Arsenite induces cell transformation by reactive oxygen species, AKT, ERK1/2, and p70S6K1

2011 ◽  
Vol 414 (3) ◽  
pp. 533-538 ◽  
Author(s):  
Richard L. Carpenter ◽  
Yue Jiang ◽  
Yi Jing ◽  
Jun He ◽  
Yon Rojanasakul ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Transformation ◽  
Reactive Oxygen ◽  
Oxygen Species

Regulation of miRNA-21 by reactive oxygen species-activated ERK/NF-κB in arsenite-induced cell transformation

2012 ◽  
Vol 52 (9) ◽  
pp. 1508-1518 ◽  
Author(s):  
Min Ling ◽  
Yuan Li ◽  
Yuan Xu ◽  
Ying Pang ◽  
Lu Shen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Transformation ◽  
Reactive Oxygen ◽  
Oxygen Species

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Fas ligand expression in rat kupffer cells in response to lipopolysaccharide is mediated by reactive oxygen species

2001 ◽  
Vol 120 (5) ◽  
pp. A361-A361
Author(s):  
K UCHIKURA ◽  
T WADA ◽  
Z SUN ◽  
S HOSHINO ◽  
G BULKLEY ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Kupffer Cells ◽  
Fas Ligand ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ligand Expression
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