scholarly journals Simultaneous Quantification of Mitochondrial DNA Damage and Copy Number in Circulating Blood: A Sensitive Approach to Systemic Oxidative Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Sam W. Chan ◽  
Simone Chevalier ◽  
Armen Aprikian ◽  
Junjian Z. Chen
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Mitochondrial Dna ◽  
Copy Number ◽  
Structural Damage ◽  
Oxidative Dna Damage ◽  
Nuclear Dna ◽  
Blood Analysis ◽  
Systemic Oxidative Stress ◽  
Wide Range

Systemic oxidative stress is associated with a wide range of pathological conditions. Oxidative DNA damage is frequently measured in circulating lymphocytes. Mitochondrial DNA (mtDNA) is known to be more sensitive to oxidative damage than nuclear DNA but is rarely used for direct measurement of DNA damage in clinical studies. Based on the supercoiling-sensitive real-time PCR method, we propose a new approach for the noninvasive monitoring of systemic oxidative stress by quantifying the mtDNA structural damage and copy number change in isolated lymphocytes in a single test. We show that lymphocytes have significantly less mtDNA content and relatively lower baseline levels of damage than cancer cell lines. In anex vivochallenge experiment, we demonstrate, for the first time, that exogenous H2O2induces a significant increase in mtDNA damage in lymphocytes from healthy individuals, but no repair activity is observed after 1 h recovery. We further demonstrate that whole blood may serve as a convenient alternative to the isolated lymphocytes in mtDNA analysis. Thus, the blood analysis with the multiple mtDNA end-points proposed in the current study may provide a simple and sensitive test to interrogate the nature and extent of systemic oxidative stress for a broad spectrum of clinical investigations.

Dietary fats modulate methylmercury-mediated systemic oxidative stress and oxidative DNA damage in rats

2008 ◽  
Vol 46 (5) ◽  
pp. 1706-1720 ◽  
Author(s):  
Xiaolei Jin ◽  
Hing Man Chan ◽  
Eric Lok ◽  
Kamla Kapal ◽  
Marnie Taylor ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Dietary Fats ◽  
Systemic Oxidative Stress

scholarly journals Viscum albumL. Extracts Protects HeLa Cells against Nuclear and Mitochondrial DNA Damage

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Evren Önay-Uçar ◽  
Özlem Erol ◽  
Başak Kandemir ◽  
Elif Mertoğlu ◽  
Ali Karagöz ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Hela Cells ◽  
Oxidative Dna Damage ◽  
Nuclear Dna ◽  
Viscum Album ◽  
Mitochondrial Dna Damage ◽  
Methanolic Extracts ◽  
Host Trees ◽  
Lime Tree

Viscum albumL. is a semiparasitic plant grown on trees and widely used for the treatment of many diseases in traditional and complementary therapy. It is well known that some activities ofViscum albumextracts are varied depending on the host trees, such as antioxidant, apoptosis-inducing, anticancer activities of the plant. The aim of the present study is to examine the comparative effects of methanolic extracts ofV. albumgrown on three different host trees (locust tree, lime tree, and hedge maple tree) on H2O2-induced DNA damage in HeLa cells. Oxidative damage in mitochondrial DNA and two nuclear regions was assessed by QPCR assay. The cells were pretreated with methanolic extracts (10 μg/mL) for 48 h, followed by the treatment with 750 μM H2O2for 1 hour. DNA damage was significantly induced by H2O2while it was inhibited byV. albumextracts. All extracts completely protected against nuclear DNA damage. While the extract from lime tree or white locust tree entirely inhibited mitochondrial DNA damage, that from hedge maple tree inhibited by only 50%. These results suggest that methanolic extracts ofV. albumcan prevent oxidative DNA damage, and the activity is dependent on the host tree.

scholarly journals PCR‐Based Analysis of Mitochondrial DNA Copy Number, Mitochondrial DNA Damage, and Nuclear DNA Damage

2016 ◽  
Vol 67 (1) ◽  
Author(s):  
Claudia P. Gonzalez‐Hunt ◽  
John P. Rooney ◽  
Ian T. Ryde ◽  
Charumathi Anbalagan ◽  
Rashmi Joglekar ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Copy Number ◽  
Nuclear Dna ◽  
Dna Copy Number ◽  
Mitochondrial Dna Damage ◽  
Mitochondrial Dna Copy Number

001. ORIGINS OF DNA DAMAGE IN SPERMATOZOA

2010 ◽  
Vol 22 (9) ◽  
pp. 1
Author(s):  
R. J. Aitken
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Sperm Nucleus ◽  
Human Spermatozoa ◽  
Environmental Toxicants ◽  
Apoptotic Pathway ◽  
Systemic Oxidative Stress ◽  
Risk Of Disease ◽  
Dna Strand

DNA damage is frequently encountered in the spermatozoa of sub-fertile male mammals and is correlated with a range of adverse clinical outcomes including impaired fertilization, disrupted embryonic development, increased rates of miscarriage and an enhanced risk of disease in the progeny. The etiology of DNA fragmentation in human spermatozoa is closely correlated with the appearance of oxidative base adducts and evidence of impaired chromatin remodelling during spermiogenesis. In light of these associations we propose a two step hypothesis for the origins of DNA damage in spermatozoa. In Step 1, a variety of intrinsic (diabetes, varicocele, testicular torsion, obesity) and extrinsic (radiofrequency electromagnetic radiation, heat, cigarette smoke, diet, environmental toxicants) factors collude to generate a state of oxidative stress in the testes. This stress impedes spermiogenesis resulting in the generation of spermatozoa with poorly remodelled chromatin. These defective cells readily default to an apoptotic pathway comprising motility loss, caspase activation, phosphatidylserine exteriorization and the production of reactive oxygen species (ROS) by the mitochondria. In Step 2, these mitochondrial ROS attack the spermatozoa inducing lipid peroxidation and oxidative DNA damage, which then leads to DNA strand breakage and cell death. Nucleases activated and released during the apoptotic process are denied access to the sperm nucleus because the unique physical architecture of this cell prevents it. For this reason, a majority of the DNA damage encountered in human spermatozoa is oxidative. Given the importance of oxidative stress in the etiology of DNA damage, there should be a significant therapeutic role for antioxidants in the treatment of this condition. Furthermore, if oxidative DNA damage in spermatozoa is providing a sensitive readout of systemic oxidative stress, the implications of these findings could stretch beyond our immediate goal of trying to minimize DNA damage in spermatozoa as a prelude to assisted conception therapy.

Serum of 8-OHdG as a potential biomarker of oxidative DNA damage in workers exposed to harmful working environments

2020 ◽  
pp. 783-783
Author(s):  
I. A. Umnyagina ◽  
L. A. Strakhova ◽  
T. V. Blinova
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Blood Serum ◽  
Oxidative Dna Damage ◽  
Working Environment ◽  
Working Environments ◽  
Potential Biomarker ◽  
High Level ◽  
Damage Marker

In the blood serum of 70% individuals exposed to harmful factors of the working environment, a high level of oxidative stress and the DNA damage marker 8-Hydroxy-2’-Deoxyguanosine (8-OHdG) were detected.

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