Critical Roles for Polymerase ζ in Cellular Tolerance to Nitric Oxide–Induced DNA Damage

2006 ◽  
Vol 66 (2) ◽  
pp. 748-754 ◽  
Author(s):  
Xiaohua Wu ◽  
Katsuya Takenaka ◽  
Eiichiro Sonoda ◽  
Helfrid Hochegger ◽  
Shosuke Kawanishi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Cellular Tolerance

2118-P: Regulation of Ataxia-Telangiectasia and Rad3-Related (ATR)–Dependent DNA Damage Response by Nitric Oxide in ß-Cells

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 2118-P
Author(s):  
CHAY TENG YEO ◽  
BRYNDON OLESON ◽  
JOHN A. CORBETT ◽  
JAMIE K. SCHNUCK
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Ataxia Telangiectasia ◽  
Damage Response

scholarly journals Genotoxic and oxidative effect of duloxetine on mouse brain and liver tissues

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Isela Álvarez-González ◽  
Scarlett Camacho-Cantera ◽  
Patricia Gómez-González ◽  
Michael J. Rendón Barrón ◽  
José A. Morales-González ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Mouse Brain ◽  
Control Level ◽  
Dna Oxidation ◽  
Methyl Methanesulfonate ◽  
Control Group ◽  
Oxidative Potential ◽  
The Brain ◽  
Oxidative Effect

AbstractWe evaluated the duloxetine DNA damaging capacity utilizing the comet assay applied to mouse brain and liver cells, as well as its DNA, lipid, protein, and nitric oxide oxidative potential in the same cells. A kinetic time/dose strategy showed the effect of 2, 20, and 200 mg/kg of the drug administered intraperitoneally once in comparison with a control and a methyl methanesulfonate group. Each parameter was evaluated at 3, 9, 15, and 21 h postadministration in five mice per group, except for the DNA oxidation that was examined only at 9 h postadministration. Results showed a significant DNA damage mainly at 9 h postexposure in both organs. In the brain, with 20 and 200 mg/kg we found 50 and 80% increase over the control group (p ≤ 0.05), in the liver, the increase of 2, 20, and 200 mg/kg of duloxetine was 50, 80, and 135% in comparison with the control level (p ≤ 0.05). DNA, lipid, protein and nitric oxide oxidation increase was also observed in both organs. Our data established the DNA damaging capacity of duloxetine even with a dose from the therapeutic range (2 mg/kg), and suggest that this effect can be related with its oxidative potential.

scholarly journals Modulation of Carcinogen Metabolism by Nitric Oxide-Aspirin 2 Is Associated with Suppression of DNA Damage and DNA Adduct Formation

2009 ◽  
Vol 284 (33) ◽  
pp. 22099-22107 ◽  
Author(s):  
Christopher J. MacDonald ◽  
Robert Y. S. Cheng ◽  
David D. Roberts ◽  
David A. Wink ◽  
Grace Chao Yeh
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Adduct Formation ◽  
Dna Adduct ◽  
Carcinogen Metabolism

scholarly journals Immunosuppressive Myeloid Cells Induce Nitric Oxide–Dependent DNA Damage and p53 Pathway Activation in CD8+ T Cells

2021 ◽  
Author(s):  
Adam N.R. Cartwright ◽  
Shengbao Suo ◽  
Soumya Badrinath ◽  
Sushil Kumar ◽  
Johannes Melms ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
T Cells ◽  
Cd8 T Cells ◽  
Myeloid Cells ◽  
P53 Pathway ◽  
Pathway Activation

scholarly journals Bioflavonoid-Induced Apoptosis and DNA Damage in Amastigotes and Promastigotes of Leishmania donovani: Deciphering the Mode of Action

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5843
Author(s):  
Shaila Mehwish ◽  
Sanjay Varikuti ◽  
Mubarak Ali Khan ◽  
Tariq Khan ◽  
Imdad Ullah Khan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Leishmania Donovani ◽  
Genetic Material ◽  
Mechanisms Of Action ◽  
Pcr Analysis ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Ic50 Values

Natural products from plants contain many interesting biomolecules. Among them, quercetin (Q), gallic acid (GA), and rutin (R) all have well-reported antileishmanial activity; however, their exact mechanisms of action are still not known. The current study is a step forward towards unveil the possible modes of action of these compounds against Leishmania donovani (the causative agent of visceral leishmaniasis). The selected compounds were checked for their mechanisms of action against L. donovani using different biological assays including apoptosis and necrosis evaluation, effects on genetic material (DNA), quantitative testing of nitric oxide production, ultrastructural modification via transmission electron microscopy, and real-time PCR analysis. The results confirmed that these compounds are active against L. donovani, with IC50 values of 84.65 µg/mL, 86 µg/mL, and 98 µg/mL for Q, GA, and R, respectively. These compounds increased nitric oxide production and caused apoptosis and DNA damage, which led to changes in the treated cells’ ultrastructural behavior and finally to the death of L. donovani. These compounds also suppressed essential enzymes like trypanothione reductase and trypanothione synthetase, which are critical for leishmanial survival. The selected compounds have high antileishmanial potentials, and thus in-vivo testing and further screening are highly recommended.

The suppression of immunity by ultraviolet radiation: UVA, nitric oxide and DNA damage

2004 ◽  
Vol 3 (8) ◽  
pp. 736 ◽  
Author(s):  
Gary M. Halliday ◽  
Scott N. Byrne ◽  
Johanna M. Kuchel ◽  
Terence S. C. Poon ◽  
Ross St. C. Barnetson
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Ultraviolet Radiation

scholarly journals DNA damage and mutation in human cells exposed to nitric oxide in vitro.

1992 ◽  
Vol 89 (7) ◽  
pp. 3030-3034 ◽  
Author(s):  
T. Nguyen ◽  
D. Brunson ◽  
C. L. Crespi ◽  
B. W. Penman ◽  
J. S. Wishnok ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Human Cells

Apoptotic cascade initiated by angiotensin II in neonatal cardiomyocytes: role of DNA damage

2003 ◽  
Vol 285 (6) ◽  
pp. H2364-H2372 ◽  
Author(s):  
Valentina Grishko ◽  
Viktor Pastukh ◽  
Viktoriya Solodushko ◽  
Mark Gillespie ◽  
Junichi Azuma ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Ventricular Remodeling ◽  
Oxidase Inhibitor ◽  
Neonatal Cardiomyocytes ◽  
Diphenylene Iodonium ◽  
Nitric Oxide Inhibitor

Angiotensin II contributes to ventricular remodeling by promoting both cardiac hypertrophy and apoptosis; however, the mechanism underlying the latter phenomenon is poorly understood. One possibility that has been advanced is that angiotensin II activates NADPH oxidase, generating free radicals that trigger apoptosis. In apparent support of this notion, it was found that angiotensin II-mediated apoptosis in the cardiomyocyte is blocked by the NADPH oxidase inhibitor diphenylene iodonium. However, three lines of evidence suggest that peroxynitrite, rather than superoxide, is responsible for angiotensin II-mediated DNA damage and apoptosis. First, the inducible nitric oxide inhibitor aminoguanidine prevents angiotensin II-induced DNA damage and apoptosis. Second, based on ligation-mediated PCR, the pattern of angiotensin II-induced DNA damage resembles peroxynitritemediated damage rather than damage caused by either superoxide or nitric oxide. Third, angiotensin II activates p53 through the phosphorylation of Ser15 and Ser20, residues that are commonly phosphorylated in response to DNA damage. It is proposed that angiotensin II promotes the oxidation of DNA, which in turn activates p53 to mediate apoptosis.

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