Role of xanthine oxidase in the formation and release of reactive oxygen species from cultured vascular endothelium

1990 ◽  
Vol 9 ◽  
pp. 98 ◽  
Author(s):  
Andrés Paler-Martinez ◽  
Peter Panus ◽  
Bruce Freeman
Nanoscale ◽  
2018 ◽  
Vol 10 (25) ◽  
pp. 11820-11830 ◽  
Author(s):  
Marco Pelin ◽  
Laura Fusco ◽  
Cristina Martín ◽  
Silvio Sosa ◽  
Javier Frontiñán-Rubio ◽  
...  

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


2006 ◽  
Vol 96 (S1) ◽  
pp. S31-S33 ◽  
Author(s):  
Mari-Carmen Gomez-Cabrera ◽  
Agustín Martínez ◽  
Gustavo Santangelo ◽  
Federico V. Pallardó ◽  
Juan Sastre ◽  
...  

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.


1991 ◽  
Vol 260 (4) ◽  
pp. G556-G563 ◽  
Author(s):  
H. Hiraishi ◽  
A. Terano ◽  
S. Ota ◽  
H. Mutoh ◽  
M. Razandi ◽  
...  

The gastric epithelium is exposed to oxygen species that are generated within the lumen. Reactive oxygen species, enzymatically generated, cause injury to cultured rat gastric mucosal cells. Much interest has been focused on the role of iron in producing oxidant-mediated injury to the gastric mucosa, because iron is a catalyst that promotes the production of .OH possibly from O2-. and H2O2 (Haber-Weiss reaction) or from H2O2 alone (Fenton reaction). With the use of an iron chelator and an iron binding protein, we examined the role of iron in producing oxidant-mediated injury to cultured gastric mucosal cells. Reactive oxygen species and H2O2 were generated by hypoxanthine-xanthine oxidase and glucose-glucose oxidase, respectively, in buffer without iron. Pretreatment with deferoxamine diminished hypoxanthine-xanthine oxidase-induced 51Cr release from prelabeled cells, dose dependently. Furthermore, addition of deferoxamine to the reactive oxygen species-generating system also protected against the injury. However, apotransferrin (which binds extracellular iron) failed to protect cells. Pretreatment with .OH scavengers was partially protective. Depletion of glutathione with diethyl maleate enhanced reactive oxygen species-mediated cytolysis; such cytolysis was inhibited by deferoxamine. Deferoxamine also decreased 51Cr release induced by glucose-glucose oxidase. We conclude that intracellular iron plays a crucial role in mediating oxygen radical damage to gastric mucosal cells. The .OH, produced from H2O2 by the iron-catalyzed Fenton reaction, seems to be the main mediator of oxidant-induced cytotoxicity to gastric mucosal cells in vitro.


2013 ◽  
Vol 20 (2) ◽  
pp. 149-155
Author(s):  
Mircea Munteanu ◽  
Adrian Sturza ◽  
Adalbert Schiller ◽  
Romulus Timar

Abstract Cardiovascular disease is the leading cause of disease / mortality worldwide. It is generally accepted that increased production of reactive oxygen species (ROS) has an important role in cardiovascular pathology, contributing to endothelial dysfunction and to the aggravation of atherosclerosis. Among all cardiovascular risk factors, diabetes mellitus is one of the most important. The worldwide prevalence of diabetes has increased rapidly even in developing countries, doubling the combined risk of cardiovascular events in patients with hypertension. In diabetes, increased reactive oxygen species (ROS) production leads to endothelial dysfunction, recognized by the presence of impaired vascular relaxation, increased vascular smooth muscle cells growth and hypertrophy, all together contributing to atherosclerotic plaque formation. On this basis, the vascular endothelium has emerged as a therapeutic target, with the aim to improve systemic metabolic state by improving vascular function. In this review we have focused on the most important sources of reactive oxygen species generated by vascular endothelium in diabetic patients (NADPH Oxidases, eNOS uncoupling, Xanthine oxidase). The importance of oxidative stress in mediating the vascular complications of diabetes is supported by studies showing that antioxidant therapy correct the vascular function in humans or in experimental models of diabetes. Therefore, understanding the physiological mechanisms involved in vascular disorders resulting from hyperglycemia is essential for the proper use of available therapeutic resources.


Sign in / Sign up

Export Citation Format

Share Document