Reactive Oxygen Species (ROS) Protection via Cysteine Oxidation in the Epidermal Cornified Cell Envelope

2013 ◽  
pp. 157-169 ◽  
Author(s):  
Wilbert P. Vermeij ◽  
Claude Backendorf
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Envelope ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cysteine Oxidation ◽  
Cornified Cell Envelope

scholarly journals Reactive Oxygen Species-Mediated Cezanne Inactivation by Oxidation of its Catalytic Cysteine Residue in Hepatocellular Carcinoma

2019 ◽  
Vol 27 (9) ◽  
pp. 1069-1077
Author(s):  
Zhongyuan Yin ◽  
Lin Yang ◽  
Feng Wu ◽  
Jinshuo Fan ◽  
Juanjuan Xu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Matrix Metalloproteinase 2 ◽  
Intercellular Adhesion Molecule ◽  
Oxygen Species ◽  
Cysteine Oxidation ◽  
Diphenylene Iodonium ◽  
Hcc Cells ◽  
Inflammatory Effect

Cysteine oxidation occurs at the active site of deubiquitinases (DUBs) during many biologic signaling cascades. Here we report that hepatocellular carcinoma cells (HCCs) generated higher levels of endogenous reactive oxygen species (ROS). This elevated ROS production was inhibited by NADPH oxidase inhibitor diphenylene iodonium (DPI) and mitochondria electron chain inhibitor rotenone in HCC cells. Moreover, we found that H2O2 could activate NF-κB-dependent inflammatory effect through increased induction of matrix metalloproteinase 2 (MMP2), MMP9, and intercellular adhesion molecule 1 (ICAM1) expression levels. In addition, we found that H2O2 could prolong NF-κB activation by suppressing the negative regulatory functions of Cezanne in HCC cells. Ubiquitin-derived thiol-reactive probe (HA-UbVME) assay and biotin-tagged 1,3-cyclohexadione derivative (DCP-Bio1) assay showed that H2O2 has the capacity to inhibit the catalytic activity of Cezanne, and the reducing agent, DTT, could reactivate the Cezanne deubiquitinating enzyme activity. Taken all together, these findings demonstrated an important role for oxidation of Cezanne by ROS in regulation of the inflammatory effect of hepatocellular carcinoma.

scholarly journals Introduction to approaches and tools for the evaluation of protein cysteine oxidation

2020 ◽  
Vol 64 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Leslie B. Poole ◽  
Cristina M. Furdui ◽  
S. Bruce King
Keyword(s):  
Reactive Oxygen Species ◽  
Best Practices ◽  
Reactive Oxygen ◽  
Cellular Proteins ◽  
Oxygen Species ◽  
Cysteine Oxidation ◽  
Oxidative Modifications ◽  
Cysteine Thiols ◽  
The Way

Abstract Oxidative modifications of cysteine thiols in cellular proteins are pivotal to the way signal-stimulated reactive oxygen species are sensed and elicit appropriate or sometimes pathological responses, but the dynamic and often transitory nature of these modifications offer a challenge to the investigator trying to identify such sites and the responses they elicit. A number of reagents and workflows have been developed to identify proteins undergoing oxidation and to query the timing, extent and location of such modifications, as described in this minireview. While no approach is perfect to capture all the redox information in a functioning cell, best practices described herein can enable considerable insights into the “redox world” of cells and organisms.

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
Sign in / Sign up

Export Citation Format

Share Document