Testosterone induces leucocyte migration by NADPH oxidase-driven ROS- and COX2-dependent mechanisms

2015 ◽  
Vol 129 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Andreia Z. Chignalia ◽  
Maria Aparecida Oliveira ◽  
Victor Debbas ◽  
Randal O. Dull ◽  
Francisco R.M. Laurindo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Risk ◽  
Cardiovascular Diseases ◽  
Nadph Oxidase ◽  
Vascular Disease ◽  
Leucocyte Migration ◽  
And Oxidative Stress

Testosterone triggers leucocyte migration and oxidative stress, important features in inflammation and in the development of cardiovascular diseases. The mechanisms by which testosterone increase cardiovascular risk are unknown. We describe one pathway whereby testosterone can potentially contribute to vascular disease.

scholarly journals Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

2017 ◽  
Vol 5 (1) ◽  
pp. 71 ◽  
Author(s):  
Wael Alanazi ◽  
Mohammad Uddin ◽  
Selim Fakhruddin ◽  
Keith Jackson
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Kidney Injury ◽  
Organ Damage ◽  
Day Surgery ◽  
Receptor Expression ◽  
Sprague Dawley ◽  
Subunit Expression ◽  
Renal Biomarker ◽  
And Oxidative Stress

Background: Recurrent insulin-induced hypoglycemia (RIIH) is an avoidable consequence in the therapeutic management of diabetes mellitus. RIIH has been implicated in causing hypertension through an increase in renal and systemic AngII production.Objective: The present study was performed to assess the hypothesis that chronic insulin treatment enhances AngII and COX2 formation which in turn increases (pro) renin receptor (PRR) expression and NADPH oxidase-mediated oxidative stress, leading to renal and cardiac injury.Methods: The present studies were conducted in Male Sprague Dawley rats treated with daily subcutaneous injections of 7u/kg insulin or saline for 14 days. On the 14th day, surgery was performed for treatment infusion (captopril 12mg/kg, NS398 0.3mg/kg or vehicle), and renal interstitial fluid sample and urine collections for biomarker measurements. At the end of the experiments, kidneys and hearts were harvested to evaluate PRR and NOX2 (NADPH oxidase subunit) expression and oxidative stress.Results: We found that RIIH enhanced AngII and COX2 activity, leading to renal PRR expression and NADPH oxidase-induced oxidative stress in the heart and kidney. 8-isoprostane was evaluated as a renal biomarker of oxidative stress, which was induced in insulin treated animals and modulated by captopril and NS398. In addition, there was a slight increase in NGAL, a urinary biomarker of acute kidney injury (AKI), in insulin treated animals when compared to control.Conclusion: These results demonstrate that RIIH induces renal PRR expression and oxidative stress through increasing AngII and COX2 in the heart and kidney, leading to end-organ damage.

scholarly journals Aging increases vulnerability to stress-induced depression via upregulation of NADPH oxidase in mice

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Jung-Eun Lee ◽  
Hye-Jin Kwon ◽  
Juli Choi ◽  
Ji-Seon Seo ◽  
Pyung-Lim Han
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Chronic Stress ◽  
Brain Aging ◽  
Aged Mice ◽  
Upstream Regulator ◽  
Underlying Mechanisms ◽  
Old Mice ◽  
And Oxidative Stress ◽  
Young Mice

AbstractBrain aging proceeds with cellular and molecular changes in the limbic system. Aging-dependent changes might affect emotion and stress coping, yet the underlying mechanisms remain unclear. Here, we show aged (18-month-old) mice exhibit upregulation of NADPH oxidase and oxidative stress in the hippocampus, which mirrors the changes in young (2-month-old) mice subjected to chronic stress. Aged mice that lack p47phox, a key subunit of NADPH oxidase, do not show increased oxidative stress. Aged mice exhibit depression-like behavior following weak stress that does not produce depressive behavior in young mice. Aged mice have reduced expression of the epigenetic factor SUV39H1 and its upstream regulator p-AMPK, and increased expression of Ppp2ca in the hippocampus—changes that occur in young mice exposed to chronic stress. SUV39H1 mediates stress- and aging-induced sustained upregulation of p47phox and oxidative stress. These results suggest that aging increases susceptibility to stress by upregulating NADPH oxidase in the hippocampus.

scholarly journals Role of Gender and Physical Activity Level on Cardiovascular Risk Factors and Biomarkers of Oxidative Stress in the Elderly

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Antoine Raberin ◽  
Philippe Connes ◽  
Jean-Claude Barthélémy ◽  
Pia Robert ◽  
Sébastien Celle ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Diseases ◽  
Cardiovascular Risk Factors ◽  
The Elderly ◽  
Activity Level ◽  
Advanced Oxidation Protein Products ◽  
The Impact

Background. Cardiovascular diseases remain as the leading cause of morbidity and mortality in industrialized countries. Ageing and gender strongly modulate the risk to develop cardiovascular diseases but very few studies have investigated the impact of gender on cardiovascular diseases in the elderly, which represents a growing population. The purpose of this study was to test the impact of gender and physical activity level on several biochemical and clinical markers of cardiovascular risk in elderly individuals. Methods. Elderly individuals (318 women (75.8±1.2 years-old) and 227 men (75.8±1.1 years-old)) were recruited. Physical activity was measured by a questionnaire. Metabolic syndrome was defined using the National Cholesterol Education Program Expert Panel’s definition. Polysomnography and digital tonometry were used to detect obstructive sleep apnea and assess vascular reactivity, respectively. Blood was sampled to measure several oxidative stress markers and adhesion molecules. Results. The frequency of cardiovascular diseases was significantly higher in men (16.4%) than in women (6.1%) (p<0.001). Body mass index (25.0±4.3 vs. 25.8±3.13 kg.m−2) and glycaemia (94.9±16.5 vs. 101.5±22.6 mg.dL−1) were lower, and High Density Lipoprotein (HDL) (74.6±17.8 vs. 65.0±17.2 mg.dL−1) was higher in women compared to men (p<0.05). Oxidative stress was lower in women than in men (uric acid: 52.05±13.78 vs. 59.84±13.58, advanced oxidation protein products: 223±94 vs. 246±101 μmol.L−1, malondialdehyde: 22.44±6.81 vs. 23.88±9.74 nmol.L−1). Physical activity was not associated with lower cardiovascular risk factors in both genders. Multivariate analyses showed an independent effect of gender on acid uric (β=0.182; p=0.020), advanced oxidation protein products (β=0.257; p<0.001), and HDL concentration (β=−0.182; p=0.026). Conclusion. These findings suggest that biochemical cardiovascular risk factors are lower in women than men which could explain the lower cardiovascular disease proportion observed in women in the elderly.

scholarly journals Biomechanical Forces and Oxidative Stress: Implications for Pulmonary Vascular Disease

2019 ◽  
Vol 31 (12) ◽  
pp. 819-842 ◽  
Author(s):  
Evgeny A. Zemskov ◽  
Qing Lu ◽  
Wojciech Ornatowski ◽  
Christina N. Klinger ◽  
Ankit A. Desai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vascular Disease ◽  
Pulmonary Vascular Disease ◽  
Biomechanical Forces ◽  
And Oxidative Stress

scholarly journals Autophagy and oxidative stress in cardiovascular diseases

2015 ◽  
Vol 1852 (2) ◽  
pp. 243-251 ◽  
Author(s):  
Yu Mei ◽  
Melissa D. Thompson ◽  
Richard A. Cohen ◽  
XiaoYong Tong
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
And Oxidative Stress

scholarly journals Review of polymorphisms, associated with cardiovascular diseases

2021 ◽  
pp. 333-338
Author(s):  
A. A. Akopyan ◽  
I. D. Strazhesko ◽  
O. N. Tkacheva ◽  
A. P. Yesakova ◽  
I. A. Orlova
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiovascular Diseases ◽  
Chronic Inflammation ◽  
Gene Polymorphisms ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
System Activation ◽  
And Oxidative Stress

In this research we examined studies of gene polymorphisms, associated with cardiovascular diseases through renin-angiotensin-aldosterone system activation (AGT с.521С>Т, AСE Ins>Del), nitric oxide decline (NOS3 с.894G>T), chronic inflammation (TNF -238G>A, MMP9 -1562С>T) and oxidative stress (CYBA c.214Т>С).

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