scholarly journals The oxidation state of the cytoplasmic glutathione redox system does not correlate with replicative lifespan in yeast

2016 ◽  
Vol 2 (1) ◽  
Author(s):  
Robert A Knieß ◽  
Matthias P Mayer
2020 ◽  
Vol 104 (5) ◽  
pp. 1531-1539
Author(s):  
Benjamin Kövesi ◽  
Csilla Pelyhe ◽  
Erika Zándoki ◽  
Miklós Mézes ◽  
Krisztián Balogh

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e108115 ◽  
Author(s):  
Kazuma Izawa ◽  
Motoi Okada ◽  
Kazuhiro Sumitomo ◽  
Naoki Nakagawa ◽  
Yoshiaki Aizawa ◽  
...  

1999 ◽  
Vol 29 (6) ◽  
pp. 543-568 ◽  
Author(s):  
Qamar Rahman ◽  
Parveen Abidi ◽  
Farrukh Afaq ◽  
D. Schiffmann ◽  
Brooke T. Mossman ◽  
...  

2008 ◽  
Vol 83 (5) ◽  
pp. 2338-2348 ◽  
Author(s):  
Misao Kuroki ◽  
Yasuo Ariumi ◽  
Masanori Ikeda ◽  
Hiromichi Dansako ◽  
Takaji Wakita ◽  
...  

ABSTRACT Arsenic trioxide (ATO), a therapeutic reagent used for the treatment of acute promyelocytic leukemia, has recently been reported to increase human immunodeficiency virus type 1 infectivity. However, in this study, we have demonstrated that replication of genome-length hepatitis C virus (HCV) RNA (O strain of genotype 1b) was notably inhibited by ATO at submicromolar concentrations without cell toxicity. RNA replication of HCV-JFH1 (genotype 2a) and the release of core protein into the culture supernatants were also inhibited by ATO after the HCV infection. To clarify the mechanism of the anti-HCV activity of ATO, we examined whether or not PML is associated with this anti-HCV activity, since PML is known to be a target of ATO. Interestingly, we observed the cytoplasmic translocation of PML after treatment with ATO. However, ATO still inhibited the HCV RNA replication even in the PML knockdown cells, suggesting that PML is dispensable for the anti-HCV activity of ATO. In contrast, we found that N-acetyl-cysteine, an antioxidant and glutathione precursor, completely and partially eliminated the anti-HCV activity of ATO after 24 h and 72 h of treatment, respectively. In this context, it is worth noting that we found an elevation of intracellular superoxide anion radical, but not hydrogen peroxide, and the depletion of intracellular glutathione in the ATO-treated cells. Taken together, these findings suggest that ATO inhibits the HCV RNA replication through modulation of the glutathione redox system and oxidative stress.


2010 ◽  
Vol 34 (1) ◽  
pp. 123-130 ◽  
Author(s):  
Theresa W. Gauthier ◽  
Julie A. Kable ◽  
Leandrea Burwell ◽  
Claire D. Coles ◽  
Lou Ann S. Brown

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