scholarly journals DNA Damage/Repair and Polymorphism of thehOGG1Gene in Lymphocytes of AMD Patients

2009 ◽  
Vol 2009 ◽  
pp. 1-9 ◽  
Author(s):  
Katarzyna Wozniak ◽  
Jacek P. Szaflik ◽  
Malgorzata Zaras ◽  
Anna Sklodowska ◽  
Katarzyna Janik-Papis ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Oxidative Dna Damage ◽  
Age Related Macular Degeneration ◽  
Repair Enzymes ◽  
Age Related ◽  
Damage Repair ◽  
Ser326cys Polymorphism ◽  
Kinetics Of ◽  
Wet Amd

Oxidative stress is thought to play a role in the pathogenesis of age-related macular degeneration (AMD). We determined the extent of oxidative DNA damage and the kinetics of its removal as well as the genotypes of the Ser326Cys polymorphism of thehOGG1gene in lymphocytes of 30 wet AMD patients and 30 controls. Oxidative DNA damage induced by hydrogen peroxide and its repair were evaluated by the comet assay and DNA repair enzymes. We observed a higher extent of endogenous oxidative DNA damage and a lower efficacy of its repair in AMD patients as compared with the controls. We did not find any correlation between the extent of DNA damage and efficacy of DNA repair with genotypes of the Ser326Cys polymorphism. The results obtained suggest that oxidative DNA damage and inefficient DNA repair can be associated with AMD and the variability of thehOOG1gene may not contribute to this association.

Kinetics of DNA Repair Under Chronic Irradiation at Low and Medium Dose Rates in Repair Proficient and Repair Compromised Normal Fibroblasts

2021 ◽  
Author(s):  
Elena K. Zaharieva ◽  
Megumi Sasatani ◽  
Kenji Kamiya
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Dose Rate ◽  
Dose Response ◽  
Chronic Irradiation ◽  
Dose Rates ◽  
Chronic Radiation ◽  
Damage Repair ◽  
Kinetics Of ◽  
Medium Dose

We present time and dose dependencies for the formation of 53BP1 and γH2AX DNA damage repair foci after chronic radiation exposure at dose rates of 140, 250 and 450 mGy/day from 3 to 96 h, in human and mouse repair proficient and ATM or DNA-PK deficient repair compromised cell models. We describe the time/dose-response curves using a mathematical equation which contains a linear component for the induction of DNA damage repair foci after irradiation, and an exponential component for their resolution. We show that under conditions of chronic irradiation at low and medium dose rates, the processes of DNA double-strand breaks (DSBs) induction and repair establish an equilibrium, which in repair proficient cells manifests as a plateau-shaped dose-response where the plateau is reached within the first 24 h postirradiation, and its height is proportionate to the radiation dose rate. In contrast, in repair compromised cells, where the rate of repair may be exceeded by the DSB induction rate, DNA damage accumulates with time of exposure and total absorbed dose. In addition, we discuss the biological meaning of the observed dependencies by presenting the frequency of micronuclei formation under the same irradiation conditions as a marker of radiation-induced genomic instability. We believe that the data and analysis presented here shed light on the kinetics of DNA repair under chronic radiation and are useful for future studies in the low-to-medium dose rate range.

scholarly journals Salidroside stimulates DNA repair enzyme Parp-1 activity in mouse HSC maintenance

Blood ◽  
2012 ◽  
Vol 119 (18) ◽  
pp. 4162-4173 ◽  
Author(s):  
Xue Li ◽  
Jared Sipple ◽  
Qishen Pang ◽  
Wei Du
Keyword(s):  
Oxidative Stress ◽  
Bone Marrow ◽  
Dna Damage ◽  
Dna Repair ◽  
Oxidative Dna Damage ◽  
Dna Damage Repair ◽  
Hematopoietic Stem ◽  
Damage Repair ◽  
Parp 1 ◽  
Quiescent Hscs

Abstract Salidroside is a phenylpropanoid glycoside isolated from the medicinal plant Rhodiola rosea, which has potent antioxidant properties. Here we show that salidroside prevented the loss of hematopoietic stem cells (HSCs) in mice under oxidative stress. Quiescent HSCs were recruited into cell cycling on in vivo challenge with oxidative stress, which was blocked by salidroside. Surprisingly, salidroside does not prevent the production of reactive oxygen species but reduces hydrogen peroxide–induced DNA-strand breaks in bone marrow cells enriched for HSCs. We tested whether salidroside enhances oxidative DNA damage repair in mice deficient for 5 DNA repair pathways known to be involved in oxidative DNA damage repair; we found that salidroside activated poly(ADP-ribose)polymerase-1 (PARP-1), a component of the base excision repair pathway, in mouse bone marrow HSCs as well as primary fibroblasts and human lymphoblasts. PARP-1 activation by salidroside protects quiescent HSCs from oxidative stress–induced cycling in native animals and self-renewal defect in transplanted recipients, which was abrogated by genetic ablation or pharmacologic inhibition of PARP-1. Together, these findings suggest that activation of PARP-1 by salidroside could affect the homeostasis and function of HSCs and contribute to the antioxidant effects of salidroside.

scholarly journals Elevated Levels of Oxidative DNA Damage and DNA Repair Enzymes in Human Atherosclerotic Plaques

Circulation ◽  
2002 ◽  
Vol 106 (8) ◽  
pp. 927-932 ◽  
Author(s):  
Wim Martinet ◽  
Michiel W.M. Knaapen ◽  
Guido R.Y. De Meyer ◽  
Arnold G. Herman ◽  
Mark M. Kockx
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Oxidative Dna Damage ◽  
Atherosclerotic Plaques ◽  
Dna Repair Enzymes ◽  
Repair Enzymes

scholarly journals MicroRNAs Modulate Oxidative Stress in Hypertension through PARP-1 Regulation

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Douglas F. Dluzen ◽  
Yoonseo Kim ◽  
Paul Bastian ◽  
Yongqing Zhang ◽  
Elin Lehrmann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Cell Survival ◽  
Oxidative Dna Damage ◽  
White Women ◽  
Luciferase Reporter ◽  
Coding Region ◽  
Age Related ◽  
Parp 1

Oxidative stress is thought to contribute to aging and age-related diseases, such as cardiovascular and neurodegenerative diseases, and is a risk factor for systemic arterial hypertension. Previously, we reported differential mRNA and microRNA (miRNA) expression between African American (AA) and white women with hypertension. Here, we found that the poly-(ADP-ribose) polymerase 1 (PARP-1), a DNA damage sensor protein involved in DNA repair and other cellular processes, is upregulated in AA women with hypertension. To explore this mechanism, we identified two miRNAs, miR-103a-2-5p and miR-585-5p, that are differentially expressed with hypertension and were predicted to target PARP1. Through overexpression of each miRNA-downregulated PARP-1 mRNA and protein levels and using heterologous luciferase reporter assays, we demonstrate that miR-103a-2-5p and miR-585-5p regulate PARP1 through binding within the coding region. Given the important role of PARP-1 in DNA repair, we assessed whether overexpression of miR-103a-2-5p or miR-585-5p affected DNA damage and cell survival. Overexpression of these miRNAs enhanced DNA damage and decreased both cell survival and colony formation. These findings highlight the role for PARP-1 in regulating oxidative DNA damage in hypertension and identify important new miRNA regulators of PARP-1 expression. These insights may provide additional avenues to understand hypertension health disparities.

The role of oxidative DNA damage, DNA repair, GSTM1, SOD2 and OGG1 polymorphisms in individual susceptibility to Barrett’s esophagus

2010 ◽  
Vol 26 (2) ◽  
pp. 67-79 ◽  
Author(s):  
Ela Kadioglu ◽  
Semra Sardas ◽  
Meltem Ergun ◽  
Selahattin Unal ◽  
Ali Esat Karakaya
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Oxidative Dna Damage ◽  
Repair Capacity ◽  
Base Damage ◽  
Purine Base ◽  
Dna Repair Capacity ◽  
Individual Susceptibility ◽  
Damage Repair

Determination of the genetic alterations, which play a role in the etiology of Barrett’s esophagus (BE), could help identify high-risk individuals for esophageal adenocarcinoma (EA). The aim of the present study was to investigate the role of oxidative DNA damage, glutathione (GSH) concentration as oxidative stress parameters and DNA repair capacity, GSTM1, SOD1 Ala16Val and OGG1 Ser326Cys genetic polymorphisms as individual susceptibility parameters in the etiology of BE. The study groups comprised BE patients who were clinically diagnosed (n = 40) and a healthy control group (n = 40). Basal DNA damage, pyrimidine and purine base damage after H2O2 induction, H 2O2 sensitivity, DNA repair capacity, oxidized pyrimidine and purine base damage repair were evaluated in peripheral blood lymphocytes with a modified comet assay using specific endonucleases (Endo III and Fpg). Polymerase chain reaction—restriction length polymorphism (PCR-RFLP)-based assays were used for genotyping. The patient group showed elevated levels of basal DNA damage, pyrimidine base damage and H2O2 sensitivity as compared to controls (p < .05). DNA repair capacity, oxidized pyrimidine and purine base damage repair capacity, were not statistically different between patients and controls. GSH concentration was found to be significantly lower in smoking patients than in the controls (p < .05). None of the genetic variations changed the risk of having BE disease. However, patients carrying the variant OGG1 Cys allele showed elevated levels of pyrimidine base damage as compared to patients carrying the wild-type OGG1 Ser (p < .05). The results of this study point to a role of oxidative DNA damage in BE. However, DNA repair capacity, GSTM1, SOD1 Ala16Val and OGG1 Ser326Cys genetic polymorphisms appeared to play no role in the individual susceptibility to this disease.

Development of age-related loss of muscle mass and function – role of oxidative DNA damage repair systems

2021 ◽  
Vol 165 ◽  
pp. 30-31
Author(s):  
Kat Kumiscia ◽  
Shahjahan Shigdar ◽  
Carole Proctor ◽  
Daryl Shanley ◽  
Euan Owen ◽  
...  
Keyword(s):  
Dna Damage ◽  
Muscle Mass ◽  
Oxidative Dna Damage ◽  
Dna Damage Repair ◽  
Age Related ◽  
Damage Repair ◽  
Repair Systems ◽  
And Function

scholarly journals The Effects of 1‐Nitropyrene on Oxidative DNA Damage and Expression of DNA Repair Enzymes

2005 ◽  
Vol 47 (3) ◽  
pp. 261-266 ◽  
Author(s):  
Yong‐Dae Kim ◽  
Young‐Jun Ko ◽  
Toshihiro Kawamoto ◽  
Heon Kim
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Oxidative Dna Damage ◽  
Dna Repair Enzymes ◽  
Repair Enzymes
Sign in / Sign up

Export Citation Format

Share Document