Improved co-oxidation of β-carotene to β-ionone using xanthine oxidase-generated reactive oxygen species in a multiphasic system

2008 ◽  
Vol 3 (2) ◽  
pp. 220-225 ◽  
Author(s):  
Mai Huong Ly ◽  
Lan Cao Hoang ◽  
Jean-Marc Belin ◽  
Yves Waché
Keyword(s):  
Reactive Oxygen Species ◽  
Co Oxidation ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Β Carotene

scholarly journals Graphene and graphene oxide induce ROS production in human HaCaT skin keratinocytes: the role of xanthine oxidase and NADH dehydrogenase

Nanoscale ◽  
2018 ◽  
Vol 10 (25) ◽  
pp. 11820-11830 ◽  
Author(s):  
Marco Pelin ◽  
Laura Fusco ◽  
Cristina Martín ◽  
Silvio Sosa ◽  
Javier Frontiñán-Rubio ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Graphene Oxide ◽  
Xanthine Oxidase ◽  
Nadh Dehydrogenase ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Depolarization ◽  
Skin Keratinocytes

Graphene based nanomaterials induce a reactive oxygen species-mediated mitochondrial depolarization, caused by the activation of NADH dehydrogenase and xanthine oxidase.

scholarly journals NADPH oxidase-derived reactive oxygen species contribute to impaired cutaneous microvascular function in chronic kidney disease

2014 ◽  
Vol 306 (12) ◽  
pp. F1499-F1506 ◽  
Author(s):  
Jennifer J. DuPont ◽  
Meghan G. Ramick ◽  
William B. Farquhar ◽  
Raymond R. Townsend ◽  
David G. Edwards
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Nadph Oxidase ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Oxidase Inhibition

Oxidative stress promotes vascular dysfunction in chronic kidney disease (CKD). We utilized the cutaneous circulation to test the hypothesis that reactive oxygen species derived from NADPH oxidase and xanthine oxidase impair nitric oxide (NO)-dependent cutaneous vasodilation in CKD. Twenty subjects, 10 stage 3 and 4 patients with CKD (61 ± 4 yr; 5 men/5 women; eGFR: 39 ± 4 ml·min−1·1.73 m−2) and 10 healthy controls (55 ± 2 yr; 4 men/6 women; eGFR: >60 ml·min−1·1.73 m−2) were instrumented with 4 intradermal microdialysis fibers for the delivery of 1) Ringer solution (Control), 2) 10 μM tempol (scavenge superoxide), 3) 100 μM apocynin (NAD(P)H oxidase inhibition), and 4) 10 μM allopurinol (xanthine oxidase inhibition). Skin blood flow was measured via laser-Doppler flowmetry during standardized local heating (42°C). Ng-nitro-l-arginine methyl ester (l-NAME; 10 mM) was infused to quantify the NO-dependent portion of the response. Cutaneous vascular conductance (CVC) was calculated as a percentage of the maximum CVC achieved during sodium nitroprusside infusion at 43°C. Cutaneous vasodilation was attenuated in patients with CKD (77 ± 3 vs. 88 ± 3%, P = 0.01), but augmented with tempol and apocynin (tempol: 88 ± 2 ( P = 0.03), apocynin: 91 ± 2% ( P = 0.001). The NO-dependent portion of the response was reduced in patients with CKD (41 ± 4 vs. 58 ± 2%, P = 0.04), but improved with tempol and apocynin (tempol: 58 ± 3 ( P = 0.03), apocynin: 58 ± 4% ( P = 0.03). Inhibition of xanthine oxidase did not alter cutaneous vasodilation in either group ( P > 0.05). These data suggest that NAD(P)H oxidase is a source of reactive oxygen species and contributes to microvascular dysfunction in patients with CKD.

scholarly journals Malaria inflammation by xanthine oxidase‐produced reactive oxygen species

2019 ◽  
Vol 11 (8) ◽  
Author(s):  
Maureen C Ty ◽  
Marisol Zuniga ◽  
Anton Götz ◽  
Sriti Kayal ◽  
Praveen K Sahu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Annato extract and β-carotene modulate the production of reactive oxygen species/nitric oxide in neutrophils from diabetic rats

2012 ◽  
Vol 50 (3) ◽  
pp. 177-183 ◽  
Author(s):  
Joamyr Victor Rossoni-Júnior ◽  
Glaucy Rodrigues Araújo ◽  
Bruno da Cruz Pádua ◽  
Míriam Martins Chaves ◽  
Maria Lúcia Pedrosa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Diabetic Rats ◽  
Oxygen Species ◽  
Β Carotene

Xanthine oxidase-derived reactive oxygen species contribute to the development ofd-galactosamine-induced liver injury in rats

2007 ◽  
Vol 41 (2) ◽  
pp. 135-144 ◽  
Author(s):  
Yoshiji Ohta ◽  
Tatsuya Matsura ◽  
Akira Kitagawa ◽  
Kenji Tokunaga ◽  
Kazuo Yamada
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Oxidative stress in marathon runners: interest of antioxidant supplementation

2006 ◽  
Vol 96 (S1) ◽  
pp. S31-S33 ◽  
Author(s):  
Mari-Carmen Gomez-Cabrera ◽  
Agustín Martínez ◽  
Gustavo Santangelo ◽  
Federico V. Pallardó ◽  
Juan Sastre ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Xanthine Oxidase ◽  
Cell Signalling ◽  
Reactive Oxygen ◽  
Peripheral Blood Lymphocytes ◽  
Signalling Pathways ◽  
Marathon Running ◽  
Oxygen Species ◽  
Marathon Runners

We have recently reported that xanthine oxidase is involved in the generation of free radicals in exhaustive exercise. Allopurinol, an inhibitor of xanthine oxidase, prevents it. The aim of the present work was to elucidate the role of exercise-derived reactive oxygen species in the cell signalling pathways involved in the adaptation to exercise in man. We have found that exercise causes an increase in the activity of plasma xanthine oxidase and an activation of NF-κB in peripheral blood lymphocytes after marathon running. This activation is dependent on free radical formation in exercise: treatment with allopurinol completely prevents it. In animal models, we previously showed that NF-κB activation induced by exhaustive physical exercise leads to an increase in the expression of superoxide dismutase, an enzyme involved in antioxidant defence. We report evidence in man that reactive oxygen species act as signals in exercise as decreasing their formation prevents activation of important signalling pathways which can cause useful adaptations in cells.

scholarly journals Role of TNF-α-induced reactive oxygen species in endothelial dysfunction during reperfusion injury

2008 ◽  
Vol 295 (6) ◽  
pp. H2242-H2249 ◽  
Author(s):  
Xue Gao ◽  
Hanrui Zhang ◽  
Souad Belmadani ◽  
Junxi Wu ◽  
Xiangbin Xu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Myocardial Ischemia ◽  
Endothelial Function ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Neutrophil Activation ◽  
Superoxide Production ◽  
Oxygen Species ◽  
Tnf Α

We hypothesized that neutralization of TNF-α at the time of reperfusion exerts a salubrious role on endothelial function and reduces the production of reactive oxygen species. We employed a mouse model of myocardial ischemia-reperfusion (I/R, 30 min/90 min) and administered TNF-α neutralizing antibodies at the time of reperfusion. I/R elevated TNF-α expression (mRNA and protein), whereas administration of anti-TNF-α before reperfusion attenuated TNF-α expression. We detected TNF-α expression in vascular smooth muscle cells, mast cells, and macrophages, but not in the endothelial cells. I/R induced endothelial dysfunction and superoxide production. Administration of anti-TNF-α at the onset of reperfusion partially restored nitric oxide-mediated coronary arteriolar dilation and reduced superoxide production. I/R increased the activity of NAD(P)H oxidase and of xanthine oxidase and enhanced the formation of nitrotyrosine residues in untreated mice compared with shams. Administration of anti-TNF-α before reperfusion blocked the increase in activity of these enzymes. Inhibition of xanthine oxidase (allopurinol) or NAD(P)H oxidase (apocynin) improved endothelium-dependent dilation and reduced superoxide production in isolated coronary arterioles following I/R. Interestingly, I/R enhanced superoxide generation and reduced endothelial function in neutropenic animals and in mice treated with a neutrophil NAD(P)H oxidase inhibitor, indicating that the effects of TNF-α are not through neutrophil activation. We conclude that myocardial ischemia initiates TNF-α expression, which induces vascular oxidative stress, independent of neutrophil activation, and leads to coronary endothelial dysfunction.

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