Oxidative DNA damage in human cells: the influence of antioxidants and DNA repair

1997 ◽  
Vol 25 (1) ◽  
pp. 326-331 ◽  
Author(s):  
A. R. Collins ◽  
S. J. Duthie ◽  
L. Fillion ◽  
C. M. Gedik ◽  
N. Vaughan ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Oxidative Dna Damage ◽  
Human Cells

scholarly journals NEIL2 Protects against Oxidative DNA Damage Induced by Sidestream Smoke in Human Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e90261 ◽  
Author(s):  
Altaf H. Sarker ◽  
Arpita Chatterjee ◽  
Monique Williams ◽  
Sabrina Lin ◽  
Christopher Havel ◽  
...  
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Human Cells ◽  
Sidestream Smoke

scholarly journals The transcription-coupled DNA repair-initiating protein CSB promotes XRCC1 recruitment to oxidative DNA damage

2018 ◽  
Vol 46 (15) ◽  
pp. 7747-7756 ◽  
Author(s):  
Hervé Menoni ◽  
Franziska Wienholz ◽  
Arjan F Theil ◽  
Roel C Janssens ◽  
Hannes Lans ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Oxidative Dna Damage

Oxidative DNA damage and inflammatory responses in cultured human cells and in humans exposed to traffic-related particles

2014 ◽  
Vol 217 (1) ◽  
pp. 23-33 ◽  
Author(s):  
Udomratana Vattanasit ◽  
Panida Navasumrit ◽  
Man Bahadur Khadka ◽  
Jantamas Kanitwithayanun ◽  
Jeerawan Promvijit ◽  
...  
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Inflammatory Responses ◽  
Human Cells ◽  
Cultured Human Cells

Mutations in CREBBP and EP300 genes affect DNA repair of oxidative damage in Rubinstein-Taybi syndrome cells

2019 ◽  
Vol 41 (3) ◽  
pp. 257-266
Author(s):  
Ilaria Dutto ◽  
Claudia Scalera ◽  
Micol Tillhon ◽  
Giulio Ticli ◽  
Gianluca Passaniti ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Genome Stability ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Control Cell ◽  
Nuclear Antigen ◽  
Autosomal Dominant Disorder ◽  
Cell Extracts ◽  
Increased Risk

Abstract Rubinstein-Taybi syndrome (RSTS) is an autosomal-dominant disorder characterized by intellectual disability, skeletal abnormalities, growth deficiency and an increased risk of tumors. RSTS is predominantly caused by mutations in CREBBP or EP300 genes encoding for CBP and p300 proteins, two lysine acetyl-transferases (KAT) playing a key role in transcription, cell proliferation and DNA repair. However, the efficiency of these processes in RSTS cells is still largely unknown. Here, we have investigated whether pathways involved in the maintenance of genome stability are affected in lymphoblastoid cell lines (LCLs) obtained from RSTS patients with mutations in CREBBP or in EP300 genes. We report that RSTS LCLs with mutations affecting CBP or p300 protein levels or KAT activity, are more sensitive to oxidative DNA damage and exhibit defective base excision repair (BER). We have found reduced OGG1 DNA glycosylase activity in RSTS compared to control cell extracts, and concomitant lower OGG1 acetylation levels, thereby impairing the initiation of the BER process. In addition, we report reduced acetylation of other BER factors, such as DNA polymerase β and Proliferating Cell Nuclear Antigen (PCNA), together with acetylation of histone H3. We also show that complementation of CBP or p300 partially reversed RSTS cell sensitivity to DNA damage. These results disclose a mechanism of defective DNA repair as a source of genome instability in RSTS cells.

scholarly journals Dynamic Compartmentalization of Base Excision Repair Proteins in Response to Nuclear and Mitochondrial Oxidative Stress

2008 ◽  
Vol 29 (3) ◽  
pp. 794-807 ◽  
Author(s):  
Lyra M. Griffiths ◽  
Dan Swartzlander ◽  
Kellen L. Meadows ◽  
Keith D. Wilkinson ◽  
Anita H. Corbett ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Base Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Intracellular Localization ◽  
Genotoxic Stress ◽  
Mitochondrial Oxidative Stress ◽  
Base Excision

ABSTRACT DNAs harbored in both nuclei and mitochondria of eukaryotic cells are subject to continuous oxidative damage resulting from normal metabolic activities or environmental insults. Oxidative DNA damage is primarily reversed by the base excision repair (BER) pathway, initiated by N-glycosylase apurinic/apyrimidinic (AP) lyase proteins. To execute an appropriate repair response, BER components must be distributed to accommodate levels of genotoxic stress that may vary considerably between nuclei and mitochondria, depending on the growth state and stress environment of the cell. Numerous examples exist where cells respond to signals, resulting in relocalization of proteins involved in key biological transactions. To address whether such dynamic localization contributes to efficient organelle-specific DNA repair, we determined the intracellular localization of the Saccharomyces cerevisiae N-glycosylase/AP lyases, Ntg1 and Ntg2, in response to nuclear and mitochondrial oxidative stress. Fluorescence microscopy revealed that Ntg1 is differentially localized to nuclei and mitochondria, likely in response to the oxidative DNA damage status of the organelle. Sumoylation is associated with targeting of Ntg1 to nuclei containing oxidative DNA damage. These studies demonstrate that trafficking of DNA repair proteins to organelles containing high levels of oxidative DNA damage may be a central point for regulating BER in response to oxidative stress.

Oxidative DNA Damage in Human Cells Induced by Paraquat

1999 ◽  
Vol 27 (3) ◽  
pp. 387-395 ◽  
Author(s):  
Helena Petrovská ◽  
Mária Dušinská
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Human Cells
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