OXIDATIVE STRESS PARTICIPATES IN THE CARDIOVASCULAR RISKS INCREASING IN JAPANESE-HAWAIIAN WOMEN

2004 ◽  
Vol 22 (Suppl. 1) ◽  
pp. S107
Author(s):  
H Negishi ◽  
K Ikeda ◽  
Y Yamori
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Risks ◽  
Hawaiian Women

Cardiovascular risks in patients with psoriasis (literature review)

2021 ◽  
pp. 12-17
Author(s):  
A. A. Hotko ◽  
N. S. Rudneva
Keyword(s):  
Oxidative Stress ◽  
Genetic Factors ◽  
Mortality Rates ◽  
Cardiovascular Risks ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Cardiovascular Pathology ◽  
Lipoprotein Composition ◽  
And Function ◽  
The Relationship

The article is of an overview nature and contains up-to-date information on comorbid cardiovascular pathology in psoriasis. Various studies have shown that psoriasis is associated with a higher prevalence of CVD risk factors, including hypertension, diabetes mellitus, dyslipidemia, obesity, and metabolic syndrome. The relationship between the severity of psoriasis and the risk of cardiovascular disease, as well as the prognostic risks with mortality rates, are discussed. Proposed common pathogenetic mechanisms include genetic factors, inflammatory pathways, adipokine secretion, insulin resistance, lipoprotein composition and function, angiogenesis, oxidative stress, and hypercoagulability.

scholarly journals Autonomic impairment and oxidative stress: Relationship in PCOS patients

2020 ◽  
Vol 14 (2) ◽  
pp. 82-88
Author(s):  
Musfika Mostafa ◽  
Sultana Ferdousi ◽  
Shamima Sultana ◽  
Ayesha Akhter
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Heart Rate ◽  
Standard Deviation ◽  
Polycystic Ovary ◽  
Digital Data ◽  
Autonomic Nerve ◽  
Cardiovascular Risks ◽  
Rr Intervals ◽  
And Oxidative Stress

Background: Polycystic ovary syndrome (PCOS) is one of the most common, heterogeneous endocrine disorder of reproductive aged women. Association of autonomic impairment and elevated oxidative stress may predispose these patients to increased cardiovascular risks. Objective: To evaluate the relationship between cardiac autonomic nerve function (CANF) and oxidative stress in patients with PCOS. Methods: This cross sectional study was conducted in Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Shahbag, Dhaka from September, 2018 to August, 2019. For this study, 30 newly diagnosed PCOS patients aged 20-35 years were recruited and similar age, body mass index (BMI) 30 apparently healthy, regularly menstruating women were enrolled as control. CANF was assessed by analyzing time domain measures of Heart Rate Variability (HRV). HRV data were recorded by a digital data acquisition device, Powerlab 8/35 (AD instruments, Australia). For evaluation of oxidative stress, plasma catalase and plasma Malondialdehyde (MDA) levels were measured. Statistical analysis was done by unpaired “t” test and Pearson’s correlation test as applicable. Results: In this study, resting pulse rate, systolic blood pressure (SBP), diastolic blood pressure (DBP) were significantly higher (p<0.001, p<0.01, p<0.01 respectively) and standard deviation of the RR intervals (SDRR) (p<0.01), mean R-R interval, standard deviation of the difference between successive RR intervals (SDSD), square root of mean squared differences of successive RR intervals (RMSSD), proportion of RR interval with duration >50 ms (pRR50%) were significantly lower (p<0.001) in PCOS than healthy controls. In addition, plasma catalase was significantly lower (p<0.01) and plasma MDA was significantly higher (p<0.001) in PCOS patients compared to controls. On correlation analysis, mean heart rate, SDRR, SDSD, RMSSD and pRR50% showed negative correlation with plasma catalase and plasma MDA (p<0.05) in PCOS patients but these were not significant. Conclusion: The present study reveals that reduced parasympathetic activity in PCOS patients may be related to oxidative stress. J Bangladesh Soc Physiol. 2019, December; 14(2): 82-88

Abstract 500: Impact of Oxidative Stress and Fancj on Heart Health

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Kaitlin A Lowran ◽  
Mikayla McCarthy ◽  
Laura Campbell ◽  
Colin Wu
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Sequences ◽  
Oxidative Dna Damage ◽  
Dna Helicase ◽  
Cardiac Cells ◽  
Cardiovascular Risks ◽  
Hydrogen Peroxide Treatment ◽  
Modified Dna ◽  
In Cells

G-quadruplexes (or G4s) are structures formed by guanine-rich nucleic acid sequences. G4s must be promptly unfolded in cells; otherwise, they can interfere with DNA replication, RNA transcription, and other essential processes. Guanines bases are susceptible to oxidative stress forming 8-oxoguanines (8oxoG). Although 8oxoG-modified DNA sequences can still fold into stable G4s, it is not known how 8oxoG4s are repaired in human cells. In our previous study, we have shown that the FANCJ DNA helicase targets G4s using an AKKQ amino acid motif. Here, we have examined the interactions of FANCJ with various 8oxoG4s using biolayer interferometry and fluorescence spectroscopy. We show that a FANCJ AKKQ peptide alone can recognize G4s with an affinity of 3.7uM. Moreover, this motif binds to 8oxoG4s with greater affinities of 1.3 to 2.3uM. A detailed description of the mechanisms by which 8oxoG4s are repaired is essential for understanding how human hearts respond to oxidative stress. To test the importance of FANCJ AKKQ-G4 interactions in cells, we measured the total extent of oxidative DNA damage in human cardiac cells by single-cell electrophoresis. Cells that overexpress FANCJ can readily overcome the chemical stress induced by hydrogen peroxide treatment and the G4-stabilizing compound telomestatin. On the contrary, cells that produce a FANCJ AAAQ mutant, which cannot interact with G4s, resulted in an accumulation of 8oxoG4s. Based on this evidence, FANCJ plays an important role to alleviate the damage caused by oxidative stress. In future experiments, we plan to further examine the cardiovascular risks of DNA damage caused by FANCJ malfunctions.

scholarly journals Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-26 ◽  
Author(s):  
Sebastian Steven ◽  
Katie Frenis ◽  
Matthias Oelze ◽  
Sanela Kalinovic ◽  
Marin Kuntic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Clinical Trials ◽  
Large Scale ◽  
Heme Oxygenase 1 ◽  
Cardiovascular Risks ◽  
Close Link ◽  
Defense Proteins ◽  
Inflammatory Disorders ◽  
Immunomodulatory Properties

Cardiovascular disease is a leading cause of death and reduced quality of life, proven by the latest data of the Global Burden of Disease Study, and is only gaining in prevalence worldwide. Clinical trials have identified chronic inflammatory disorders as cardiovascular risks, and recent research has revealed a contribution by various inflammatory cells to vascular oxidative stress. Atherosclerosis and cardiovascular disease are closely associated with inflammation, probably due to the close interaction of inflammation with oxidative stress. Classical therapies for inflammatory disorders have demonstrated protective effects in various models of cardiovascular disease; especially established drugs with pleiotropic immunomodulatory properties have proven beneficial cardiovascular effects; normalization of oxidative stress seems to be a common feature of these therapies. The close link between inflammation and redox balance was also supported by reports on aggravated inflammatory phenotype in the absence of antioxidant defense proteins (e.g., superoxide dismutases, heme oxygenase-1, and glutathione peroxidases) or overexpression of reactive oxygen species producing enzymes (e.g., NADPH oxidases). The value of immunomodulation for the treatment of cardiovascular disease was recently supported by large-scale clinical trials demonstrating reduced cardiovascular mortality in patients with established atherosclerotic disease when treated by highly specific anti-inflammatory therapies (e.g., using monoclonal antibodies against cytokines). Modern antidiabetic cardiovascular drugs (e.g., SGLT2 inhibitors, DPP-4 inhibitors, and GLP-1 analogs) seem to share these immunomodulatory properties and display potent antioxidant effects, all of which may explain their successful lowering of cardiovascular risk.

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.

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