Equine Estrogen Metabolite 4-Hydroxyequilenin Induces DNA Damage in the Rat Mammary Tissues:  Formation of Single-Strand Breaks, Apurinic Sites, Stable Adducts, and Oxidized Bases

2001 ◽  
Vol 14 (12) ◽  
pp. 1654-1659 ◽  
Author(s):  
Fagen Zhang ◽  
Steven M. Swanson ◽  
Richard B. van Breemen ◽  
Xuemei Liu ◽  
Yanan Yang ◽  
...  
2018 ◽  
Vol 19 (8) ◽  
pp. 2389 ◽  
Author(s):  
Md. Hossain ◽  
Yunfeng Lin ◽  
Shan Yan

DNA single-strand breaks (SSBs) occur more than 10,000 times per mammalian cell each day, representing the most common type of DNA damage. Unrepaired SSBs compromise DNA replication and transcription programs, leading to genome instability. Unrepaired SSBs are associated with diseases such as cancer and neurodegenerative disorders. Although canonical SSB repair pathway is activated to repair most SSBs, it remains unclear whether and how unrepaired SSBs are sensed and signaled. In this review, we propose a new concept of SSB end resection for genome integrity. We propose a four-step mechanism of SSB end resection: SSB end sensing and processing, as well as initiation, continuation, and termination of SSB end resection. We also compare different mechanisms of SSB end resection and DSB end resection in DNA repair and DNA damage response (DDR) pathways. We further discuss how SSB end resection contributes to SSB signaling and repair. We focus on the mechanism and regulation by APE2 in SSB end resection in genome integrity. Finally, we identify areas of future study that may help us gain further mechanistic insight into the process of SSB end resection. Overall, this review provides the first comprehensive perspective on SSB end resection in genome integrity.


2012 ◽  
Vol 19 (11) ◽  
pp. 1741-1749 ◽  
Author(s):  
P Fortini ◽  
C Ferretti ◽  
B Pascucci ◽  
L Narciso ◽  
D Pajalunga ◽  
...  

1998 ◽  
Vol 11 (9) ◽  
pp. 1105-1111 ◽  
Author(s):  
Yumei Chen ◽  
Li Shen ◽  
Fagen Zhang ◽  
Serrine S. Lau ◽  
Richard B. van Breemen ◽  
...  

2000 ◽  
Vol 20 (4) ◽  
pp. 1206-1218 ◽  
Author(s):  
Jonathan G. Moggs ◽  
Paola Grandi ◽  
Jean-Pierre Quivy ◽  
Zophonías O. Jónsson ◽  
Ulrich Hübscher ◽  
...  

ABSTRACT Sensing DNA damage is crucial for the maintenance of genomic integrity and cell cycle progression. The participation of chromatin in these events is becoming of increasing interest. We show that the presence of single-strand breaks and gaps, formed either directly or during DNA damage processing, can trigger the propagation of nucleosomal arrays. This nucleosome assembly pathway involves the histone chaperone chromatin assembly factor 1 (CAF-1). The largest subunit (p150) of this factor interacts directly with proliferating cell nuclear antigen (PCNA), and critical regions for this interaction on both proteins have been mapped. To isolate proteins specifically recruited during DNA repair, damaged DNA linked to magnetic beads was used. The binding of both PCNA and CAF-1 to this damaged DNA was dependent on the number of DNA lesions and required ATP. Chromatin assembly linked to the repair of single-strand breaks was disrupted by depletion of PCNA from a cell-free system. This defect was rescued by complementation with recombinant PCNA, arguing for role of PCNA in mediating chromatin assembly linked to DNA repair. We discuss the importance of the PCNA–CAF-1 interaction in the context of DNA damage processing and checkpoint control.


2010 ◽  
Vol 402 (1) ◽  
pp. 70-82 ◽  
Author(s):  
Petra Groth ◽  
Simon Ausländer ◽  
Muntasir Mamun Majumder ◽  
Niklas Schultz ◽  
Fredrik Johansson ◽  
...  

1984 ◽  
Vol 218 (1) ◽  
pp. 273-275 ◽  
Author(s):  
A C Mello Filho ◽  
M E Hoffmann ◽  
R Meneghini

Phenanthroline, a strong iron chelator, prevents both the formation of DNA single-strand breaks and the killing of mouse cells produced by H2O2. These results, taken together with our previous findings, indicate that the DNA damage is produced by hydroxyl radicals formed when H2O2 reacts with chromatin-bound Fe2+ and that this damage is responsible for the killing effect.


2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Ptumporn Muangphra ◽  
Ravi Gooneratne

To determine genotoxicity to coelomocytes,Pheretima peguanaearthworms were exposed in filter paper studies to cadmium (Cd) and lead (Pb) for 48 h, at concentrations less than the LC10—Cd: 0.09, 0.19, 0.38, 0.75, and 1.50 μg cm−2; Pb: 1.65, 3.29, 6.58, 13.16, and 26.32 μg cm−2. For Cd at 0.75 μg cm−2, in the micronucleus test (detects chromosomal aberrations), significant increases () in micronuclei and binucleate cells were observed, and in the comet assay (detects DNA single-strand breaks), tail DNA% was significantly increased. Lead was less toxic with minimal effects on DNA, but the binucleates were significantly increased by Pb at 3.29 μg cm−2. This study shows that Cd is more acutely toxic and sublethally genotoxic than Pb toP. peguana. Cadmium caused chromosomal aberrations and DNA single-strand breaks at 45% of the LC10concentration. Lead, in contrast, did not induce DNA damage but caused cytokinesis defects.


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