Ofloxacin-associated retinopathy in rabbits: role of oxidative stress

2008 ◽  
Vol 27 (5) ◽  
pp. 409-415 ◽  
Author(s):  
S Rampal ◽  
R Kaur ◽  
R Sethi ◽  
O Singh ◽  
N Sood
Keyword(s):  
Oxidative Stress ◽  
Cell Layer ◽  
Enzymic Activity ◽  
Cellular Infiltration ◽  
Significant Elevation ◽  
Glutathione S Transferase ◽  
Glutathione Redox Cycle ◽  
Histopathological Studies ◽  
Glutathione Redox

Ofloxacin, a quinolone, is an extensively used, well-tolerated antibacterial agent but has been reported to induce photosensitivity at low incidences. In the present investigation, the possible role of oxidative stress in ofloxacin-induced retinopathy in rabbits was evaluated. It was observed that ofloxacin at a dose rate of 10 and 20 mg/rabbit, twice daily for 21 consecutive days, resulted in significant elevation in the extent of lipid peroxidation and depletion of the blood glutathione levels. Marked alterations were also observed in various parameters of the glutathione-redox cycle. There was significant increase in the enzymic activity of glutathione peroxidase and glutathione reductase, whereas a significant decrease was observed in the activities of superoxide dismutase, catalase, and glutathione-S-transferase enzymes. Histopathological studies revealed retinal damage especially in the pigmented cell layer. Degenerative changes in liver and kidneys were also observed. Liver showed focal areas of necrosis, dilation of sinusoids, and cellular infiltration, whereas in kidneys, there was glomerular and tubular degeneration, suggesting impaired renal functioning.

Reductant substrate for glutathione peroxidase modulates oxidant inhibition of Ca2+ signaling in endothelial cells

1995 ◽  
Vol 268 (1) ◽  
pp. H278-H287 ◽  
Author(s):  
S. J. Elliott ◽  
T. N. Doan ◽  
P. N. Henschke
Keyword(s):  
Endothelial Cells ◽  
Glutathione Peroxidase ◽  
Oxidant Stress ◽  
Glutathione S Transferase ◽  
Glutathione Redox Cycle ◽  
Tert Butyl Hydroperoxide ◽  
Intracellular Glutathione ◽  
Glutamylcysteine Synthetase ◽  
Dependent Signal

Oxidant stress mediated by tert-butyl hydroperoxide (t-BOOH) inhibits agonist-stimulated Ca2+ entry and internal store Ca2+ release in cultured endothelial cells. The role of intracellular glutathione in modulating the effects of oxidant stress on Ca2+ signaling was determined in cells preincubated with buthionine-[S,R]-sulfoximine (BSO), an inhibitor of gamma-glutamylcysteine synthetase, or 1-chloro-2,4-dinitrobenzene (CDNB), a cosubstrate for glutathione-S-transferase. BSO and CDNB decreased endothelial cell glutathione content by 85 and 97%, respectively (control glutathione, 21.5 +/- 2.3 nmol/mg protein). Each agent accelerated the time-dependent effects of t-BOOH on Ca2+ signaling in fura 2-loaded cells and potentiated the inhibition of bradykinin-stimulated 45Ca2+ efflux induced by t-BOOH. These results indicate that decreased availability of reduced glutathione, the primary cosubstrate for glutathione peroxidase, potentiates the effect of hydroperoxide oxidant stress on receptor-operated Ca2+ entry across the plasmalemma and Ca2+ release from internal stores. The present findings suggest that intracellular glutathione availability and/or glutathione redox cycle activity are critically important modulators of oxidant inhibition of Ca(2+)-dependent signal transduction.

Role of glutathione redox cycle in TNF-α-mediated endothelial cell dysfunction

1995 ◽  
Vol 117 (2) ◽  
pp. 179-188 ◽  
Author(s):  
Michal Toborek ◽  
Steven W. Barger ◽  
Mark P. Mattson ◽  
Craig J. McClain ◽  
Bernhard Hennig
Keyword(s):  
Endothelial Cell ◽  
Redox Cycle ◽  
Endothelial Cell Dysfunction ◽  
Cell Dysfunction ◽  
Glutathione Redox Cycle ◽  
Tnf Α ◽  
Glutathione Redox

scholarly journals Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Vladan P. Bajic ◽  
Christophe Van Neste ◽  
Milan Obradovic ◽  
Sonja Zafirovic ◽  
Djordje Radak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Redox Homeostasis ◽  
Cardiovascular Complications ◽  
Homeostatic Mechanism ◽  
Redox Mechanism ◽  
Signaling Mechanisms ◽  
Research Findings ◽  
Glutathione Redox

More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.

In vitro toxicity of hydrogen peroxide against normal vs. tumor rat hepatocytes: Role of catalase and of the glutathione redox cycle

Hepatology ◽  
1988 ◽  
Vol 8 (6) ◽  
pp. 1673-1678 ◽  
Author(s):  
Philippe Mavier ◽  
Bernard Guigui ◽  
Anne-Marie Preaux ◽  
Jean Rosenbaum ◽  
Marie-Claude Lescs ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Rat Hepatocytes ◽  
In Vitro Toxicity ◽  
Redox Cycle ◽  
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.

Influence of flavonoid extracts from celery on oxidative stress induced by dichlorvos in rats

2011 ◽  
Vol 31 (6) ◽  
pp. 617-625 ◽  
Author(s):  
J Cao ◽  
X Zhang ◽  
Q Wang ◽  
L Jia ◽  
Y Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treated Group ◽  
Protective Role ◽  
Normal Diet ◽  
Intragastric Administration ◽  
Glutathione S Transferase ◽  
Male Wistar Rats ◽  
Mda Content ◽  
Gpx Activity

The present work was to investigate the effects of flavonoid extracts from celery on oxidative stress induced by dichlorvos (DIC) in male Wistar rats maintained on a normal diet. The rats were given DIC through intragastric administration by the dose of 7.2 mg/kg·body weight (bw)/day and additionally added 5% flavonoid extracts to the diet for 4 weeks continuously. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione- S-transferase (GST) and the content of malondialdehyde (MDA) in livers of rats were measured at the end of the experiment. Under the influence of DIC, there were significant decrease in the activities of SOD, CAT and GST and significant increase in GPx activity and MDA content. The results also showed that the activities of SOD, GST and CAT in the DIC-treated group declined significantly when compared with the flavonoid extracts group and the DIC + flavonoid extracts group, respectively. With regard to GPx activity and MDA content, significant increase were showed in the DIC-treated group in comparison to those in the flavonoid extracts group and the DIC + flavonoid extracts group, respectively. The observations presented lead us to conclude the harmful effects of DIC during the exposure and the protective role of flavonoids in minimizing these effects.

Role of Oxidative Stress Mediated by Glutathione-S-transferase in Thiopurines’ Toxic Effects

2015 ◽  
Vol 28 (6) ◽  
pp. 1186-1195 ◽  
Author(s):  
Marco Pelin ◽  
Sara De Iudicibus ◽  
Laura Fusco ◽  
Eleonora Taboga ◽  
Giulia Pellizzari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Toxic Effects ◽  
Glutathione S Transferase
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