Concurrent Increase of Oxidative DNA Damage and Lipid Peroxidation Together with Mitochondrial DNA Mutation in Human Lung Tissues During Aging—Smoking Enhances Oxidative Stress on the Aged Tissues

1999 ◽  
Vol 362 (2) ◽  
pp. 309-316 ◽  
Author(s):  
Hsin-Chen Lee ◽  
Maria L.R. Lim ◽  
Ching-You Lu ◽  
Vincent W.S. Liu ◽  
Huei-Jyh Fahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Mitochondrial Dna ◽  
Oxidative Dna Damage ◽  
Human Lung ◽  
Mitochondrial Dna Mutation ◽  
Dna Mutation

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.

scholarly journals Nonthermal Dielectric-Barrier Discharge Plasma-Induced Inactivation Involves Oxidative DNA Damage and Membrane Lipid Peroxidation inEscherichia coli

2011 ◽  
Vol 55 (3) ◽  
pp. 1053-1062 ◽  
Author(s):  
Suresh G. Joshi ◽  
Moogega Cooper ◽  
Adam Yost ◽  
Michelle Paff ◽  
Utku K. Ercan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Dielectric Barrier Discharge ◽  
Oxidative Dna Damage ◽  
Barrier Discharge ◽  
Membrane Lipid ◽  
Membrane Lipid Peroxidation ◽  
Dbd Plasma ◽  
Dielectric Barrier

ABSTRACTOxidative stress leads to membrane lipid peroxidation, which yields products causing variable degrees of detrimental oxidative modifications in cells. Reactive oxygen species (ROS) are the key regulators in this process and induce lipid peroxidation inEscherichia coli. Application of nonthermal (cold) plasma is increasingly used for inactivation of surface contaminants. Recently, we reported a successful application of nonthermal plasma, using a floating-electrode dielectric-barrier discharge (FE-DBD) technique for rapid inactivation of bacterial contaminants in normal atmospheric air (S. G. Joshi et al., Am. J. Infect. Control 38:293-301, 2010). In the present report, we demonstrate that FE-DBD plasma-mediated inactivation involves membrane lipid peroxidation inE. coli. Dose-dependent ROS, such as singlet oxygen and hydrogen peroxide-like species generated during plasma-induced oxidative stress, were responsible for membrane lipid peroxidation, and ROS scavengers, such as α-tocopherol (vitamin E), were able to significantly inhibit the extent of lipid peroxidation and oxidative DNA damage. These findings indicate that this is a major mechanism involved in FE-DBD plasma-mediated inactivation of bacteria.

scholarly journals Mitochondrial DNA damage associated with lipid peroxidation of the mitochondrial membrane induced by Fe2+-citrate

2006 ◽  
Vol 78 (3) ◽  
pp. 505-514 ◽  
Author(s):  
Andréa M. Almeida ◽  
Clélia R.A. Bertoncini ◽  
Jiri Borecký ◽  
Nadja C. Souza-Pinto ◽  
Aníbal E. Vercesi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Mitochondrial Dna ◽  
Dna Fragmentation ◽  
Hereditary Hemochromatosis ◽  
Beta Thalassemia ◽  
Rat Liver Mitochondria ◽  
Small Molecular Weight ◽  
Mitochondrial Dna Damage

Iron imbalance/accumulation has been implicated in oxidative injury associated with many degenerative diseases such as hereditary hemochromatosis, beta-thalassemia, and Friedreich's ataxia. Mitochondria are particularly sensitive to iron-induced oxidative stress - high loads of iron cause extensive lipid peroxidation and membrane permeabilization in isolated mitochondria. Here we detected and characterized mitochondrial DNA damage in isolated rat liver mitochondria exposed to a Fe2+-citrate complex, a small molecular weight complex. Intense DNA fragmentation was induced after the incubation of mitochondria with the iron complex. The detection of 3' phosphoglycolate ends at the mtDNA strand breaks by a 32P-postlabeling assay, suggested the involvement of hydroxyl radical in the DNA fragmentation induced by Fe2+-citrate. Increased levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine also suggested that Fe2+-citrate-induced oxidative stress causes mitochondrial DNA damage. In conclusion, our results show that iron-mediated lipid peroxidation was associated with intense mtDNA damage derived from the direct attack of reactive oxygen species.

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