Oxidative stress: a baystander or a causal contributor to atrial remodelling and fibrillation?

BACKGROUND: Atrial fibrillation (AF) could be triggered by inflammation and oxidative stress. Ganoderma lucidum has an active substance in the form of β-glucan that can reduce inflammatory process and oxidative stress in rats. The objective of this study was to evaluate the effect of Ganoderma lucidum polysaccharide peptide (GLPP) in paroxysmal AF subjects with parameters of anti-inflammatory antioxidant, electrocardiography and health-related quality of life (HRQoL).METHODS: A randomized closed-label clinical trial with pre- and post-test design was conducted. After AF subjects selection, the subjects were randomized, interviewed and veni-punctured to isolate blood plasma. AF Subjects were then treated with placebo or GLPP for 90 days. Post-test blood plasma was collected on the following day after the 90th day. Then anti-inflammatory and antioxidant parameters were measured. After that, echocardiographic and HRQoL assessments were performed.RESULTS: A total of 38 subjects, 11 males and 27 females, completed the study with no significant changes in diets, physical activities, or medications. Comparing to control, the 90-days GLPP-treated subject characteristics were significant difference in systolic blood pressure, heart rate, malondialdehyde, high-sensitivity C-reactive protein, tumor necrosis factor-a, interleukin (IL)-1b, IL-6, primary (P)-wave dispersion, P-max, physical functioning, limitation to physical health, energy/fatigue, pain, and physical limitation.CONCLUSION: GLPP has several potential effects in AF subjects, including anti-inflammatory, antioxidant, and atrial remodelling, so that HRQoL of AF subjects could be improved. Hence, GLPP could suggested as a potential supplementing agent for AF management.KEYWORDS: atrial fibrillation, Ganoderma lucidum, inflammation, antioxidant, atrial remodelling, quality of life

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

Food & Function ◽

10.1039/d0fo01638a ◽

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.

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

Biochemical Journal ◽

10.1042/bcj20190591 ◽

2019 ◽

Vol 476 (24) ◽

pp. 3705-3719 ◽

Cited By ~ 2

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.

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Clinical aspects of reactive oxygen and nitrogen species

Biochemical Society Symposium ◽

10.1042/bss0710121 ◽

2004 ◽

Vol 71 ◽

pp. 121-133 ◽

Cited By ~ 25

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.

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