Relevant bibliographies by topics / Antioxidants Heart cells. Oxidative stress. Enzyme activation

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Antioxidants Heart cells. Oxidative stress. Enzyme activation'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Antioxidants Heart cells. Oxidative stress. Enzyme activation"

1

Maldonado, Edio, Diego A. Rojas, Fabiola Urbina, and Aldo Solari. "The Use of Antioxidants as Potential Co-Adjuvants to Treat Chronic Chagas Disease." Antioxidants 10, no. 7 (2021): 1022. http://dx.doi.org/10.3390/antiox10071022.

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Chagas disease is a neglected tropical disease caused by the flagellated protozoa Trypanosome cruzi. This illness affects to almost 8–12 million people worldwide, however, is endemic to Latin American countries. It is mainly vectorially transmitted by insects of the Triatominae family, although other transmission routes also exist. T. cruzi-infected cardiomyocytes at the chronic stage of the disease display severe mitochondrial dysfunction and high ROS production, leading to chronic myocardial inflammation and heart failure. Under cellular stress, cells usually can launch mitochondrial biogene
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Sun, Jing, Guibo Sun, Xiaolan Cui, Xiangbao Meng, Meng Qin, and Xiaobo Sun. "Myricitrin Protects against Doxorubicin-Induced Cardiotoxicity by Counteracting Oxidative Stress and Inhibiting Mitochondrial Apoptosis via ERK/P53 Pathway." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/6093783.

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Doxorubicin (Dox) is one of the most effective and widely used anthracycline antineoplastic antibiotics. Unfortunately, the use of Dox is limited by its cumulative and dose-dependent cardiac toxicity. Myricitrin, a natural flavonoid which is isolated from the ground bark ofMyrica rubra, has recently been found to have a strong antioxidative effect. This study aimed to evaluate the possible protective effect of myricitrin against Dox-induced cardiotoxicity and the underlying mechanisms. An in vivo investigation in SD rats demonstrated that myricitrin significantly reduced the Dox-induced myocar
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Martínez-Álvarez, R. M., M. C. Hidalgo, A. Domezain, A. E. Morales, M. García-Gallego, and A. Sanz. "Physiological changes of sturgeon Acipenser naccarii caused by increasing environmental salinity." Journal of Experimental Biology 205, no. 23 (2002): 3699–706. http://dx.doi.org/10.1242/jeb.205.23.3699.

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SUMMARY The possible repercussions of osmoregulatory processes on some indicators of classical and oxidative stress were examined during gradual acclimation of sturgeons (Acipenser naccarii) to full seawater (35% salinity) and after a period of 20∼days at this salinity. Erythrocyte constants and levels of cortisol, protein and glucose in the plasma were determined. In addition, plasma osmolality and muscle-hydration values, as well as liver and heart protein, were determined. Catalase, glutathione peroxidase and superoxide dismutase activities and lipidperoxidation levels were measured in bloo
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4

Grudinin, N. V., V. K. Bogdanov, M. G. Sharapov, et al. "Use of peroxiredoxin for preconditioning of heterotopic heart transplantation in a rat." Russian Journal of Transplantology and Artificial Organs 22, no. 2 (2020): 158–64. http://dx.doi.org/10.15825/1995-1191-2020-2-158-164.

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Peroxiredoxin 6 (Prdx6) is an antioxidant enzyme in the human body that performs a number of important functions in the cell. Prdx6 restores a wide range of peroxide substrates, thus playing a leading role in maintaining redox homeostasis in mammalian cells. In addition to peroxidase activity, Prdx6 has an activity of phospholipase A2, thus taking part in membrane phospholipid metabolism. Due to its peroxidase and phospholipase activity, Prdx6 participates in intracellular and intercellular signal transmission, thereby facilitating the initiation of regenerative processes in the cell, suppress
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5

Li, Jian-Mei, and Ajay M. Shah. "Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 5 (2004): R1014—R1030. http://dx.doi.org/10.1152/ajpregu.00124.2004.

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The endothelial generation of reactive oxygen species (ROS) is important both physiologically and in the pathogenesis of many cardiovascular disorders. ROS generated by endothelial cells include superoxide (O2−·), hydrogen peroxide (H2O2), peroxynitrite (ONOO−·), nitric oxide (NO), and hydroxyl (·OH) radicals. The O2−· radical, the focus of the current review, may have several effects either directly or through the generation of other radicals, e.g., H2O2 and ONOO−·. These effects include 1) rapid inactivation of the potent signaling molecule and endothelium-derived relaxing factor NO, leading
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Rochette, Luc, and Steliana Ghibu. "Mechanics Insights of Alpha-Lipoic Acid against Cardiovascular Diseases during COVID-19 Infection." International Journal of Molecular Sciences 22, no. 15 (2021): 7979. http://dx.doi.org/10.3390/ijms22157979.

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Coronavirus disease 2019 (COVID-19) was first reported in Wuhan, China, in late December 2019. Since then, COVID-19 has spread rapidly worldwide and was declared a global pandemic on 20 March 2020. Cardiovascular complications are rapidly emerging as a major peril in COVID-19 in addition to respiratory disease. The mechanisms underlying the excessive effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on patients with cardiovascular comorbidities remain only partly understood. SARS-CoV-2 infection is caused by binding of the viral surface spike (S) protein to the h
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7

Hamilton, Thais Rose dos Santos, Gabriela Esteves Duarte, José Antonio Visintin, and Mayra Elena Ortiz D’Ávila Assumpção. "Immunolocalization of antioxidant enzymes in testis of rams submitted to long-term heat stress." Zygote 27, no. 6 (2019): 432–35. http://dx.doi.org/10.1017/s0967199419000467.

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SummaryLong-term heat stress (HS) induced by testicular insulation generates oxidative stress (OS) on the testicular environment; consequently activating antioxidant enzymes such as superoxide dismutase (SOD), glutathione reductase (GR) and glutathione peroxidase (GPx). The aim of this work was to immunolocalize antioxidant enzymes present in different cells within the seminiferous tubule when rams were submitted to HS. Rams were divided into control (n = 6) and treated group (n = 6), comprising rams subjected to testicular insulation for 240 h. After the testicular insulation period, rams wer
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8

Surai, Kochish, Fisinin, and Kidd. "Antioxidant Defence Systems and Oxidative Stress in Poultry Biology: An Update." Antioxidants 8, no. 7 (2019): 235. http://dx.doi.org/10.3390/antiox8070235.

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Poultry in commercial settings are exposed to a range of stressors. A growing body of information clearly indicates that excess ROS/RNS production and oxidative stress are major detrimental consequences of the most common commercial stressors in poultry production. During evolution, antioxidant defence systems were developed in poultry to survive in an oxygenated atmosphere. They include a complex network of internally synthesised (e.g., antioxidant enzymes, (glutathione) GSH, (coenzyme Q) CoQ) and externally supplied (vitamin E, carotenoids, etc.) antioxidants. In fact, all antioxidants in th
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Guan, Xiao-Hui, Xiao-Hong Liu, Xuan Hong, et al. "CD38 Deficiency Protects the Heart from Ischemia/Reperfusion Injury through Activating SIRT1/FOXOs-Mediated Antioxidative Stress Pathway." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/7410257.

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Ischemia/reperfusion (I/R) injury induces irreversible oxidative stress damage to the cardiac muscle. We previously observed that CD38 deficiency remarkably protects mouse embryonic fibroblasts (MEFs) from oxidative stress-induced injury. However, whether CD38 deficiency protects from I/R injury in the heart is not explored. Here, we showed that the hearts of CD38 deficient mice or wild type mice supplied with exogenous NAD were significantly protected from ischemia/reperfusion injury, seen as reduction of the myocardial infarct sizes when the mice were subjected to 30 min ischemia followed by
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Zhou, Shanshan, Wanqing Sun, Zhiguo Zhang, and Yang Zheng. "The Role of Nrf2-Mediated Pathway in Cardiac Remodeling and Heart Failure." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/260429.

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Heart failure (HF) is frequently the consequence of sustained, abnormal neurohormonal, and mechanical stress and remains a leading cause of death worldwide. The key pathophysiological process leading to HF is cardiac remodeling, a term referring to maladaptation to cardiac stress at the molecular, cellular, tissue, and organ levels. HF and many of the conditions that predispose one to HF are associated with oxidative stress. Increased generation of reactive oxygen species (ROS) in the heart can directly lead to increased necrosis and apoptosis of cardiomyocytes which subsequently induce cardia
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Dissertations / Theses on the topic "Antioxidants Heart cells. Oxidative stress. Enzyme activation"

1

Edwards, Heather Gray. "Protection from oxidative stress in the cardiac H9C2-cell line by the transcription factor NRF2." Auburn, Ala., 2007. http://repo.lib.auburn.edu/07M%20Dissertations/GRAY-EDWARDS_HEATHER_53.pdf.

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