scholarly journals The Biological and Metabolic Fates of Endogenous DNA Damage Products

2010 ◽  
Vol 2010 ◽  
pp. 1-13 ◽  
Author(s):  
Simon Wan Chan ◽  
Peter C. Dedon
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Chemical Reactions ◽  
Human Disease ◽  
Interindividual Variations ◽  
Physiological Processes ◽  
Potential Source ◽  
Cellular Repair ◽  
Repair Pathways ◽  
Significant Effort

DNA and other biomolecules are subjected to damaging chemical reactions during normal physiological processes and in states of pathophysiology caused by endogenous and exogenous mechanisms. In DNA, this damage affects both the nucleobases and 2-deoxyribose, with a host of damage products that reflect the local chemical pathology such as oxidative stress and inflammation. These damaged molecules represent a potential source of biomarkers for defining mechanisms of pathology, quantifying the risk of human disease and studying interindividual variations in cellular repair pathways. Toward the goal of developing biomarkers, significant effort has been made to detect and quantify damage biomolecules in clinically accessible compartments such as blood and and urine. However, there has been little effort to define the biotransformational fate of damaged biomolecules as they move from the site of formation to excretion in clinically accessible compartments. This paper highlights examples of this important problem with DNA damage products.

scholarly journals DNA Damage and Oxidative Stress in Human Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-2 ◽  
Author(s):  
Sharbel Weidner Maluf ◽  
Norma Possa Marroni ◽  
Vanina D. Heuser ◽  
Daniel Prá
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Human Disease ◽  
And Oxidative Stress

scholarly journals Chapter 11. Alternative DNA Repair Pathways to Handle Complex DNA Damage Generated by Oxidative Stress and Anticancer Drugs

2020 ◽  
pp. 249-278 ◽  
Author(s):  
E. Matta ◽  
U. Aliyaskarova ◽  
A. A. Kuznetsova ◽  
B. T. Matkarimov ◽  
O. S. Fedorova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Anticancer Drugs ◽  
Repair Pathways

scholarly journals Bilirubin-Induced Oxidative Stress Leads to DNA Damage in the Cerebellum of Hyperbilirubinemic Neonatal Mice and Activates DNA Double-Strand Break Repair Pathways in Human Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Vipin Rawat ◽  
Giulia Bortolussi ◽  
Silvia Gazzin ◽  
Claudio Tiribelli ◽  
Andrés F. Muro
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Strand Break ◽  
Adaptive Responses ◽  
Repair Pathways ◽  
Bilirubin Toxicity ◽  
The Brain

Unconjugated bilirubin is considered a potent antioxidant when present at moderate levels. However, at high concentrations, it produces severe neurological damage and death associated with kernicterus due to oxidative stress and other mechanisms. While it is widely recognized that oxidative stress by different toxic insults results in severe damage to cellular macromolecules, especially to DNA, no data are available either on DNA damage in the brain triggered by hyperbilirubinemia during the neonatal period or on the activation of DNA repair mechanisms. Here, using a mouse model of neonatal hyperbilirubinemia, we demonstrated that DNA damage occurs in vivo in the cerebellum, the brain region most affected by bilirubin toxicity. We studied the mechanisms associated with potential toxic action of bilirubin on DNA in in vitro models, which showed significant increases in DNA damage when neuronal and nonneuronal cells were treated with 140 nM of free bilirubin (Bf), as determined by γH2AX Western blot and immunofluorescence analyses. Cotreatment of cells with N-acetyl-cysteine, a potent oxidative-stress inhibitor, prevented DNA damage by bilirubin, supporting the concept that DNA damage was caused by bilirubin-induced oxidative stress. Bilirubin treatment also activated the main DNA repair pathways through homologous recombination (HR) and nonhomologous end joining (NHEJ), which may be adaptive responses to repair bilirubin-induced DNA damage. Since DNA damage may be another important factor contributing to neuronal death and bilirubin encephalopathy, these results contribute to the understanding of the mechanisms associated with bilirubin toxicity and may be of relevance in neonates affected with severe hyperbilirubinemia.

366-OR: TCF19 Promotes Functional Beta-Cell Mass and Proliferative Capacity by Regulating DNA Damage Repair Pathways

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 366-OR
Author(s):  
GRACE H. YANG ◽  
JEE YOUNG HAN ◽  
SUKANYA LODH ◽  
JOSEPH T. BLUMER ◽  
DANIELLE FONTAINE ◽  
...  
Keyword(s):  
Dna Damage ◽  
Beta Cell ◽  
Dna Damage Repair ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Proliferative Capacity ◽  
Damage Repair ◽  
Repair Pathways

Serum of 8-OHdG as a potential biomarker of oxidative DNA damage in workers exposed to harmful working environments

2020 ◽  
pp. 783-783
Author(s):  
I. A. Umnyagina ◽  
L. A. Strakhova ◽  
T. V. Blinova
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Blood Serum ◽  
Oxidative Dna Damage ◽  
Working Environment ◽  
Working Environments ◽  
Potential Biomarker ◽  
High Level ◽  
Damage Marker

In the blood serum of 70% individuals exposed to harmful factors of the working environment, a high level of oxidative stress and the DNA damage marker 8-Hydroxy-2’-Deoxyguanosine (8-OHdG) were detected.

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