Oxidative stress is involved in the pathogenesis of atherosclerosis. A variety of antioxidants has been used in clinical studies, during the past few years, for the prevention and treatment of atherosclerosis. In small clinical studies it was found that both vitamins C and E may improve endothelial function in high risk patients. However, interventional trials have been controversial, with some positive findings, many null findings, and some suggestion of harm in certain high-risk populations. Therefore, treatment with antioxidant vitamins C and E should not be recommended for the prevention or treatment of coronary atherosclerosis. New antioxidant strategies are needed to clarify the exact role of antioxidant treatment in coronary atherosclerosis.
"An increasing number of studies focus on the role of reactive oxygen species (ROS) in the pathogenesis of premature ageing as well as of numerous civilization diseases, such as cardiovascular diseases [1–3]. It has been suggested that higher antioxidant potential can protect the organism against undesirable ROS activity and thus prevent disease incidence . However, the present state of knowledge on such dependence is still not complete . "
[Show abstract][Hide abstract] ABSTRACT: Whether the incidence of coronary heart disease (CHD) is related to a decrease in total antioxidant capacity (TAC) has not yet been completely clarified. We assessed TAC of blood serum in a group of 163 men with CHD aged 34.8-77.0 years and in 163 age-matched peers without CHD. Two spectrophotometric methods were applied to assess TAC: ferric reducing ability of serum (TAC-FRAS) and 2.2-diphenyl-1-picryl-hydrazyl (TAC-DPPH) tests. In the CHD group, multivariate analysis revealed that uric acid (UA), triglycerides, and systolic blood pressure contributed independently to the TAC-FRAS variance. TAC-DPPH was favorably predicted by UA concentration, but negatively so by current smoking and glucose levels. In men without CHD, UA was the only independent determinant of both TAC-FRAS and TAC-DPPH. Presence of CHD was not an independent predictor of TAC-observed between-group differences (higher TAC in CHD patients) disappeared after adjustment for other confounders. We conclude that UA is the main determinant of TAC of blood serum in men. TAC is not directly influenced by age or CHD but is related to several indices of overweight/obesity and laboratory measures of metabolic syndrome, especially in patients with CHD.
BioMed Research International 08/2014; 2014:216964. DOI:10.1155/2014/216964 · 3.17 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The angle θ that a rigid gravity pendulum driven by
sinusoidal torque makes with the vertical satisfies d <sup>2
</sup>θ/ dt <sup>2</sup>+(2π Q <sub>I</sub>)
<sup>2</sup> sin(θ)= D
cos(2π Q <sub>M</sub> t ). The undriven average tune
Q <sub>free</sub> is Q <sub>I</sub> for small angle
oscillations, but decreases to zero as the amplitude is increased to
π. In general, the driven system behavior depends on D and
Q <sub>M</sub>, the amplitude and tune of the driving torque.
One of four dynamical phases which exist in the ( D , Q
<sub>M</sub>) parameter space exhibits massive chaos. The tune
modulation part of the E778 nonlinear dynamics experiment tests the
validity of the theoretical models which describe three phases, in an
accelerator representation of this extremely simple system. The authors
describe the models and present some of the experimental rules. Tune
modulation is shown to play an important role in limiting the
performance of proton storage rings like the SSC (Superconducting Super
Particle Accelerator Conference, 1989. Accelerator Science and Technology., Proceedings of the 1989 IEEE; 04/1989
[Show abstract][Hide abstract] ABSTRACT: Recent studies from our laboratory and others have shown that increases in cytoplasmic superoxide (O(2)(·-)) levels and Akt activation play a key role in agonist-stimulated NF-κB activation and cardiomyocyte hypertrophy in vitro. In this study, we tested the hypothesis that adenovirus (Ad)-mediated intramyocardial gene transfer of cytoplasmic superoxide dismutase (AdCu/ZnSOD) or a dominant-negative form of Akt (AdDNAkt) in mice would attenuate pressure overload-induced increases in activation of the redox-sensitive transcription factor NF-κB and cardiac hypertrophy. Adult C57BL/6 mice were subjected to thoracic aortic banding (TAB) or sham surgery, and intramyocardial injections of viral vectors (AdCu/ZnSOD, AdDNAkt, or control) were performed. There was robust transgene expression in the heart, which peaked 6-7 days after injection and then declined to undetectable levels by 12-14 days. In mice injected with AdBgL II, TAB caused a significant increase in O(2)(·-) generation and cardiac mass at 1 wk, and these responses were markedly attenuated by AdCu/ZnSOD. In addition, TAB induced time-dependent activation of NF-κB in the myocardium as measured longitudinally by in vivo bioluminescent imaging of NF-κB-dependent luciferase expression. This was also abolished by intracardiac AdCu/ZnSOD or AdDNAkt, but not the control vector. The inhibition of Akt and O(2)(·-)-mediated NF-κB activation in TAB hearts was associated with an attenuation of cardiac hypertrophy. Since a direct cause-and-effect relationship between NF-κB activation and cardiomyocyte hypertrophy has been established previously, our data support the hypothesis that increased O(2)(·-) generation and Akt activation are key signaling intermediates in pressure overload-induced activation of NF-κB and cardiac hypertrophy.
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