Differential influences of various arsenic compounds on glutathione redox status and antioxidative enzymes in porcine endothelial cells

2002 ◽  
Vol 59 (11) ◽  
pp. 1972-1982 ◽  
Author(s):  
J. Y. Yeh ◽  
L. C. Cheng ◽  
B. R. Ou ◽  
P. D. Whanger ◽  
L. W. Chang
Keyword(s):  
Endothelial Cells ◽  
Antioxidative Enzymes ◽  
Redox Status ◽  
Arsenic Compounds ◽  
Porcine Endothelial Cells ◽  
Glutathione Redox

Resveratrol and grape juice: Effects on redox status and nitric oxide production of endothelial cells in in vitro preeclampsia model

2021 ◽  
Vol 23 ◽  
pp. 205-210
Author(s):  
Mayara Caldeira-Dias ◽  
Sarah Viana-Mattioli ◽  
Jackeline de Souza Rangel Machado ◽  
Mattias Carlström ◽  
Ricardo de Carvalho Cavalli ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Grape Juice ◽  
Redox Status ◽  
Nitric Oxide Production ◽  
Oxide Production

scholarly journals Induction of nitric oxide synthesis in J774 cells lowers intracellular glutathione: effect of modulated glutathione redox status on nitric oxide synthase induction

1997 ◽  
Vol 322 (2) ◽  
pp. 477-481 ◽  
Author(s):  
John S. HOTHERSALL ◽  
Fernando Q. CUNHA ◽  
Guy H. NEILD ◽  
Alberto A. NOROHNA-DUTRA
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
De Novo ◽  
Redox Status ◽  
No Production ◽  
Duration Of Treatment ◽  
Intracellular Glutathione ◽  
J774 Cells ◽  
Oxide Synthase ◽  
Glutathione Redox

Under pathological conditions, the induction of nitric oxide synthase (NOS) in macrophages is responsible for NO production to a cytotoxic concentration. We have investigated changes to, and the role of, intracellular glutathione in NO production by the activated murine macrophage cell line J774. Total glutathione concentrations (reduced, GSH, plus the disulphide, GSSG) were decreased to 45% of the control 48 h after cells were activated with bacterial lipopolysaccharide plus interferon γ. This was accompanied by a decrease in the GSH/GSSG ratio from 12:1 to 2:1. The intracellular decrease was not accounted for by either GSH or GSSG efflux; on the contrary, rapid export of glutathione in control cells was abrogated during activation. The loss of intra- and extracellular glutathione indicates either a decrease in synthesis de novo, or an increase in utilization, rather than competition for available NADPH. All changes in activated cells were prevented by pretreatment with the NOS inhibitor l-N-(1-iminoethyl)ornithine. Basal glutathione levels in J774 cells were manipulated by pretreatment with (1) buthionine sulphoximine (glutathione synthase inhibitor), (2) acivicin (γ-glutamyltranspeptidase inhibitor), (3) bromo-octane (glutathione S-transferase substrate) and (4) diamide/zinc (thiol oxidant and glutathione reductase inhibitor). All treatments significantly decreased the output of NO following activation. The degree of inhibition was dependent on (i) duration of treatment prior to activation, (ii) rate of depletion or subsequent recovery and (iii) thiol end product. The level of GSH did not significantly affect the production of NO, after induction of NOS. Thus, glutathione redox status appears to plays an important role in NOS induction during macrophage activation.

scholarly journals The Effectiveness of Glutathione Redox Status as a Possible Tumor Marker in Colorectal Cancer

2021 ◽  
Vol 22 (12) ◽  
pp. 6183
Author(s):  
Delia Acevedo-León ◽  
Lidia Monzó-Beltrán ◽  
Segundo Ángel Gómez-Abril ◽  
Nuria Estañ-Capell ◽  
Natalia Camarasa-Lillo ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Redox State ◽  
Reduced Glutathione ◽  
Redox Status ◽  
Oxidation Products ◽  
Interventional Study ◽  
Thiol Redox State ◽  
Thiol Redox ◽  
Glutathione Redox

The role of oxidative stress (OS) in cancer is a matter of great interest due to the implication of reactive oxygen species (ROS) and their oxidation products in the initiation of tumorigenesis, its progression, and metastatic dissemination. Great efforts have been made to identify the mechanisms of ROS-induced carcinogenesis; however, the validation of OS byproducts as potential tumor markers (TMs) remains to be established. This interventional study included a total of 80 colorectal cancer (CRC) patients and 60 controls. By measuring reduced glutathione (GSH), its oxidized form (GSSG), and the glutathione redox state in terms of the GSSG/GSH ratio in the serum of CRC patients, we identified significant changes as compared to healthy subjects. These findings are compatible with the effectiveness of glutathione as a TM. The thiol redox state showed a significant increase towards oxidation in the CRC group and correlated significantly with both the tumor state and the clinical evolution. The sensitivity and specificity of serum glutathione levels are far above those of the classical TMs CEA and CA19.9. We conclude that the GSSG/GSH ratio is a simple assay which could be validated as a novel clinical TM for the diagnosis and monitoring of CRC.

scholarly journals Impact of a dietary challenge with peroxidized oil on the glutathione redox status and integrity of the small intestine in weaned piglets

animal ◽  
2019 ◽  
Vol 13 (8) ◽  
pp. 1641-1650 ◽  
Author(s):  
J. Degroote ◽  
W. Wang ◽  
H. Vergauwen ◽  
S. De Smet ◽  
C. Van Ginneken ◽  
...  
Keyword(s):  
Small Intestine ◽  
Redox Status ◽  
Weaned Piglets ◽  
Glutathione Redox

Intracellular redox status affects transplasma membrane electron transport in pulmonary arterial endothelial cells

2002 ◽  
Vol 282 (1) ◽  
pp. L36-L43 ◽  
Author(s):  
Marilyn P. Merker ◽  
Robert D. Bongard ◽  
Nicholas J. Kettenhofen ◽  
Yoshiyuki Okamoto ◽  
Christopher A. Dawson
Keyword(s):  
Endothelial Cells ◽  
Electron Transport ◽  
Control Level ◽  
Redox Status ◽  
Cellular Mechanisms ◽  
Control Activity ◽  
Transplasma Membrane Electron Transport ◽  
Cell Extracts ◽  
Pulmonary Arterial ◽  
Arterial Endothelial Cells

Pulmonary arterial endothelial cells possess transplasma membrane electron transport (TPMET) systems that transfer intracellular reducing equivalents to extracellular electron acceptors. As one aspect of determining cellular mechanisms involved in one such TPMET system in pulmonary arterial endothelial cells in culture, glycolysis was inhibited by treatment with iodoacetate (IOA) or by replacing the glucose in the cell medium with 2-deoxy-d-glucose (2-DG). TPMET activity was measured as the rate of reduction of the extracellular electron acceptor polymer toluidine blue O polyacrylamide. Intracellular concentrations of NADH, NAD+, NADPH, and NADP+ were determined by high-performance liquid chromatography of KOH cell extracts. IOA decreased TPMET activity to 47% of control activity concomitant with a decrease in the NADH/NAD+ ratio to 34% of the control level, without a significant change in the NADPH/NADP+ ratio. 2-DG decreased TPMET activity to 53% of control and decreased both NADH/NAD+ and NADPH/NADP+ ratios to 51% and 55%, respectively, of control levels. When lactate was included in the medium along with the inhibitors, the effects of IOA and 2-DG on both TPMET activity and the NADPH/NADP+ ratios were prevented. The results suggest that cellular redox status is a determinant of pulmonary arterial endothelial cell TPMET activity, with TPMET activity more highly correlated with the poise of the NADH/NAD+redox pair.

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