scholarly journals The role of oxidative stress and NADPH oxidase in the pathogenesis of atherosclerosis

2017 ◽  
Vol 71 (1) ◽  
pp. 57-68
Author(s):  
Dorota Bryk ◽  
Wioletta Olejarz ◽  
Danuta Zapolska-Downar

Reactive oxygen species (ROS) play a key role in the pathogenesis of atherosclerosis. The main mechanisms which are involved are low-density lipoprotein oxidative modification, inactivation of nitric oxide and modulation of redox-sensitive signaling pathways. ROS contribute to several aspects of atherosclerosis including endothelial cell dysfunction, monocyte/macrophage recruitment and activation, stimulation of inflammation, and inducing smooth muscle cell migration and proliferation. NADPH oxidase is the main source of ROS in the vasculature. This enzyme consists of a membrane-bound heterodimer of gp91phox and p22phox, cytosolic regulatory subunits p47phox, p67phox and p40phox, and small GTP-binding proteins rac1 and rac 2. Seven distinct isoforms of this enzyme have been identified, of which four (NOX1, 2, 4 and 5) may have cardiovascular function. In this paper, we review the current state of knowledge concerning the role of oxidative stress and NOX enzymes in pathogenesis of atherosclerosis. Moreover, we analyze the experimental studies that explore the relationship between the NOX family and atherosclerosis.

Lupus ◽  
1998 ◽  
Vol 7 (2_suppl) ◽  
pp. 132-134 ◽  
Author(s):  
O Vaarala

In prospective studies, increased levels of cardiolipin-biding antibodies and autoantibodies to oxidized low-density lipoprotein (LDL) have been observed in patients with myocardial infarction (MI). These findings suggest that antiphospholipid antibodies may contribute to the development of MI. The ‘oxidative-modification hypothesis’ in the pathogenesis of atherosclerotic heart disease is based on the oxidation of LDL, its accumulation into arterial wall, and the development of chronic inflammation in the atheroma. Evidence of enhanced lipid peroxidation and its association with antiphospholipid antibodies has been recently reported in SLE patients. There is also epidemiological data showing a remarkably increased risk of MI in SLE. In this review, the role of different types of antiphospholipid antibodies in the development of atherosclerotic heart disease is evaluated with particular attention to their potential pathogenic mechanisms and the possibilities in the prevention of MI associated with antiphospholipid antibodies.


Metabolism ◽  
1999 ◽  
Vol 48 (12) ◽  
pp. 1503-1508 ◽  
Author(s):  
Antonio Ceriello ◽  
Nadia Bortolotti ◽  
Enrico Motz ◽  
Carlo Pieri ◽  
Michele Marra ◽  
...  

SURG Journal ◽  
2008 ◽  
Vol 1 (2) ◽  
pp. 82-90
Author(s):  
Cristina Cuda

The metabolic consequences of obesity have made this highly prevalent condition one of the most common risk factors for type 2 diabetes, hypertension and atherosclerosis. Simultaneous occurrence of these conditions can be explained through the manifestations of metabolic syndrome [MetS]. Clinical indication of MetS is characterized by a clustering of risk factors for complex chronic diseases which all feature metabolic deterioration as a common component. Diagnosis of MetS can be made if a patient exhibits three of the identified risk factors, some of which include: elevated waist circumference, elevated triglycerides, low high density lipoprotein levels, hypertension and elevated blood glucose. The progression from obesity to MetS involves an alteration in body metabolism mediated by cytokines- signalling molecules that coordinate the inflammatory response. Increased visceral adipose tissue contributes to augmented secretion of pro-inflammatory cytokines which can activate several transcription factors, including NF-κB, which promote these inflammatory conditions and lead to increased oxidative stress. Exacerbation of the condition then ensues as oxidative stress results in oxidized low density lipoprotein, dyslipidemia, insulin resistance, hypertension and atherogenesis. This review will not only focus on the role of inflammation in the manifestations of MetS, but also outlines some lifestyle and nutritional treatments that can be used to treat the condition and reduce the risk of chronic disease.


1995 ◽  
Vol 61 ◽  
pp. 55-63 ◽  
Author(s):  
B. Kalyanaraman

Thiyl radicals are formed from one-electron oxidation of thiols. Thiyl radicals participate in a number of reactions including electron transfer, hydrogen abstraction and addition reactions with several biological constituents and xenobiotics. Thiyl radicals can be detected by optical spectroscopy or by electron spin resonance (ESR) spectroscopy. Thiyl radicals appear to play a role in the nitrosylation of thiols and protein thiols. The exact mechanism of thiol-induced enhancement of oxidative modification of low-density lipoprotein remains questionable. The proposed role of thiyl radicals in lipid peroxidation needs to be re-examined. It has been proposed that thiyl radicals are detoxified by superoxide dismutase in mammalian cells and by a thiol-specific enzyme in bacterial systems. We propose that thiols or protein thiols act as potent antioxidants in radical-induced damage via formation of thiyl radicals.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Sultan Alouffi ◽  
Mohammad Faisal ◽  
Abdulrahman A. Alatar ◽  
Saheem Ahmad

Background. Pro- and antiatherogenic properties of oxidised low density lipoprotein (Ox-LDL) are responsible for different chronic diseases including diabetes and cardiovascular diseases (CVD). The constant attack on the body from oxidative stress makes the quantification of various oxidation products necessary. In this study, the oxidative stress causing the structural and chemical changes occurring in the LDL molecule is comprehensively done. Moreover, the prevalence of the autoantibodies against the oxidised LDL is also determined. Methods. Our study made an attempt to see the effect of Ox-LDL as an enhancer of type 2 diabetes mellitus (T2DM) coupled with CVD. Primarily, we detected the oxidation of LDL with different concentration of Fenton reaction. The biochemical parameters were assessed for the changes occurring in the LDL molecule. In a clinical set up, 20 sera samples were taken from patients who are healthy, 30 from those with diabetes, 20 from those with CVD, and 30 from diabetes with CVD patients. Results. In biochemical assays there were markedly increased TBARS, carbonyl, and HMF content in Ox-LDL as compared to native LDL. The prevalence of autoantibodies against the T2DM was recorded to be 36%, while for CVD it was recorded to be 29%. However, it was found that 50% of the sera samples showed autoantibodies against oxidized LDL in the sera of T2DM with CVD complications as compared to the native analogue. Conclusion. There is significant change in the LDL molecule as revealed by various physicochemical analysis. The change in the LDL macromolecule as a result of oxidation triggered the development of the autoantibodies against it.


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