Oxidative Stress and Labile Zinc in Heart Dysfunction Under Hyperglycemia

2019 ◽  
pp. 397-412
Author(s):  
Belma Turan
Keyword(s):  
Oxidative Stress ◽  
Heart Dysfunction

Exenatide alleviates adriamycin-induced heart dysfunction in mice: Modulation of oxidative stress, apoptosis and inflammation

2019 ◽  
Vol 304 ◽  
pp. 186-193 ◽  
Author(s):  
Juntao Fang ◽  
Yida Tang ◽  
Xianwu Cheng ◽  
Lijuan Wang ◽  
Can Cai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Dysfunction ◽  
Apoptosis And Inflammation

Oxidative Stress and Apoptosis in Heart Dysfunction

Herz ◽  
2002 ◽  
Vol 27 (7) ◽  
pp. 662-668 ◽  
Author(s):  
Dinender Kumar ◽  
Huiquan Lou ◽  
Pawan K. Singal
Keyword(s):  
Oxidative Stress ◽  
Heart Dysfunction

Honokiol attenuates oxidative stress-dependent heart dysfunction in chronic Chagas disease by targeting AMPK / NFE2L2 / SIRT3 signaling pathway

2020 ◽  
Vol 156 ◽  
pp. 113-124 ◽  
Author(s):  
Eugenia Pérez Caballero ◽  
Nilo Mariz-Ponte ◽  
Cristina S. Rigazio ◽  
Miguel H. Santamaría ◽  
Ricardo S. Corral
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Chagas Disease ◽  
Heart Dysfunction ◽  
Stress Dependent ◽  
Chronic Chagas Disease

Secoisolariciresinol diglucoside attenuates cardiac hypertrophy and oxidative stress in monocrotaline-induced right heart dysfunction

2017 ◽  
Vol 432 (1-2) ◽  
pp. 33-39 ◽  
Author(s):  
Stephanie Puukila ◽  
Rafael Oliveira Fernandes ◽  
Patrick Türck ◽  
Cristina Campos Carraro ◽  
Jéssica Hellen Poletto Bonetto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Hypertrophy ◽  
Secoisolariciresinol Diglucoside ◽  
Right Heart ◽  
Heart Dysfunction ◽  
Right Heart Dysfunction ◽  
And Oxidative Stress

Abstract 325: Dissociation of Oxidative Stress from High Fatty Acid-Induced Cardiac Myocyte Death

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Nicolas Gutierrez Cortes ◽  
Huiliang Zhang ◽  
Shangcheng Xu ◽  
Guohua Gong ◽  
Wang Wang
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Cardiac Myocytes ◽  
Mitochondrial Respiration ◽  
High Fat Diet ◽  
High Fatty Acid ◽  
Ros Production ◽  
High Fat ◽  
Heart Dysfunction

Metabolic syndrome, featured by obesity and diabetes, is an independent risk factor for cardiovascular disease. The high availability of free fatty acids characteristic of obesity has been proposed to increase fatty acid oxidation, impair mitochondrial function, stimulate reactive oxygen species (ROS) production and eventually lead to oxidative stress, which then would cause myocyte damage and heart dysfunction. However, the role of oxidative stress as the initial cause of obesity-induced heart failure is controversial. We evaluated the time-dependent effect of fatty acids in vitro in adult rat cardiac myocytes (treated with palmitate and oleate, the major saturated and unsaturated fatty acids in the plasma, respectively), and in vivo in mice fed a high-fat diet (fat calories = 60%). Palmitate and oleate dose-dependently stimulated mitochondrial respiration and superoxide flash activity, a respiration-coupled bursting ROS production event in single mitochondria. The flash frequency increased 2-fold (0.1 mM, the physiological level in plasma) and 3-fold (0.3 mM, the plasma level found in obese subjects) after only 2 hr incubation and up to 24 hr, increase that could be blocked by the CPT1 inhibitor etomoxir (100uM). Surprisingly, there was no obvious mitochondrial oxidative stress, although the high level of fatty acids caused mPTP opening and cell death at 48 hr. Further, aconitase activity was normal and NAD/NADH ratio was decreased, indicating a more reduced status rather than oxidative stress. Intriguingly, mitochondrial membrane potential was slightly lowered after only 2 hr of treatment. Finally, the high-fat diet-fed mice developed heart dysfunction after 12 weeks of treatment, but oxidative stress only appeared after 18 weeks. In the light of these results, we hypothesize that high fatty acid supply induced multiple adaptive and mal-adaptive responses in cardiac myocytes. The increased mitochondrial respiration and bursting ROS production is offset by a mild uncoupling and increased reducing equivalents. Therefore, oxidative stress is unlikely an initial cause of myocyte death and heart dysfunction in obesity, but rather a consequence of mitochondrial dysfunction, although the exact cause of this dysfunction remains to be elucidated.

Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp (Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Secondary Metabolites ◽  
Human Health ◽  
Grass Carp ◽  
Aquatic Environment ◽  
Ctenopharyngodon Idellus

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.

Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov
Keyword(s):  
Oxidative Stress ◽  
Head And Neck ◽  
Transcriptional Activation ◽  
Platinum Resistance ◽  
Mrna Levels ◽  
Strong Positive Correlation ◽  
Platinum Compounds ◽  
Copper Chelation ◽  
Novel Approach ◽  
Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Pancreatic stones shockwave lithotripsy induces oxidative stress. A study of lipoperoxidation products in pure pancreatic juice

2001 ◽  
Vol 120 (5) ◽  
pp. A217-A217
Author(s):  
C SPADA ◽  
S SANTINI ◽  
F FOSCHIA ◽  
M PANDOLFI ◽  
V PERRI ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Juice ◽  
Shockwave Lithotripsy ◽  
Pure Pancreatic Juice ◽  
Pancreatic Stones

Dilinoleoylphosphatidylcholine (DLPC) protects against alcohol-induced oxidative stress in rats

2001 ◽  
Vol 120 (5) ◽  
pp. A116-A116
Author(s):  
S ALEYNIK ◽  
M ALEYNIK ◽  
C LIEBER
Keyword(s):  
Oxidative Stress
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