scholarly journals Melatonin restores neutrophil functions and prevents apoptosis amid dysfunctional glutathione redox system

2020 ◽  
Vol 69 (3) ◽  
Author(s):  
Somanathapura K. NaveenKumar ◽  
Mahadevappa Hemshekhar ◽  
Swamy Jagadish ◽  
Kurnegala Manikanta ◽  
Gopalapura J. Vishalakshi ◽  
...  
Keyword(s):  
Redox System ◽  
Glutathione Redox System ◽  
Glutathione Redox

scholarly journals Combined effects of aflatoxin B1 and deoxynivalenol on the expression of glutathione redox system regulatory genes in common carp

2020 ◽  
Vol 104 (5) ◽  
pp. 1531-1539
Author(s):  
Benjamin Kövesi ◽  
Csilla Pelyhe ◽  
Erika Zándoki ◽  
Miklós Mézes ◽  
Krisztián Balogh
Keyword(s):  
Common Carp ◽  
Aflatoxin B1 ◽  
Redox System ◽  
Regulatory Genes ◽  
Combined Effects ◽  
Glutathione Redox System ◽  
Glutathione Redox

scholarly journals Impaired Glutathione Redox System Paradoxically Suppresses Angiotensin II-Induced Vascular Remodeling

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e108115 ◽  
Author(s):  
Kazuma Izawa ◽  
Motoi Okada ◽  
Kazuhiro Sumitomo ◽  
Naoki Nakagawa ◽  
Yoshiaki Aizawa ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Vascular Remodeling ◽  
Redox System ◽  
Glutathione Redox System ◽  
Glutathione Redox

Glutathione Redox System in Oxidative Lung Injury

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

scholarly journals Arsenic Trioxide Inhibits Hepatitis C Virus RNA Replication through Modulation of the Glutathione Redox System and Oxidative Stress

2008 ◽  
Vol 83 (5) ◽  
pp. 2338-2348 ◽  
Author(s):  
Misao Kuroki ◽  
Yasuo Ariumi ◽  
Masanori Ikeda ◽  
Hiromichi Dansako ◽  
Takaji Wakita ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Arsenic Trioxide ◽  
Redox System ◽  
Rna Replication ◽  
Hcv Rna ◽  
Glutathione Redox System ◽  
And Oxidative Stress ◽  
Glutathione Redox

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.

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