scholarly journals A direct and continuous assay for the determination of thioredoxin reductase activity in cell lysates

2013 ◽  
Vol 443 (1) ◽  
pp. 34-40 ◽  
Author(s):  
Brian Cunniff ◽  
Gregg W. Snider ◽  
Nicholas Fredette ◽  
Robert J. Hondal ◽  
Nicholas H. Heintz
1997 ◽  
Vol 253 (1) ◽  
pp. 123-125 ◽  
Author(s):  
Kristina E. Hill ◽  
Gary W. McCollum ◽  
Raymond F. Burk

2021 ◽  
Vol 3 ◽  
pp. 100127
Author(s):  
Tendai J. Mafireyi ◽  
Jorge O. Escobedo ◽  
Robert M. Strongin

1989 ◽  
Vol 21 (4) ◽  
pp. 285-291 ◽  
Author(s):  
Otto Hockwin ◽  
Peter Müller ◽  
Jan Krolczyk ◽  
Bette A. McCue ◽  
Philip R. Mayer

2009 ◽  
Vol 2009 ◽  
pp. 1-10 ◽  
Author(s):  
Andrean L. Simons ◽  
Arlene D. Parsons ◽  
Katherine A. Foster ◽  
Kevin P. Orcutt ◽  
Melissa A. Fath ◽  
...  

The hypothesis that the Akt inhibitor, perifosine (PER), combined with inhibitors of glutathione (GSH) and thioredoxin (Trx) metabolism will induce cytotoxicity via metabolic oxidative stress in human head and neck cancer (HNSCC) cells was tested. PER induced increases in glutathione disulfide (%GSSG) in FaDu, Cal-27, and SCC-25 HNSCCs as well as causing significant clonogenic cell killing in FaDu and Cal-27, which was suppressed by simultaneous treatment with N-acetylcysteine (NAC). An inhibitor of GSH synthesis, buthionine sulfoximine (BSO), sensitized Cal-27 and SCC-25 cells to PER-induced clonogenic killing as well as decreased total GSH and increased %GSSG. Additionally, inhibition of thioredoxin reductase activity (TrxRed) with auranofin (AUR) was able to induce PER sensitization in SCC-25 cells that were initially refractory to PER. These results support the conclusion that PER induces oxidative stress and clonogenic killing in HNSCC cells that is enhanced with inhibitors of GSH and Trx metabolism.


1996 ◽  
Vol 80 (2) ◽  
pp. 215-219 ◽  
Author(s):  
Sylke Müller ◽  
Tim-Wolf Gilberger ◽  
Petra M. Färber ◽  
Katja Becker ◽  
R. Heiner Schirmer ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document