Effects of an acute exposure to toluene on the DNA repair activity of the human 8-oxoguanine DNA glycosylase 1 (hOGG1) in healthy subjects

2009 ◽  
Vol 83 (8) ◽  
pp. 777-784
Author(s):  
P. Finkenwirth ◽  
U. Spelmeyer ◽  
G. Hommel ◽  
D.-M. Rose ◽  
D. Jung ◽  
...  
Author(s):  
Philip A.J. Crosbie ◽  
Amanda J. Watson ◽  
Raymond Agius ◽  
Philip V. Barber ◽  
Geoffrey P. Margison ◽  
...  

2001 ◽  
Vol 486 (3) ◽  
pp. 207-216 ◽  
Author(s):  
Kai Janssen ◽  
Kirsten Schlink ◽  
Walter Götte ◽  
Birgit Hippler ◽  
Bernd Kaina ◽  
...  

2014 ◽  
Vol 290 (8) ◽  
pp. 4966-4980 ◽  
Author(s):  
Sanjay Adhikari ◽  
Mahandranauth A. Chetram ◽  
Jordan Woodrick ◽  
Partha S. Mitra ◽  
Praveen V. Manthena ◽  
...  

2020 ◽  
Vol 401 (12) ◽  
pp. 1487-1493
Author(s):  
Stephan Kiontke ◽  
Tanja Göbel ◽  
Annika Brych ◽  
Alfred Batschauer

AbstractDrosophila, Arabidopsis, Synechocystis, human (DASH)-type cryptochromes (cry-DASHs) form one subclade of the cryptochrome/photolyase family (CPF). CPF members are flavoproteins that act as DNA-repair enzymes (DNA-photolyases), or as ultraviolet(UV)-A/blue light photoreceptors (cryptochromes). In mammals, cryptochromes are essential components of the circadian clock feed-back loop. Cry-DASHs are present in almost all major taxa and were initially considered as photoreceptors. Later studies demonstrated DNA-repair activity that was, however, restricted to UV-lesions in single-stranded DNA. Very recent studies, particularly on microbial organisms, substantiated photoreceptor functions of cry-DASHs suggesting that they could be transitions between photolyases and cryptochromes.


Oncotarget ◽  
2017 ◽  
Vol 8 (28) ◽  
pp. 45072-45087 ◽  
Author(s):  
Li-Fang Lin ◽  
Ming-Hsi Wu ◽  
Vijaya Kumar Pidugu ◽  
I-Ching Ho ◽  
Tsann-Long Su ◽  
...  

2000 ◽  
Vol 19 (10-12) ◽  
pp. 1505-1516 ◽  
Author(s):  
Angelika Rösler ◽  
George Panayotou ◽  
David P. Hornby ◽  
Tom Barlow ◽  
Tom Brown ◽  
...  

1992 ◽  
Vol 12 (12) ◽  
pp. 5536-5540
Author(s):  
R J Boorstein ◽  
L N Chiu ◽  
G W Teebor

We isolated a mutant mammalian cell line lacking activity for the DNA repair enzyme 5-hydroxymethyluracil-DNA glycosylase (HmUra-DNA glycosylase). The mutant was isolated through its resistance to the thymidine analog 5-hydroxymethyl-2'-deoxyuridine (HmdUrd). The mutant incorporates HmdUrd into DNA to the same extent as the parent line but, lacking the repair enzyme, does not remove it. The phenotype of the mutant demonstrates that the toxicity of HmdUrd does not result from substitution of thymine in DNA by HmUra but rather from the removal via base excision of large numbers of HmUra residues in DNA. This finding elucidates a novel mechanism of toxicity for a xenobiotic nucleoside. Furthermore, the isolation of this line supports our hypothesis that the enzymatic repairability of HmUra derives not from its formation opposite adenine via the oxidation of thymine, but rather from its formation opposite guanine as a product of the oxidation and subsequent deamination of 5-methylcytosine.


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