scholarly journals NOX4 NADPH Oxidase-Dependent Mitochondrial Oxidative Stress in Aging-Associated Cardiovascular Disease

2015 ◽  
Vol 23 (18) ◽  
pp. 1389-1409 ◽  
Author(s):  
Aleksandr E. Vendrov ◽  
Kimberly C. Vendrov ◽  
Alberto Smith ◽  
Jinling Yuan ◽  
Arihiro Sumida ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Nadph Oxidase ◽  
Mitochondrial Oxidative Stress

scholarly journals Relation between Development of Cardiovascular Disease and the C242T CYBA Polymorphism of the NADPH Oxidase in ESRD Patients

2010 ◽  
Vol 29 (2) ◽  
pp. 89-93 ◽  
Author(s):  
Feng-Ying Tang ◽  
Ying Zhu ◽  
Gui Hua Wang ◽  
Xiong-Wei Xie
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Nadph Oxidase ◽  
Multiple Logistic Regression Analysis ◽  
Smoking History ◽  
Multiple Logistic Regression ◽  
Disease Group ◽  
Independent Variables ◽  
Group D ◽  
Esrd Patients

Background: The development of cardiovascular disease in ESRD patients is considered to be associated with oxidative stress. NAD(P)H oxidase has attracted attention as mechanisms of generating oxidative stress. We investigated the relation between the genotype of the C242T CYBA polymorphism of the NADPH oxidase and the development of cardiovascular disease in ESRD patients.Methods: A total of 289 ESRD patients were recruited and allocated to one of the two groups: patients without cardiovascular disease (group N; n=192) and patients developing cardiovascular disease (group D; n=97). The C242T CYBA polymorphism was determined by RFLP-PCR methods.Results: The frequency of the C242T CT+TT genotype was significantly lower in group D than in group N (9.1 vs. 20.2%). In multiple Logistic regression analysis, systolic blood pressure, smoking history and this gene polymorphism were shown to be independent variables for the development of cardiovascular disease in ESRD patients.Conclusions: These results suggest that assessment of the C242T CYBA polymorphism of the NADPH oxidase may be useful in identifying the risk for developing cardiovascular disease in ESRD patients.

Activation of NADPH oxidase mediates mitochondrial oxidative stress and atrial remodeling in diabetic rabbits

Life Sciences ◽  
2021 ◽  
Vol 272 ◽  
pp. 119240
Author(s):  
Lingling Zhou ◽  
Yang Liu ◽  
Zhaojia Wang ◽  
Daiqi Liu ◽  
Bingxin Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Atrial Remodeling ◽  
Mitochondrial Oxidative Stress ◽  
Diabetic Rabbits

Folic acid supplementation inhibits NADPH oxidase-mediated superoxide anion production in the kidney

2011 ◽  
Vol 300 (1) ◽  
pp. F189-F198 ◽  
Author(s):  
Sun-Young Hwang ◽  
Yaw L. Siow ◽  
Kathy K. W. Au-Yeung ◽  
James House ◽  
Karmin O
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Folic Acid ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Folic Acid Supplementation ◽  
Sod Activity ◽  
Superoxide Anion Production ◽  
Acid Supplementation ◽  
Anion Production

Hyperhomocysteinemia, a condition of elevated blood homocysteine (Hcy) levels, is a metabolic disease. It is a common clinical finding in patients with chronic kidney diseases and occurs almost uniformly in patients with end-stage renal disease. Hyperhomocysteinemia is also a risk factor for cardiovascular disease. Our recent studies indicate that hyperhomocysteinemia can lead to renal injury by inducing oxidative stress. Oxidative stress is one of the important mechanisms contributing to Hcy-induced tissue injury. Folic acid supplementation is regarded as a promising approach for prevention and treatment of cardiovascular disease associated with hyperhomocysteinemia due to its Hcy-lowering effect. However, its effect on the kidney is not clear. The aim of this study was to examine the effect of folic acid supplementation on Hcy-induced superoxide anion production via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in the kidney during hyperhomocysteinemia. Hyperhomocysteinemia was induced in male Sprague-Dawley rats fed a high-methionine diet for 12 wk with or without folic acid supplementation. A group of rats fed a regular diet was used as control. There was a significant increase in levels of superoxide anions and lipid peroxides in kidneys isolated from hyperhomocysteinemic rats. Activation of NADPH oxidase was responsible for hyperhomocysteinemia-induced oxidative stress in the kidney. Folic acid supplementation effectively antagonized hyperhomocysteinemia-induced oxidative stress via its Hcy-lowering and Hcy-independent effect. In vitro study also showed that 5-methyltetrahydrofolate, an active form of folate, effectively reduced Hcy-induced superoxide anion production via NADPH oxidase. Xanthine oxidase activity was increased and superoxide dismutase (SOD) activity was decreased in the kidney of hyperhomocysteinemic rats, which might also contribute to an elevation of superoxide anion level in the kidney. Folic acid supplementation attenuated xanthine oxidase activity and restored SOD activity in the kidney of hyperhomocysteinemic rats. These results suggest that folic acid supplementation may offer renal protective effect against oxidative stress.

scholarly journals Vascular Calcification—New Insights into Its Mechanism

2020 ◽  
Vol 21 (8) ◽  
pp. 2685 ◽  
Author(s):  
Sun Joo Lee ◽  
In-Kyu Lee ◽  
Jae-Han Jeon
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Vascular Calcification ◽  
Mitochondrial Oxidative Stress ◽  
The Past ◽  
Defensive Mechanisms ◽  
Osteogenic Signaling ◽  
Multiple Signaling ◽  
Medial Calcification

Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

scholarly journals Effects of p67phox on the mitochondrial oxidative state in the kidney of Dahl salt-sensitive rats: optical fluorescence 3-D cryoimaging

2015 ◽  
Vol 309 (4) ◽  
pp. F377-F382 ◽  
Author(s):  
F. Salehpour ◽  
Z. Ghanian ◽  
C. Yang ◽  
N. N. Zheleznova ◽  
T. Kurth ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Three Dimensional ◽  
Renal Medulla ◽  
Mitochondrial Oxidative Stress ◽  
Redox States ◽  
Salt Level ◽  
Transport Chain ◽  
Optical Fluorescence ◽  
Nadph Oxidase 2

The goal of the present study was to quantify and correlate the contribution of the cytosolic p67 phox subunit of NADPH oxidase 2 to mitochondrial oxidative stress in the kidneys of the Dahl salt-sensitive (SS) hypertensive rat. Whole kidney redox states were uniquely assessed using a custom-designed optical fluorescence three-dimensional cryoimager to acquire multichannel signals of the intrinsic fluorophores NADH and FAD. SS rats were compared with SS rats in which the cytosolic subunit p67 phox was rendered functionally inactive by zinc finger nuclease mutation of the gene (SSp67 phox-null rats). Kidneys of SS rats fed a 0.4% NaCl diet exhibited significantly ( P = 0.023) lower tissue redox ratio (NADH/FAD; 1.42 ± 0.06, n = 5) than SSp67 phox-null rats (1.64 ± 0.07, n = 5), indicating reduced levels of mitochondrial electron transport chain metabolic activity and enhanced oxidative stress in SS rats. When fed a 4.0% salt diet for 21 days, both strains exhibited significantly lower tissue redox ratios ( P < 0.001; SS rats: 1.03 ± 0.05, n = 9, vs. SSp67 phox-null rats: 1.46 ± 0.04, n = 7) than when fed a 0.4% salt, but the ratio was still significantly higher in SSp67 phox rats at the same salt level as SS rats. These results are consistent with results from previous studies that found elevated medullary interstitial fluid concentrations of superoxide and H2O2 in the medulla of SS rats. We conclude that the p67 phox subunit of NADPH oxidase 2 plays an important role in the excess production of ROS from mitochondria in the renal medulla of the SS rat.

Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress

2007 ◽  
Vol 293 (2) ◽  
pp. C584-C596 ◽  
Author(s):  
Yuri Y. Sautin ◽  
Takahiko Nakagawa ◽  
Sergey Zharikov ◽  
Richard J. Johnson
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Uric Acid ◽  
Nadph Oxidase ◽  
Map Kinases ◽  
Nitrosative Stress ◽  
Experimental Studies ◽  
Increased Risk ◽  
And Oxidative Stress

Uric acid is considered a major antioxidant in human blood that may protect against aging and oxidative stress. Despite its proposed protective properties, elevated levels of uric acid are commonly associated with increased risk for cardiovascular disease and mortality. Furthermore, recent experimental studies suggest that uric acid may have a causal role in hypertension and metabolic syndrome. All these conditions are thought to be mediated by oxidative stress. In this study we demonstrate that differentiation of cultured mouse adipocytes is associated with increased production of reactive oxygen species (ROS) and uptake of uric acid. Soluble uric acid stimulated an increase in NADPH oxidase activity and ROS production in mature adipocytes but not in preadipocytes. The stimulation of NADPH oxidase-dependent ROS by uric acid resulted in activation of MAP kinases p38 and ERK1/2, a decrease in nitric oxide bioavailability, and an increase in protein nitrosylation and lipid oxidation. Collectively, our results suggest that hyperuricemia induces redox-dependent signaling and oxidative stress in adipocytes. Since oxidative stress in the adipose tissue has recently been recognized as a major cause of insulin resistance and cardiovascular disease, hyperuricemia-induced alterations in oxidative homeostasis in the adipose tissue might play an important role in these derangements.

NADPH oxidase p22phox gene variants are associated with systemic oxidative stress biomarker responses to exercise training

2005 ◽  
Vol 99 (5) ◽  
pp. 1905-1911 ◽  
Author(s):  
Joon-Young Park ◽  
Robert E. Ferrell ◽  
Jung-Jun Park ◽  
James M. Hagberg ◽  
Dana A. Phares ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Exercise Training ◽  
Nadph Oxidase ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cardiovascular Disease Risk Factors ◽  
Tbars Level ◽  
Systemic Oxidative Stress

Systemic oxidative stress plays a role in many degenerative diseases. Although regular physical activity has been known as the most effective nonpharmacological intervention to alleviate the oxidative stress, the beneficial effect varies between individuals. We investigated whether NADPH oxidase p22phox gene C242T and A640G polymorphisms are associated with systemic oxidative stress level response to exercise training (ExTr). Fifty-nine sedentary middle-aged to older Caucasians with relatively high cardiovascular disease risk factors underwent a 6-mo standardized ExTr program. Body mass index, plasma lipoprotein-lipid profiles, cardiovascular fitness, and plasma thiobarbituric acid reactive substances (TBARS) were measured before and after ExTr. Demographic and initial levels of cardiovascular disease risk factors were similar among genotype groups for both polymorphisms. Overall, TBARS was decreased by 16% with ExTr in the entire group ( P < 0.001). There was no significant difference in TBARS changes with ExTr among the C242T genotype groups. However, A allele carriers showed greater reduction in TBARS than noncarriers at the A640G locus ( P = 0.05). There was a significant interaction ( P = 0.05) between ExTr and A640G polymorphism in TBARS changes with ExTr. This interaction remained after accounting for age and baseline TBARS level. Furthermore, diplotype analysis showed that TBARS was decreased to a greater extent in the C242/A640 haplotype carriers compared with the noncarriers ( P < 0.05). We found that p22phox polymorphisms, especially A640G, were associated with differential changes in systemic oxidative stress with aerobic exercise training.

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