scholarly journals Uric Acid in Cardiovascular Diseases: A Factor or an Incident?

2020 ◽  
Vol 70 (12) ◽  
pp. 4442-4444
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular Disease ◽  
Uric Acid ◽  
Reactive Oxygen ◽  
Medical Community ◽  
Xanthine Oxidoreductase ◽  
Oxygen Species ◽  
Cardiac Events ◽  
Target Organs ◽  
Complex Approach

The pathophysiological involvement of uric acid in cardiovascular disease has been intensively addressed in the last decades by the medical community. The tendencies to elucidate its role in cardiac events have been carried out in numerous researches with controversial results. In an attempt to understand this phenomenon, the existence of a paradox is admited, according to which uric acid behaves as an antioxidant, capturing reactive oxygen species, and in the context of an existing cardiac pathology, manifests a precipitating oxidative effect of circulating lipids, there being also present. inflammatory substrate. The involvement of the target organs in hypertension, along with other factors such as hyperlipidemia, obesity, pathologies of the valvular apparatus, contributes to the appearance of hyperuricemia of excretory cause. The ability of xanthine oxidoreductase to produce reactive oxygen species that contribute to the occurrence of oxidative stress and endothelial dysfunction has redirected our visions to a more complex approach to ischemic heart disease. And the use of xanthine oxidoreductase inhibitors in cardiovascular disease in patients with hyperuricemia has allowed to appreciate real benefits in improving renal function and preventing atherosclerosis. Keywords: uric acid, cardiovascular disease, factor

scholarly journals A Monitoring of Allantoin, Uric Acid, and Malondialdehyde Levels in Plasma and Erythrocytes After Ten Minutes of Running Activity

2014 ◽  
pp. 753-762
Author(s):  
R. KANĎÁR ◽  
X. ŠTRAMOVÁ ◽  
P. DRÁBKOVÁ ◽  
J. KŘENKOVÁ
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Uric Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Intense Exercise ◽  
Suitable Candidate ◽  
Running Activity ◽  
Plasma Malondialdehyde

Uric acid is the final product of human purine metabolism. It was pointed out that this compound acts as an antioxidant and is able to react with reactive oxygen species forming allantoin. Therefore, the measurement of allantoin levels may be used for the determination of oxidative stress in humans. The aim of the study was to clarify the antioxidant effect of uric acid during intense exercise. Whole blood samples were obtained from a group of healthy subjects. Allantoin, uric acid, and malondialdehyde levels in plasma and erythrocytes were measured using a HPLC with UV/Vis detection. Statistical significant differences in allantoin and uric acid levels during short-term intense exercise were found. Immediately after intense exercise, the plasma allantoin levels increased on the average of 200 % in comparison to baseline. Plasma uric acid levels increased slowly, at an average of 20 %. On the other hand, there were no significant changes in plasma malondialdehyde. The results suggest that uric acid, important antioxidant, is probably oxidized by reactive oxygen species to allantoin. Therefore allantoin may be suitable candidate for a marker of acute oxidative stress.

Accelerated senescence in kidneys of low-birth-weight rats after catch-up growth

2009 ◽  
Vol 297 (6) ◽  
pp. F1697-F1705 ◽  
Author(s):  
Valerie A. Luyckx ◽  
Catharine A. Compston ◽  
Thomas Simmen ◽  
Thomas F. Mueller
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Normal Birth Weight ◽  
Normal Birth ◽  
Catch Up

Epidemiological studies show a strong association between low birth weight and hypertension, renal, and cardiovascular disease, especially after catch-up growth. Senescence is an important contributor to the progression of chronic disease. Developmentally programmed premature senescence may be a link among low birth weight, catch-up growth, and adult disease. Low birth weight was induced by feeding pregnant rats a low-protein diet from day 12 of gestation to 10 days postdelivery. Low- and normal-birth-weight male offspring were weaned onto regular or high-calorie diets to enhance catch-up growth. Kidneys and hearts of offspring were analyzed for RNA and protein markers of stress-induced senescence (p16, p21, p53, Rb). Markers of mitochondrial stress (p66Shc) and activation of endoplasmic reticulum protein secretion (Ero1α) were analyzed as regulators of reactive oxygen species generation. Reactive oxygen species are known to be associated with premature aging. Senescence markers were not different in low- or normal-birth-weight kidneys at birth. During rapid catch-up growth, p16 and p21 increased significantly in low-birth-weight kidneys and hearts ( P < 0.01). Renal p16 levels increased progressively and were significantly higher in low-birth-weight kidneys at 3 and 6 mo ( P ≤ 0.02). Renal p66Shc and Ero1α were significantly higher in low- compared with normal- birth-weight kidneys at 6 mo, suggesting reactive oxygen species generation ( P ≤ 0.03). Low-birth-weight rats exhibit accelerated senescence in kidneys and hearts after rapid catch-up growth, a likely important link between early growth and subsequent hypertension, renal, and cardiovascular disease.

scholarly journals Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Nhat-Tu Le ◽  
James P. Corsetti ◽  
Janet L. Dehoff-Sparks ◽  
Charles E. Sparks ◽  
Keigi Fujiwara ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Subsequent Development ◽  
Hdl Cholesterol ◽  
Specific Protein ◽  
Oxygen Species ◽  
Cardiac Events ◽  
Inflammatory Conditions ◽  
Endothelial Inflammation ◽  
Coronary Events

Although the exact mechanism through which NADPH oxidases (Nox’s) generate reactive oxygen species (ROS) is still not completely understood, it is widely considered that ROS accumulation is the cause of oxidative stress in endothelial cells. Increasing pieces of evidence strongly indicate the role for ROS in endothelial inflammation and dysfunction and subsequent development of atherosclerotic plaques, which are causes of various pathological cardiac events. An overview for a causative relationship between ROS and endothelial inflammation will be provided in this review. Particularly, a crucial role for specific protein SUMOylation in endothelial inflammation will be presented. Given that SUMOylation of specific proteins leads to increased endothelial inflammation, targeting specific SUMOylated proteins may be an elegant, effective strategy to control inflammation. In addition, the involvement of ROS production in increasing the risk of recurrent coronary events in a sub-group of non-diabetic, post-infarction patients with elevated levels of HDL-cholesterol will be presented with the emphasis that elevated HDL-cholesterol under certain inflammatory conditions can lead to increased incidence of cardiovascular events.

scholarly journals Lycopene Deficiency in Ageing and Cardiovascular Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Ivan M. Petyaev
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cardiovascular Disease ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
Nutritional Intervention ◽  
Peroxyl Radicals ◽  
Oxygen Species ◽  
Apo B ◽  
Poor Outcomes

Lycopene is a hydrocarbon phytochemical belonging to the tetraterpene carotenoid family and is found in red fruit and vegetables. Eleven conjugated double bonds predetermine the antioxidant properties of lycopene and its ability to scavenge lipid peroxyl radicals, reactive oxygen species, and nitric oxide. Lycopene has a low bioavailability rate and appears in the blood circulation incorporated into chylomicrons and other apo-B containing lipoproteins. The recent body of evidence suggests that plasma concentration of lycopene is not only a function of intestinal absorption rate but also lycopene breakdown via enzymatic and oxidative pathways in blood and tissues. Oxidative stress and the accumulation of reactive oxygen species and nitric oxide may represent a major cause of lycopene depletion in ageing, cardiovascular disease, and type 2 diabetes mellitus. It has been shown recently that low carotenoid levels, and especially decreased serum lycopene levels, are strongly predictive of all-cause mortality and poor outcomes of cardiovascular disease. However, there is a poor statistical association between dietary and serum lycopene levels which occurs due to limited bioavailability of lycopene from dietary sources. Hence, it is very unlikely that nutritional intervention alone could be instrumental in the correction of lycopene and carotenoid deficiency. Therefore, new nutraceutical formulations of carotenoids with enhanced bioavailability are urgently needed.

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