scholarly journals Berichtigung: Probing the Intracellular Glutathione Redox Potential by In-Cell NMR Spectroscopy

2014 ◽  
Vol 126 (11) ◽  
pp. 2838-2838
Author(s):  
Steve Y. Rhieu ◽  
Aaron A. Urbas ◽  
Daniel W. Bearden ◽  
John P. Marino ◽  
Katrice A. Lippa ◽  
...  
2013 ◽  
Vol 126 (2) ◽  
pp. 457-460 ◽  
Author(s):  
Steve Y. Rhieu ◽  
Aaron A. Urbas ◽  
Daniel W. Bearden ◽  
John P. Marino ◽  
Katrice A. Lippa ◽  
...  

2013 ◽  
Vol 53 (2) ◽  
pp. 447-450 ◽  
Author(s):  
Steve Y. Rhieu ◽  
Aaron A. Urbas ◽  
Daniel W. Bearden ◽  
John P. Marino ◽  
Katrice A. Lippa ◽  
...  

2014 ◽  
Vol 53 (11) ◽  
pp. 2797-2797
Author(s):  
Steve Y. Rhieu ◽  
Aaron A. Urbas ◽  
Daniel W. Bearden ◽  
John P. Marino ◽  
Katrice A. Lippa ◽  
...  

2019 ◽  
Vol 476 (13) ◽  
pp. 1857-1873 ◽  
Author(s):  
Shambhu Yadav ◽  
Bindia Chawla ◽  
Mohammad Anwar Khursheed ◽  
Rajesh Ramachandran ◽  
Anand Kumar Bachhawat

Abstract Calcium signaling is essential for embryonic development but the signals upstream of calcium are only partially understood. Here, we investigate the role of the intracellular glutathione redox potential in calcium signaling using the Chac1 protein of zebrafish. A member of the γ-glutamylcyclotransferase family of enzymes, the zebrafish Chac1 is a glutathione-degrading enzyme that acts only on reduced glutathione. The zebrafish chac1 expression was seen early in development, and in the latter stages, in the developing muscles, brain and heart. The chac1 knockdown was embryonic lethal, and the developmental defects were seen primarily in the myotome, brain and heart where chac1 was maximally expressed. The phenotypes could be rescued by the WT Chac1 but not by the catalytically inactive Chac1 that was incapable of degrading glutathione. The ability of chac1 to alter the intracellular glutathione redox potential in the live animals was examined using Grx1-roGFP2. The chac1 morphants lacked the increased degree of cellular oxidation seen in the WT zebrafish. As calcium is also known to be critical for the developing myotomes, brain and heart, we further investigated if the chac1 knockdown phenotypes were a consequence of the lack of calcium signals. We observed using GCaMP6s, that calcium transients normally seen in the developing embryos were strongly attenuated in these knockdowns. The study thus identifies Chac1 and the consequent change in intracellular glutathione redox potential as important upstream activators of calcium signaling during development.


2008 ◽  
Vol 5 (6) ◽  
pp. 553-559 ◽  
Author(s):  
Marcus Gutscher ◽  
Anne-Laure Pauleau ◽  
Laurent Marty ◽  
Thorsten Brach ◽  
Guido H Wabnitz ◽  
...  

1997 ◽  
Vol 322 (2) ◽  
pp. 477-481 ◽  
Author(s):  
John S. HOTHERSALL ◽  
Fernando Q. CUNHA ◽  
Guy H. NEILD ◽  
Alberto A. NOROHNA-DUTRA

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.


2013 ◽  
Vol 162 (1) ◽  
pp. 16-25 ◽  
Author(s):  
Khaled Khazim ◽  
Daniela Giustarini ◽  
Ranieri Rossi ◽  
Darlene Verkaik ◽  
John E. Cornell ◽  
...  

2008 ◽  
Vol 10 (4) ◽  
pp. 821-828 ◽  
Author(s):  
Junying Wang ◽  
Hiroyuki Mochizuki ◽  
Makoto Todokoro ◽  
Hirokazu Arakawa ◽  
Akihiro Morikawa

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