Dithiocarbamate Toxicity toward Thymocytes Involves Their Copper-Catalyzed Conversion to Thiuram Disulfides, Which Oxidize Glutathione in a Redox Cycle without the Release of Reactive Oxygen Species

1998 ◽  
Vol 353 (1) ◽  
pp. 73-84 ◽  
Author(s):  
Mark J. Burkitt ◽  
Hugh S. Bishop ◽  
Lesley Milne ◽  
Shui Ying Tsang ◽  
Gordon J. Provan ◽  
...  
2018 ◽  
Vol 78 (6) ◽  
pp. 1390-1399 ◽  
Author(s):  
Wenshu Li ◽  
Peng Zhou ◽  
Jing Zhang ◽  
Yongli Zhang ◽  
Gucheng Zhang ◽  
...  

Abstract This study investigated the generation of reactive oxygen species (ROS) (O2−•, H2O2, and HO•) by promoting the Cu(II)/Cu(I) redox cycle with certain reducing agents (RAs) in aerobic aqueous solution, and benzoic acid (BA) was employed as indicator for the hydroxyl radical (HO•). Hydroxylamine (HA) can reduce Cu(II) to Cu(I) to induce chain reactions of copper species resulting in the generation of the superoxide radical (O2−•) and hydrogen peroxide (H2O2), and the intermediate Cu(I) can further activate H2O2 via a Fenton-like reaction to produce HO•, creating the remarkable BA degradation. O2 is indispensable, and unprotonated HA is the motive power in the O2/Cu/HA system. Moreover, pH is a crucial factor of the O2/Cu/HA system due to the protonated HA not being able to reduce Cu(II) into Cu(I). The oxidation of HA can be effectively induced by trace amounts of Cu(II), and both a higher HA dosage and a higher Cu(II) dosage can enhance H2O2 generation and BA degradation. In addition, some other RAs that can reduce Cu(II) into Cu(I) could replace HA in the O2/Cu/HA system to induce the generation of these ROS in aerobic aqueous solution.


2008 ◽  
Vol 393 (4) ◽  
pp. 1337-1343 ◽  
Author(s):  
Naoya Kishikawa ◽  
Nobuhiro Ohkubo ◽  
Kaname Ohyama ◽  
Kenichiro Nakashima ◽  
Naotaka Kuroda

2013 ◽  
Vol 26 (12) ◽  
pp. 1862-1871 ◽  
Author(s):  
Matthew A. Kelley ◽  
Valeria Y. Hebert ◽  
Taylor M. Thibeaux ◽  
Mackenzie A. Orchard ◽  
Farhana Hasan ◽  
...  

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

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel

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.


2001 ◽  
Vol 120 (5) ◽  
pp. A361-A361
Author(s):  
K UCHIKURA ◽  
T WADA ◽  
Z SUN ◽  
S HOSHINO ◽  
G BULKLEY ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document