Particulate matter and oxidative stress: dangerous partners in inflammation, vascular dysfunction and innate immunity

2011 ◽  
pp. 157-169
Author(s):  
Steve N. Georas ◽  
Mark W. Frampton
2016 ◽  
Vol 87 ◽  
pp. 199-208 ◽  
Author(s):  
Weerapon Sangartit ◽  
Poungrat Pakdeechote ◽  
Veerapol Kukongviriyapan ◽  
Wanida Donpunha ◽  
Shigeki Shibahara ◽  
...  

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Edward M Powers ◽  
Murat Fudim ◽  
Heidi J Silver ◽  
Robert W Fitch ◽  
Kevin D Niswender

Background: Former football players (FP) who competed with BMI > 30 have high rates of atherosclerosis and early mortality (28% by age 50). FP are disproportionately black, a group predisposed to hypertension and atherosclerosis. Hypothesis: Positive energy balance and oxidative stress lead to vascular dysfunction in black FP. Methods: High BMI college FP (n=33) underwent metabolic and vascular testing at the Vanderbilt Medical Center during the offseason training program. Endothelial function was tested using flow-mediated dilation (FMD) of the brachial artery. Arterial elasticity and vascular resistance were tested using a calibrated tonometer. Regression was performed using least squares on Stat, version 12. Results: Elevated blood pressure (EBP) (SBP > 130) was common in both black (n = 14) and white (n = 19) athletes (78% vs 63%, p = .34). Black players had significantly higher systemic vascular resistance and lower arterial elasticity. However, they had significantly better lipid profiles and body composition, and comparable insulin resistance assessed by HOMA. In black FP, EBP was associated with positive energy balance (4.3 kg gained during six weeks from enrollment to clinic visit vs. 0.7 kg, p = .05). Daily caloric intake predicted endothelial function as measured by flow mediated vasodilation (FMD) (r=.76, p=.001). Caloric intake and oxidative stress (F2-isoprostanes) trended to inversely correlate with larger artery elasticity (r=.40, p=.09 and r=.41, p=.09, respectively). HOMA did not predict FMD (r < .01, p = .56). Respiratory quotient (RQ) correlated with f2-isoprostanes (r=.53, p=.02), suggesting a link between mitochondrial dysfunction and oxidative stress. Conclusion: High BMI black FP suffer from vascular dysfunction, possibly due to oxidative stress from overfeeding. This correlates with studies of non-athlete adult population, but differs notably in being independent of insulin resistance. A larger, longitudinal study is needed to establish a link between overfeeding, vascular dysfunction and early cardiovascular morbidity and mortality in high BMI black athletes. The role of oxidative stress and selective use of nitric oxide donor drugs in black athletes should be explored.


Aging Cell ◽  
2016 ◽  
Vol 16 (1) ◽  
pp. 17-26 ◽  
Author(s):  
Lisa A. Lesniewski ◽  
Douglas R. Seals ◽  
Ashley E. Walker ◽  
Grant D. Henson ◽  
Mark W. Blimline ◽  
...  

2005 ◽  
Vol 18 (2) ◽  
pp. 213-219 ◽  
Author(s):  
M NYBY ◽  
K MATSUMOTO ◽  
K YAMAMOTO ◽  
K ABEDI ◽  
P ESLAMI ◽  
...  

Chemosphere ◽  
2017 ◽  
Vol 173 ◽  
pp. 124-134 ◽  
Author(s):  
Melissa Marcoccia ◽  
Lucilla Ronci ◽  
Elvira De Matthaeis ◽  
Andrea Setini ◽  
Cinzia Perrino ◽  
...  

2010 ◽  
Vol 95 (8) ◽  
pp. 3783-3787 ◽  
Author(s):  
Joshua A. Beckman ◽  
Allison B. Goldfine ◽  
Alison Goldin ◽  
Adnan Prsic ◽  
Sora Kim ◽  
...  

Context: Antagonism of protein kinase Cβ (PKCβ) restores endothelial function in experimental models of diabetes and prevents vascular dysfunction in response to hyperglycemia in healthy humans. Objective: We tested the hypothesis that PKCβ antagonism would improve vascular function in subjects with type 2 diabetes compared with healthy control subjects. Design: The effect of PKCβ was evaluated in a randomized, placebo-controlled, double-blinded crossover trial. Setting: The study was performed in the outpatient setting of a university medical center. Participants: Thirteen subjects with type 2 diabetes without evidence of cardiovascular disease and 15 healthy control subjects were recruited via newspaper advertisement. Intervention: Subjects underwent a randomized, double-blind, crossover, placebo-controlled trial of the selective PKCβ antagonist ruboxistaurin mesylate. Subjects received each treatment for 14 d. Main Outcome Measure: Endothelium-dependent and endothelium-independent vasodilation of forearm resistance vessels was measured with mercury-in-silastic, strain-gauge plethysmography during intraarterial administration of methacholine chloride and verapamil, respectively. Markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress were measured after each treatment. Results: Endothelium-dependent vasodilation of forearm resistance vessels was attenuated in diabetic subjects when compared with healthy subjects (P = 0.001). Endothelium-independent vasodilation did not differ between groups (P value not significant). Ruboxistaurin did not significantly change endothelium-dependent or endothelium-independent vasodilation or blood-based markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress in either diabetic or healthy subjects. Conclusion: Endothelial dysfunction of forearm resistance vessels was not improved by 2 wk of selective PKCβ inhibition in patients with diabetes. These results suggest that PKCβ does not contribute significantly to vascular dysfunction in otherwise healthy patients with type 2 diabetes.


2016 ◽  
Vol 130 (13) ◽  
pp. 1039-1050 ◽  
Author(s):  
Victoria Austin ◽  
Peter J. Crack ◽  
Steven Bozinovski ◽  
Alyson A. Miller ◽  
Ross Vlahos

Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and loss of lung function, and is currently the third largest cause of death in the world. It is now well established that cardiovascular-related comorbidities such as stroke contribute to morbidity and mortality in COPD. The mechanisms linking COPD and stroke remain to be fully defined but are likely to be interconnected. The association between COPD and stroke may be largely dependent on shared risk factors such as aging and smoking, or the association of COPD with traditional stroke risk factors. In addition, we propose that COPD-related systemic inflammation and oxidative stress may play important roles by promoting cerebral vascular dysfunction and platelet hyperactivity. In this review, we briefly discuss the pathogenesis of COPD, acute exacerbations of COPD (AECOPD) and cardiovascular comorbidities associated with COPD, in particular stroke. We also highlight and discuss the potential mechanisms underpinning the link between COPD and stroke, with a particular focus on the roles of systemic inflammation and oxidative stress.


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