Inhibition of Cu2+-Induced LDL Oxidation by Nitric Oxide: A Study Using Donors with Different Half-Time of NO Release

Seccia, M.; Perugini, C.; Albano, Emanuele; Bellomo, Giorgio

doi:10.1006/bbrc.1996.0401

Cited by 39 publications

(16 citation statements)

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“…Hypercholesterolemia and other factors predisposing to atherosclerosis, such as hypertension, diabetes, and smoking synergistically impair endothelial function [65][66][67]. Endothelial dysfunction is thought to play a key role in the onset and progression of atherosclerosis as well as in its clinical implications [68].…”

Section: Endothelial Dysfunction In Cardiovascular Diseasementioning

confidence: 99%

Influence of Statin Use on Endothelial Function: From Bench to Clinics

Martı́nez-González

Badimon

2007

CPD

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Endothelial dysfunction has been shown to be a prognostic factor for cardiovascular disease and improvement of endothelial dysfunction prevents cardiovascular event presentation. Endothelial dysfunction is associated to a reduced nitric oxide (NO) bioactivity, as a result of the impairment of NO synthesis/release by the endothelial NO synthase (eNOS) or by inactivation of NO. Endothelial dysfunction measurements are valuable surrogate markers to assess the effectiveness of interventions addressed to prevent or treat coronary heart disease (CHD). Dyslipemia and other cardiovascular risk factors promote endothelial dysfunction and life style changes and pharmacological treatment, particularly HMG-CoA reductase inhibitors (statins), have shown early improve of endothelial-dependent vasomotion. Statins efficiently reduce plasma LDL cholesterol, an effect that may account for their beneficial effect on endothelial function, but they also reduce cellular levels of isoprenoid compounds relevant for the bioavailability of NO. Statins restore NO production by several mechanisms, including up-regulation of eNOS mRNA and protein levels and preservation of NO inactivation by reactive oxygen species (ROS). These effects are mediated, at least in a part, through mechanisms independent of their lipid lowering effect (pleiotropic effects). In this article we discuss the relevance of endothelium-dependent effects on the early and delayed clinical benefit of statins, as well as the multiple ways by which statins may restore endothelial function acting not only on the endothelium but also on endothelial progenitor cells (EPC), which likely could contribute to both ischemia-induced neovascularization and endothelial regeneration after injury.

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Section: Endothelial Dysfunction In Cardiovascular Diseasementioning

confidence: 99%

Influence of Statin Use on Endothelial Function: From Bench to Clinics

Martı́nez-González

Badimon

2007

CPD

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“…NO release from NOC-18 has a half-time of more than 500 min at physiological pH. 33 Two clonal cell lines expressing the G39A mutant SOD1 were more sensitive to the toxic effects of NOC-18 than vector clones over all tested concentrations of NOC-18, with cells expressing wild-type SOD1 having an intermediate sensitivity. Two-way ANOVA revealed that the differences between cell lines were highly signi cant (P < 0.001), as was the effect of increasing concentrations of NOC18 (P < 0.001).…”

Section: Cell Death Induced By No Donorsmentioning

confidence: 99%

Cu/Zn superoxide dismutase (SOD1) mutations associated with familial amyotrophic lateral sclerosis (ALS) affect cellular free radical release in the presence of oxidative stress

Cookson

Menzies²,

Manning³

et al. 2002

ALS

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“…DETA-NO, a diazeniumdiolate-class NO donor, is a watersoluble zwitterionic triamine/NO adduct, with a half-life of approximately 20 hours (21,26,29,51,55). Diazeniumdiolates are chemical compounds that carry the [N(O)NO]Ϫ functional group (29).…”

Section: Sahmentioning

confidence: 99%