glutathione recycling assay. In all participants, the levels of 7-Ketocholesterol, 25-hydroxycholesterol and 7β-hydroxycholesterol correlated significantly and positively with the time to maximum arteriolar dilation. In addition, 25-hydroxycholesterol and 7β-hydroxycholesterol negatively correlated to the percentage of maximum arteriolar dilation. A negative correlation was observed for 27-hydroxycholesterol and 7β-hydroxycholesterol with microvascular arteriolar constriction. These results suggest that, with age, abnormal oxysterol levels correlate with early changes in microvascular bed function. This relationship could signal early risk for cardiovascular diseases (CVDs) in an ageing population. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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12 pages, 10019 KiB

Open AccessArticle

Tumor-Induced Cardiac Dysfunction: A Potential Role of ROS

by Priyanka Karekar, Haley N. Jensen, Kathryn L. G. Russart, Devasena Ponnalagu, Sarah Seeley, Shridhar Sanghvi, Sakima A. Smith, Leah M. Pyter, Harpreet Singh and Shubha Gururaja Rao

Antioxidants 2021, 10(8), 1299; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10081299 - 18 Aug 2021

Cited by 6 | Viewed by 5042

Abstract

Cancer and heart diseases are the two leading causes of mortality and morbidity worldwide. Many cancer patients undergo heart-related complications resulting in high incidences of mortality. It is generally hypothesized that cardiac dysfunction in cancer patients occurs due to cardiotoxicity induced by therapeutic agents, used to treat cancers and/or cancer-induced cachexia. However, it is not known if localized tumors or unregulated cell growth systemically affect heart function before treatment, and/or prior to the onset of cachexia, hence, making the heart vulnerable to structural or functional abnormalities in later stages of the disease. We incorporated complementary mouse and Drosophila models to establish if tumor induction indeed causes cardiac defects even before intervention with chemotherapy or onset of cachexia. We focused on one of the key pathways involved in irregular cell growth, the Hippo–Yorkie (Yki), pathway. We used overexpression of the transcriptional co-activator of the Yki signaling pathway to induce cellular overgrowth, and show that Yki overexpression in the eye tissue of Drosophila results in compromised cardiac function. We rescue these cardiac phenotypes using antioxidant treatment, with which we conclude that the Yki induced tumorigenesis causes a systemic increase in ROS affecting cardiac function. Our results show that systemic cardiac dysfunction occurs due to abnormal cellular overgrowth or cancer elsewhere in the body; identification of specific cardiac defects associated with oncogenic pathways can facilitate the possible early diagnosis of cardiac dysfunction. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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14 pages, 317 KiB

Open AccessReview

Oxidative Stress and Diseases Associated with High-Altitude Exposure

by Eduardo Pena, Samia El Alam, Patricia Siques and Julio Brito

Antioxidants 2022, 11(2), 267; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020267 - 28 Jan 2022

Cited by 47 | Viewed by 5251

Abstract

Several diseases associated with high-altitude exposure affect unacclimated individuals. These diseases include acute mountain sickness (AMS), high-altitude cerebral edema (HACE), high-altitude pulmonary edema (HAPE), chronic mountain sickness (CMS), and, notably, high-altitude pulmonary hypertension (HAPH), which can eventually lead to right ventricle hypertrophy and heart failure. The development of these pathologies involves different molecules and molecular pathways that might be related to oxidative stress. Studies have shown that acute, intermittent, and chronic exposure to hypobaric hypoxia induce oxidative stress, causing alterations to molecular pathways and cellular components (lipids, proteins, and DNA). Therefore, the aim of this review is to discuss the oxidative molecules and pathways involved in the development of high-altitude diseases. In summary, all high-altitude pathologies are related to oxidative stress, as indicated by increases in the malondialdehyde (MDA) biomarker and decreases in superoxide dismutase (SOD) and glutathione peroxidase (GPx) antioxidant activity. In addition, in CMS, the levels of 8-iso-PGF2α and H₂O₂ are increased, and evidence strongly indicates an increase in Nox4 activity in HAPH. Therefore, antioxidant treatments seem to be a promising approach to mitigating high-altitude pathologies. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

13 pages, 1610 KiB

Open AccessReview

A Cardioplegic Solution with an Understanding of a Cardiochannelopathy

by Min Jeong Ji and Jeong Hee Hong

Antioxidants 2021, 10(12), 1878; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10121878 - 25 Nov 2021

Cited by 2 | Viewed by 2933

Abstract

Cardiac surgeries have been improved by accompanying developing cardioplegia solutions. However, the cardioplegia application presents an ongoing challenge with a view of a sufficiently restored cardiac function. In this review, we focus on the cardioplegia-induced mechanism and summarize the findings of studies undertaken to improve cardioprotective strategies. Currently, and somewhat surprisingly, relatively little is known about cardiac electrolyte regulation through channel physiology. We hope that an improved understanding of the electrolyte transport through ion channels/transporters and modulations of water channel aquaporins will provide an insight into cardiac channel physiology and a channel-based cardiac pathology of a cardiochannelopathy. Full article

(This article belongs to the Special Issue Oxidative Stress in Cardiac Disease)

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