DNA repair activity of 8-oxoguanine DNA glycosylase 1 (OGG1) in human lymphocytes is not dependent on genetic polymorphism Ser326/Cys326

2001 ◽  
Vol 486 (3) ◽  
pp. 207-216 ◽  
Author(s):  
Kai Janssen ◽  
Kirsten Schlink ◽  
Walter Götte ◽  
Birgit Hippler ◽  
Bernd Kaina ◽  
...  
Keyword(s):  
Dna Repair ◽  
Genetic Polymorphism ◽  
Human Lymphocytes ◽  
Dna Glycosylase ◽  
Repair Activity

Elevated N3-methylpurine-DNA glycosylase DNA repair activity is associated with lung cancer

2012 ◽  
Vol 732 (1-2) ◽  
pp. 43-46 ◽  
Author(s):  
Philip A.J. Crosbie ◽  
Amanda J. Watson ◽  
Raymond Agius ◽  
Philip V. Barber ◽  
Geoffrey P. Margison ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Repair ◽  
Dna Glycosylase ◽  
Repair Activity ◽  
Methylpurine Dna Glycosylase

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 ◽  
...  
Keyword(s):  
Dna Repair ◽  
Healthy Subjects ◽  
Acute Exposure ◽  
Dna Glycosylase ◽  
Repair Activity

scholarly journals Germ Line Variants of HumanN-Methylpurine DNA Glycosylase Show Impaired DNA Repair Activity and Facilitate 1,N6-Ethenoadenine-induced Mutations

2014 ◽  
Vol 290 (8) ◽  
pp. 4966-4980 ◽  
Author(s):  
Sanjay Adhikari ◽  
Mahandranauth A. Chetram ◽  
Jordan Woodrick ◽  
Partha S. Mitra ◽  
Praveen V. Manthena ◽  
...  
Keyword(s):  
Dna Repair ◽  
Germ Line ◽  
Dna Glycosylase ◽  
Induced Mutations ◽  
Repair Activity ◽  
Methylpurine Dna Glycosylase

scholarly journals DASH-type cryptochromes – solved and open questions

2020 ◽  
Vol 401 (12) ◽  
pp. 1487-1493
Author(s):  
Stephan Kiontke ◽  
Tanja Göbel ◽  
Annika Brych ◽  
Alfred Batschauer
Keyword(s):  
Dna Repair ◽  
Circadian Clock ◽  
Blue Light ◽  
Dna Repair Enzymes ◽  
Repair Enzymes ◽  
Open Questions ◽  
Essential Components ◽  
Repair Activity ◽  
Almost All ◽  
Uv Lesions

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.

scholarly journals P-glycoprotein attenuates DNA repair activity in multidrug-resistant cells by acting through the Cbp-Csk-Src cascade

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 ◽  
...  
Keyword(s):  
Dna Repair ◽  
Multidrug Resistant ◽  
P Glycoprotein ◽  
Repair Activity ◽  
Resistant Cells

scholarly journals A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.

2002 ◽  
Vol 49 (1) ◽  
pp. 145-155 ◽  
Author(s):  
Janusz Błasiak ◽  
Ewa Gloc ◽  
Mariusz Warszawski
Keyword(s):  
Dna Damage ◽  
Human Lymphocytes ◽  
Dna Glycosylase ◽  
Oxygen Species ◽  
Anthracycline Antibiotic ◽  
Strand Breaks ◽  
Endonuclease Iii ◽  
Normal Human ◽  
In Vitro Genotoxicity

Idarubicin is an anthracycline antibiotic used in cancer therapy. Mitoxantrone is an anthracycline analog with presumed better antineoplastic activity and lesser toxicity. Using the alkaline comet assaywe showed that the drugs at 0.01-10 microM induced DNA damage in normal human lymphocytes. The effect induced by idarubicin was more pronounced than by mitoxantrone (P < 0.001). The cells treated with mitoxantrone at 1 microM were able to repair damage to their DNA within a 30-min incubation, whereas the lymphocytes exposed to idarubicin needed 180 min. Since anthracyclines are known to produce free radicals, we checked whether reactive oxygen species might be involved in the observed DNA damage. Catalase, an enzyme inactivating hydrogen peroxide, decreased the extent of DNA damage induced by idarubicin, but did not affect the extent evoked by mitoxantrone. Lymphocytes exposed to the drugs and treated with endonuclease III or formamidopyrimidine-DNA glycosylase (Fpg), enzymes recognizing and nicking oxidized bases, displayed a higher level of DNA damage than the untreated ones. 3-Methyladenine-DNA glycosylase II (AlkA), an enzyme recognizing and nicking mainly methylated bases in DNA, increased the extent of DNA damage caused by idarubicin, but not that induced by mitoxantrone. Our results indicate that the induction of secondary malignancies should be taken into account as side effects of the two drugs. Direct strand breaks, oxidation and methylation of the DNA bases can underlie the DNA-damaging effect of idarubicin, whereas mitoxantrone can induce strand breaks and modification of the bases, including oxidation. The observed in normal lymphocytes much lesser genotoxicity of mitoxantrone compared to idarubicin should be taken into account in planning chemotherapeutic strategies.

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