Oxidative Stress

Faraci, Frank M.

doi:10.1161/01.str.0000153067.27288.8b

Cited by 64 publications

(23 citation statements)

References 34 publications

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“…6,9,19,28 Our data support this hypothesis, as superoxide levels were significantly increased in old MnSOD ϩ/Ϫ mice and this increase could be inhibited with a scavenger of superoxide.…”

Section: Discussionsupporting

confidence: 80%

“…[1][2][3][4][5] Although vascular dysfunction can encompass a variety of defects in multiple homeostatic mechanisms, it is believed that decreased bioavailability of nitric oxide (NO, a major endothelium-derived relaxing factor) is a primary cause of endothelial dysfunction in disease. 6 The bioactivity of NO depends, in part, on its interaction with reactive oxygen species, particularly that of superoxide anion. 6 NO reacts with superoxide to form peroxynitrite at a rate 3 times faster than the dismutation of superoxide by superoxide dismutases (SODs).…”

mentioning

confidence: 99%

“…6 The bioactivity of NO depends, in part, on its interaction with reactive oxygen species, particularly that of superoxide anion. 6 NO reacts with superoxide to form peroxynitrite at a rate 3 times faster than the dismutation of superoxide by superoxide dismutases (SODs). 7 Local steady-state levels of superoxide are dependent in large part on activity of endogenous SODs, of which there are 3 isoforms: cystolic CuZn-SOD (SOD1), mitochondrial or MnSOD (SOD2), and extracellular CuZnSOD (ECSOD, SOD3).…”

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confidence: 99%

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Effect of Aging, MnSOD Deficiency, and Genetic Background on Endothelial Function

Brown

Didion

Andresen

et al. 2007

ATVB

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Objective-The goal of this study was to compare vascular function, superoxide levels, and MnSOD protein expression in young (4 to 7 months) and old (22 to 24 months) MnSOD ϩ/ϩ and MnSOD-deficient (MnSOD ϩ/Ϫ ) mice. Methods and Results-Relaxation of aorta in vitro to the endothelium-dependent dilator acetylcholine (ACh) was similar in young MnSOD ϩ/ϩ (nϭ9) and young MnSOD ϩ/Ϫ (nϭ6) mice. This response was impaired in old MnSOD ϩ/ϩ (nϭ8) mice and old MnSOD ϩ/Ϫ mice (nϭ14), with dysfunction being greater in old MnSOD-deficient mice (eg, 100 mol/L ACh produced 77Ϯ3% [meanϮSE], 77Ϯ3%, 70Ϯ4%, and 57Ϯ4% relaxation in young MnSOD ϩ/ϩ , young MnSOD ϩ/Ϫ , old MnSOD ϩ/ϩ , and old MnSOD ϩ/Ϫ mice, respectively). The endothelial dysfunction was similar in mice on both C57BL/6 and CD-1 genetic backgrounds. In contrast to ACh, responses to the endothelium-independent dilator sodium nitroprusside were enhanced in old MnSOD ϩ/ϩ and MnSOD ϩ/Ϫ mice compared with both groups of young mice (PϽ0.05). Superoxide levels, as measured using lucigenin-enhanced chemiluminescence, were increased more than 2-fold in old MnSOD ϩ/Ϫ mice compared with old MnSOD ϩ/ϩ and young mice (PϽ0.05). Conclusions-These data provide the first direct evidence that MnSOD halpoinsufficiency results in increased vascular oxidative stress and endothelial dysfunction with aging. (Arterioscler Thromb Vasc

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“…6,9,19,28 Our data support this hypothesis, as superoxide levels were significantly increased in old MnSOD ϩ/Ϫ mice and this increase could be inhibited with a scavenger of superoxide.…”

Section: Discussionsupporting

confidence: 80%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of Aging, MnSOD Deficiency, and Genetic Background on Endothelial Function

Brown

Didion

Andresen

et al. 2007

ATVB

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“…Oxidative stress has been implicated in a number of inflammatory diseases, such as type-2 diabetes (Evans et al 2002), vascular diseases (Faraci 2005) and chronic inflammatory lung disease (Rahman & MacNee 1996). Oxidative stress does compromise endothelial cell function, a crucial mechanism in the development and progression of atherosclerosis (Bonomini et al 2008).…”

Section: Oxidative Stressmentioning

confidence: 99%

Evidence that periodontal treatment improves biomarkers and CVD outcomes

D’Aiuto

Orlandi

Gunsolley

2013

Journal of Periodontology

128

137

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Evidence that periodontal treatment improves biomarkers and CVD outcomes D'Aiuto F, Orlandi M, Gunsolley JC. Evidence that periodontal treatment improves biomarkers and CVD outcomes. AbstractAim: The aim of this review was to critically appraise the evidence on the impact of periodontal treatment of cardiovascular diseases (CVDs) biomarkers and outcomes. Methods: A systematic search was performed in Cinhal, Cochrane, Embase and Medline for relevant articles up to July 2012. Duplicate screening and reference hand searching were performed. Data were then summarized and evidence graded in tables. Results: The search resulted in: (a) no evidence on the effects of periodontal therapy on subclinical atherosclerosis, serum levels of CD40 ligand, serum amyloid A and monocyte chemoattractant protein-1, (b) limited evidence on the effects of periodontal therapy on arterial blood pressure, leucocyte counts, fibrinogen, tissue necrosis factor-a, sE-selectin, von Willebrand factors, d-dimers, matrix metalloproteinases, oxidative stress and CVD events, and (c) moderate evidence suggesting a negligible effect of periodontal therapy in reducing interleukin-6 and lipids levels, whilst a positive effect in reducing serum C-reactive protein levels and improving endothelial function. Conclusions: Periodontal therapy triggers a short-term inflammatory response followed by (a) a progressive and consistent reduction of systemic inflammation and (b) an improvement in endothelial function. There is however limited evidence that these acute and chronic changes will either increase or reduce CVD burden of individuals suffering from periodontitis in the long term.

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“…[1][2][3] Increased levels of reactive oxygen species contribute to vascular pathophysiology. 4 In addition to its rate of production by superoxide dismutases (SODs), steadystate levels of H 2 O 2 are also determined by the activity of glutathione peroxidases (GPxs), which metabolize H 2 O 2 to water. [5][6][7] Increasing evidence suggests that H 2 O 2 may play diverse and important roles in vascular biology.…”

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confidence: 99%

Glutathione Peroxidase-1 Plays a Major Role in Protecting Against Angiotensin II–Induced Vascular Dysfunction

et al. 2008

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Abstract-Levels of reactive oxygen species, including hydrogen peroxide , increase in blood vessels during hypertension and in response to angiotensin II (Ang II). Although glutathione peroxidases are known to metabolize hydrogen peroxide, the role of glutathione peroxidase during hypertension is poorly defined. We tested the hypothesis that glutathione peroxidase-1 protects against Ang II-induced endothelial dysfunction. Responses of carotid arteries from Gpx1-deficient (Gpx1 ϩ/Ϫ and Gpx1 Ϫ/Ϫ ) and Gpx1 transgenic mice, and their respective littermate controls, were examined in vitro after overnight incubation with either vehicle or Ang II. Under control conditions, relaxation to acetylcholine (ACh; an endothelium-dependent agonist) was similar in control, Gpx1 ϩ/Ϫ , and Gpx1 transgenic mice, whereas in Gpx1 Ϫ/Ϫ mice, responses to ACh were impaired. In control mice, ACh-induced vasorelaxation was not affected by 1 nmol/L of Ang II. In contrast, relaxation to ACh in arteries from Gpx1 ϩ/Ϫ mice was inhibited by Ϸ60% after treatment with 1 nmol/L of Ang II, indicating that Gpx1 haploinsufficiency markedly enhances Ang II-induced endothelial dysfunction. A higher concentration of Ang II (10 nmol/L) selectively impaired relaxation to ACh in arteries from control mice, and this effect was prevented in arteries from Gpx1 transgenic mice or in arteries from control mice treated with polyethylene glycol-catalase (which degrades hydrogen peroxide). Thus, genetic and pharmacological evidence suggests a major role for glutathione peroxidase-1 and hydrogen peroxide in Ang II-induced effects on vascular function. (Hypertension. 2008;51:872-877.)

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Oxidative Stress

Cited by 64 publications

References 34 publications

Effect of Aging, MnSOD Deficiency, and Genetic Background on Endothelial Function

Effect of Aging, MnSOD Deficiency, and Genetic Background on Endothelial Function

Evidence that periodontal treatment improves biomarkers and CVD outcomes

Glutathione Peroxidase-1 Plays a Major Role in Protecting Against Angiotensin II–Induced Vascular Dysfunction

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