scholarly journals Retraction of: High Uric Acid Inhibits Cardiomyocyte Viability Through the ERK/P38 Pathway via Oxidative Stress

2021 ◽  
Vol 55 (4) ◽  
pp. 521-521
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
High Uric Acid ◽  
P38 Pathway

scholarly journals Biomarkers of Oxidative Stress in Normal and Pre-eclamptic Women

KYAMC Journal ◽  
2017 ◽  
Vol 4 (2) ◽  
pp. 406-408
Author(s):  
Shahin Ara ◽  
Taslima Nigar ◽  
Md Anwar Habib
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Pregnant Women ◽  
Control Group ◽  
Third Trimester ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Observational Group ◽  
High Uric Acid ◽  
Biomarkers Of Oxidative Stress

Preeclampsia is a serious pregnancy complication. Little is known about which clinical risk factors are associated with the progression from normal to preeclampsia. Recent evidence suggests that the oxidative stress is one of the important factor associated with preeclampsia. High uric acid and MDA levels are indicative of oxidative stress. The purpose of this study was to evaluate the possible relationship between the biochemical markers (Uric acid & MDA) of oxidative stress in preeclamptic & normal pregnant women. In our study we investigated total number of 40 healthy pregnant and clinically diagnosed preeclamtic women. Among them 20 healthy (third trimester) normal pregnant women were taken as control group and another 20 clinically diagnosed PET women (at pre labour state) were taken as observational group. MDA and uric acid level were within normal range (2.63 ± 0.66 & 337.88 ± 16.52 ?mol/l ) respectively in normal pregnant women but significantly higher (3.74 ± 1.45 & 428.50 ± 23.65 ?mol/l ) in the group of preeclamptic women. This study review our current understanding of oxidative stress biomarkers ( Uric acid & MDA ) in preeclampsia and highlights that increased MDA and Uric acid levels are associated with preeclampsia.KYAMC Journal Vol. 4, No.-2, Jan 2014, Page 406-408

Evaluation of Salivary Antioxidants and Oxidative Stress Markers in Male Smokers

2019 ◽  
Vol 22 (7) ◽  
pp. 496-501
Author(s):  
Fatemeh Ahmadi-Motamayel ◽  
Parisa Falsafi ◽  
Hamidreza Abolsamadi ◽  
Mohammad T. Goodarzi ◽  
Jalal Poorolajal
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Free Radicals ◽  
Antioxidant Capacity ◽  
Cigarette Smoke ◽  
Total Antioxidant Capacity ◽  
The Body ◽  
Total Antioxidant ◽  
The Mean ◽  
And Oxidative Stress

Background: Cigarette smoke free radicals can cause cellular damage and different diseases. All the body fluids have antioxidants which protect against free radicals. Objective: The aim of this study was to evaluate salivary total antioxidant capacity and peroxidase, uric acid and malondialdehyde levels in smokers and a nonsmoking control group. Methods: Unstimulated saliva was collected from 510 males. A total of 259 subjects were current smokers and 251 were non-smokers. The levels of salivary total antioxidant capacity, uric acid, peroxidase and malondialdehyde were measured using standard procedures. Data were analyzed with t test and ANOVA. Results: The smokers were younger and dental hygiene index was higher than healthy nonsmoking controls. The mean total antioxidant capacity in smokers and nonsmokers was 0.13±0.07 and 0.21±011, respectively (P=0.001). Smokers had significantly lower peroxidase and uric acid levels than healthy controls. In addition, the mean malondialdehyde levels in the smokers and nonsmokers were 4.55 ±2.61 and 2.79 ±2.21, respectively (P=0.001). Conclusion: Cigarette smoke produces free radical and oxidative stress, causing many side effects. Salivary antioxidant levels decreased and malondialdehyde levels increased in smokers, indicating the high oxidative stress among smokers compared to nonsmokers. Cigarette smoke had deleterious effects on main salivary antioxidants levels.

scholarly journals Uric acid promotes oxidative stress and enhances vascular endothelial cell apoptosis in rats with middle cerebral artery occlusion

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Chengfu Song ◽  
Xiangdong Zhao
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cell ◽  
Artery Occlusion ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis ◽  
Related Factors ◽  
Cerebral Artery Occlusion

In patients with cerebral infarction (CI), elevated serum uric acid (UA) level may exacerbate the occurrence and development of carotid atherosclerosis (AS). Our study intended to explore the underlying mechanism. We enrolled 86 patients with CI, and divided them into four groups: Non-AS, AS-mild, AS-moderate, and AS-severe groups; the levels of UA and oxidative stress-related factors in serum were detected. The middle cerebral artery occlusion (MCAO) model was used to stimulate CI in rats, and different doses of UA were administrated. The levels of oxidative stress-related factors in serum were detected. Hematoxylin & eosin (H&E) staining was used to observe the morphological alterations, and the apoptotic cell death detection kit was used to detect apoptotic cells. Increased UA concentration and enhanced oxidative stress were found in AS patients. H&E staining results showed that UA treatment exacerbated morphological damage in rats with MCAO, promoted oxidative stress, and enhanced vascular endothelial cell apoptosis in rats with MCAO.

scholarly journals Uric Acid, Oxidative Stress and Inflammation in Chronic Heart Failure with Reduced Ejection Fraction

2015 ◽  
Vol 23 (4) ◽  
pp. 397-406 ◽  
Author(s):  
Adriana Iliesiu ◽  
Alexandru Campeanu ◽  
Daciana Marta ◽  
Irina Parvu ◽  
Gabriela Gheorghe
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Uric Acid ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Xanthine Oxidase ◽  
Left Ventricular ◽  
Paraoxonase 1 ◽  
Lv Function ◽  
The Relationship

Abstract Background. Oxidative stress (OS) and inflammation are major mechanisms involved in the progression of chronic heart failure (CHF). Serum uric acid (sUA) is related to CHF severity and could represent a marker of xanthine-oxidase activation. The relationship between sUA, oxidative stress (OS) and inflammation markers was assessed in patients with moderate-severe CHF and reduced left ventricular (LV) ejection fraction (EF). Methods. In 57 patients with stable CHF, functional NYHA class III, with EF<40%, the LV function was assessed by N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) levels and echocardiographically through the EF and E/e’ ratio, a marker of LV filling pressures. The relationship between LV function, sUA, malondialdehyde (MDA), myeloperoxidase (MPO), paraoxonase 1 (PON-1) as OS markers and high sensitivity C-reactive protein (hsCRP) and interleukin 6 (IL-6) as markers of systemic inflammation was evaluated. Results. The mean sUA level was 7.9 ± 2.2 mg/dl, and 61% of the CHF patients had hyperuricemia. CHF patients with elevated LV filling pressures (E/e’ ≥ 13) had higher sUA (8.6 ± 2.3 vs. 7.3 ± 1.4, p=0.08) and NT-proBNP levels (643±430 vs. 2531±709, p=0.003) and lower EF (29.8 ± 3.9 % vs. 36.3 ± 4.4 %, p=0.001). There was a significant correlation between sUA and IL-6 (r = 0.56, p<0.001), MDA (r= 0.49, p= 0.001), MPO (r=0.34, p=0.001) and PON-1 levels (r= −0.39, p= 0.003). Conclusion. In CHF, hyperuricemia is associated with disease severity. High sUA levels in CHF with normal renal function may reflect increased xanthine-oxidase activity linked with chronic inflammatory response.

Balanced oxidative stress index in spite of decreased uric acid levels in multiple sclerosis patients

2015 ◽  
Vol 9 (2) ◽  
pp. 153-158 ◽  
Author(s):  
O. Aydin ◽  
F. Kurtulus ◽  
E. Eren ◽  
H. Y. Ellidag ◽  
N. Yılmaz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Uric Acid ◽  
Stress Index ◽  
Oxidative Stress Index ◽  
Multiple Sclerosis Patients

Oxidation of Uric Acid in Rheumatoid Arthritis: Is Allantoin a Marker of Oxidative Stress?

2004 ◽  
Vol 38 (6) ◽  
pp. 623-628 ◽  
Author(s):  
Sevgi Yardim-Akaydin ◽  
Aylin Sepici ◽  
Yeşim Özkan ◽  
Meral Torun ◽  
Bolkan Şimşek ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Uric Acid

Culture and establishment of self-renewing human liver 3D organoids with high uric acid for screening antihyperuricemic functional compounds

2021 ◽  
pp. 131634
Author(s):  
Chuanli Hou ◽  
Wanqian Sha ◽  
Zhenzhen Xu ◽  
Yang Hu ◽  
William Kwame Amakye ◽  
...  
Keyword(s):  
Uric Acid ◽  
Human Liver ◽  
High Uric Acid

CTRP3 protects against uric acid-induced endothelial injury by inhibiting inflammation and oxidase stress in rats

2021 ◽  
pp. 153537022110471
Author(s):  
Junxia Zhang ◽  
Xue Lin ◽  
Jinxiu Xu ◽  
Feng Tang ◽  
Lupin Tan
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Specific Inhibitor ◽  
Endothelial Damage ◽  
Endothelial Injury ◽  
Sprague Dawley ◽  
Protein Levels ◽  
And Oxidative Stress

Hyperuricemia, which contributes to vascular endothelial damage, plays a key role in multiple cardiovascular diseases. This study was designed to investigate whether C1q/tumor necrosis factor (TNF)-related protein 3 (CTRP3) has a protective effect on endothelial damage induced by uric acid and its underlying mechanisms. Animal models of hyperuricemia were established in Sprague-Dawley (SD) rats through the consumption of 10% fructose water for 12 weeks. Then, the rats were given a single injection of Ad-CTRP3 or Ad-GFP. The animal experiments were ended two weeks later. In vitro, human umbilical vein endothelial cells (HUVECs) were first infected with Ad-CTRP3 or Ad-GFP. Then, the cells were stimulated with 10 mg/dL uric acid for 48 h after pretreatment with or without a Toll-like receptor 4 (TLR4)-specific inhibitor. Hyperuricemic rats showed disorganized intimal structures, increased endothelial apoptosis rates, increased inflammatory responses and oxidative stress, which were accompanied by reduced CTRP3 and elevated TLR4 protein levels in the thoracic aorta. In contrast, CTRP3 overexpression decreased TLR4 protein levels and ameliorated inflammatory responses and oxidative stress, thereby improving the morphology and apoptosis of the aortic endothelium in rats with hyperuricemia. Similarly, CTRP3 overexpression decreased TLR4-mediated inflammation, reduced oxidative stress, and rescued endothelial damage induced by uric acid in HUVECs. In conclusion, CTRP3 ameliorates uric acid-induced inflammation and oxidative stress, which in turn protects against endothelial injury, possibly by inhibiting TLR4-mediated inflammation and downregulating oxidative stress.

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