Pyocyanin induces oxidative stress in human endothelial cells and modulates the glutathione redox cycle

2002 ◽  
Vol 33 (11) ◽  
pp. 1527-1533 ◽  
Author(s):  
Michael Muller
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Redox Cycle ◽  
Human Endothelial Cells ◽  
Glutathione Redox Cycle ◽  
Glutathione Redox

scholarly journals Riboflavin (vitamin B2) and oxidative stress: a review

2014 ◽  
Vol 111 (11) ◽  
pp. 1985-1991 ◽  
Author(s):  
Marziyeh Ashoori ◽  
Ahmad Saedisomeolia
Keyword(s):  
Oxidative Stress ◽  
Stress Reduction ◽  
Antioxidant Properties ◽  
The Body ◽  
Redox Cycle ◽  
Antioxidant Action ◽  
Glutathione Redox Cycle ◽  
Main Factors ◽  
And Oxidative Stress ◽  
Glutathione Redox

Oxidative stress is involved in the development of many chronic diseases. One of the main factors involved in oxidative stress reduction is increased antioxidant potential. Some nutrients such as vitamin C, vitamin E and carotenoids are known to act as antioxidants; however, riboflavin is one of the neglected antioxidant nutrients that may have an antioxidant action independently or as a component of the glutathione redox cycle. Herein, studies that have examined the antioxidant properties of riboflavin and its effect on oxidative stress reduction are reviewed. The results of the reviewed studies confirm the antioxidant nature of riboflavin and indicate that this vitamin can protect the body against oxidative stress, especially lipid peroxidation and reperfusion oxidative injury. The mechanisms by which riboflavin protects the body against oxidative stress may be attributed to the glutathione redox cycle and also to other possible mechanisms such as the conversion of reduced riboflavin to the oxidised form.

Effect of medium pH on glutathione redox cycle in cultured human umbilical vein endothelial cells

Metabolism ◽  
1993 ◽  
Vol 42 (9) ◽  
pp. 1121-1126 ◽  
Author(s):  
Motoyoshi Ikebuchi ◽  
Atsunori Kashiwagi ◽  
Takayuki Asahina ◽  
Yasushi Tanaka ◽  
Yoshihumi Takagi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Redox Cycle ◽  
Medium Ph ◽  
Human Umbilical Vein ◽  
Glutathione Redox Cycle ◽  
Umbilical Vein Endothelial Cells ◽  
Glutathione Redox

Glutathione redox cycle regulates nitric oxide-mediated glyceraldehyde-3-phosphate dehydrogenase inhibition

1997 ◽  
Vol 272 (1) ◽  
pp. C99-C108 ◽  
Author(s):  
C. M. Padgett ◽  
A. R. Whorton
Keyword(s):  
Nitric Oxide ◽  
Molecular Weight ◽  
Endothelial Cells ◽  
Low Molecular Weight ◽  
Redox Cycle ◽  
Gapdh Activity ◽  
Cell Extracts ◽  
Glutathione Redox Cycle ◽  
Generating System ◽  
Glutathione Redox

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) has been identified as a potential target for nitric oxide (NO)-mediated cellular toxicity. We have previously shown that NO inhibits GAPDH by S-nitrosylation of the active site cysteine residue, which is reversed by low-molecular-weight thiols. Because endothelial cells contain high concentrations of low-molecular-weight thiols, principally glutathione, we investigated the effect of NO on GAPDH activity in intact endothelial cells and the influence that cellular glutathione has on GAPDH inhibition. Our results show that incubation of cells with an exogenous NO-generating system resulted in inhibition of GAPDH activity. The mechanism for inhibition appears to involve reversible modification of GAPDH because addition of thiols to cell extracts restored activity. Furthermore, cells were able to completely recover GAPDH activity after removal of the NO-generating system. Recovery did not require de novo protein synthesis. Depletion of cellular glutathione levels by treatment of cells with buthionine sulfoximine resulted in greater NO-mediated GAPDH inhibition as well as a lesser ability to recover activity. Finally, disruption of the glutathione redox cycle with the glutathione reductase inhibitor, 1,3-bis(2-chloroethyl)-1-nitrosourea, increased the extent of NO-mediated GAPDH inhibition and decreased both the rate and degree of recovery of GAPDH-activity. These results suggest that the glutathione redox cycle plays an important role not only in regulating the extent of NO-mediated GAPDH inhibition but also in the ability of endothelial cells to recover from NO-mediated GAPDH inhibition.

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