2023 POSTER Can Radiation-Induced Chronic-Oxidative Stress in Kidney and Liver Be Prevented by Dimethyl Sulfoxide? Biochemical Determination by Serum and Tissue Markers

2011 ◽  
Vol 47 ◽  
pp. S195
Author(s):  
R. Cosar ◽  
S. Eskiocak ◽  
V. Yurut-Caloglu ◽  
A. Ozen ◽  
C. Uzal ◽  
...  
2012 ◽  
Vol 103 ◽  
pp. S604-S605
Author(s):  
R. Cosar ◽  
S. Eskiocak ◽  
V. Yurut-Caloglu ◽  
A. Ozen ◽  
C. Uzal ◽  
...  

Micron ◽  
2002 ◽  
Vol 33 (2) ◽  
pp. 133-141 ◽  
Author(s):  
Mike E.C Robbins ◽  
Weiling Zhao ◽  
Charles S Davis ◽  
Shinya Toyokuni ◽  
Stephen M Bonsib

2008 ◽  
Vol 413 (1) ◽  
pp. 185-191 ◽  
Author(s):  
Disha Dayal ◽  
Sean M. Martin ◽  
Charles L. Limoli ◽  
Douglas R. Spitz

Chronic oxidative stress has been associated with genomic instability following exposure to ionizing radiation. However, results showing direct causal linkages between specific ROS (reactive oxygen species) and the ionizing radiation-induced mutator phenotype are lacking. The present study demonstrates that ionizing radiation-induced genomically unstable cells (characterized by chromosomal instability and an increase in mutation and gene amplification frequencies) show a 3-fold increase in steady-state levels of hydrogen peroxide, but not superoxide. Furthermore, stable clones isolated from parallel studies showed significant increases in catalase and GPx (glutathione peroxidase) activity. Treatment of unstable cells with PEG-CAT (polyethylene glycol-conjugated catalase) reduced the mutation frequency and mutation rate in a dose-dependent fashion. In addition, inhibiting catalase activity in the stable clones using AT (3-aminotriazole) increased mutation frequency and rate. These results clearly demonstrate the causal relationship between chronic oxidative stress mediated by hydrogen peroxide and the mutator phenotype that persists for many generations following exposure of mammalian cells to ionizing radiation.


2012 ◽  
Vol 33 (7) ◽  
pp. 1399-1405 ◽  
Author(s):  
Nabila-Sandra Hadj-Hamou ◽  
Marick Laé ◽  
Anna Almeida ◽  
Pierre de la Grange ◽  
Youlia Kirova ◽  
...  

Author(s):  
Aiten M. Soliman ◽  
Mai H. Mekkawy ◽  
Heba M. Karam ◽  
Maureen Higgins ◽  
Albena T. Dinkova-Kostova ◽  
...  

2021 ◽  
Vol 10 (7) ◽  
pp. 1349
Author(s):  
Kamila Czubak-Prowizor ◽  
Jacek Trelinski ◽  
Paulina Stelmach ◽  
Piotr Stelmach ◽  
Agnieszka Madon ◽  
...  

Chronic oxidative stress (OS) can be an important factor of acute myeloid leukemia (AML) progression; however, there are no data on the extent/consequence of OS after transfusion of packed red blood cells (pRBCs) and platelet concentrates (PCs), which are commonly used in the treatment of leukemia-associated anemia and thrombocytopenia. We aimed to investigate the effects of pRBC/PC transfusion on the OS markers, i.e., thiol and carbonyl (CO) groups, 3-nitrotyrosine (3-NT), thiobarbituric acid reactive substances (TBARS), advanced glycation end products (AGE), total antioxidant capacity (TAC), SOD, GST, and LDH, in the blood plasma of AML patients, before and 24 h post-transfusion. In this exploratory study, 52 patients were examined, of which 27 were transfused with pRBCs and 25 with PCs. Age-matched healthy subjects were also enrolled as controls. Our results showed the oxidation of thiols, increased 3-NT, AGE levels, and decreased TAC in AML groups versus controls. After pRBC transfusion, CO groups, AGE, and 3-NT significantly increased (by approximately 30, 23, and 35%; p < 0.05, p < 0.05, and p < 0.01, respectively) while thiols reduced (by 18%; p < 0.05). The PC transfusion resulted in the raise of TBARS and AGE (by 45%; p < 0.01 and 31%; p < 0.001), respectively). Other variables showed no significant post-transfusion changes. In conclusion, transfusion of both pRBCs and PCs was associated with an increased OS; however, transfusing the former may have more severe consequences, since it is associated with the irreversible oxidative/nitrative modifications of plasma proteins.


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