Comet Assay Coupled to Repair Enzymes for the Detection of Oxidative Damage to DNA Induced by Low Doses of γ-Radiation: Use of YOYO-1, Low-Background Slides, and Optimized Electrophoresis Conditions

2002 ◽  
Vol 303 (1) ◽  
pp. 107-109 ◽  
Author(s):  
Sylvie Sauvaigo ◽  
Crina Petec-Calin ◽  
Sylvain Caillat ◽  
Francette Odin ◽  
Jean Cadet
Keyword(s):  
Comet Assay ◽  
Oxidative Damage ◽  
Low Doses ◽  
Γ Radiation ◽  
Low Background ◽  
Repair Enzymes ◽  
Oxidative Damage To Dna ◽  
Radiation Use

scholarly journals An ECVAG trial on assessment of oxidative damage to DNA measured by the comet assay

Mutagenesis ◽  
2009 ◽  
Vol 25 (2) ◽  
pp. 125-132 ◽  
Author(s):  
C. Johansson ◽  
P. Moller ◽  
L. Forchhammer ◽  
S. Loft ◽  
R. W. L. Godschalk ◽  
...  
Keyword(s):  
Comet Assay ◽  
Oxidative Damage ◽  
Oxidative Damage To Dna

Measuring oxidative damage to DNA; HPLC and the comet assay compared

1998 ◽  
Vol 29 (6) ◽  
pp. 609-615 ◽  
Author(s):  
Catherine M. Gedik ◽  
Sharon G. Wood ◽  
Andrew R. Collins
Keyword(s):  
Comet Assay ◽  
Oxidative Damage ◽  
Oxidative Damage To Dna

Biomarkers of oxidative damage to DNA and repair

2008 ◽  
Vol 36 (5) ◽  
pp. 1071-1076 ◽  
Author(s):  
Steffen Loft ◽  
Pernille Høgh Danielsen ◽  
Lone Mikkelsen ◽  
Lotte Risom ◽  
Lykke Forchhammer ◽  
...  
Keyword(s):  
Comet Assay ◽  
Oxidative Damage ◽  
Urinary Excretion ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Population Based ◽  
Base Excision ◽  
Cellular Dna ◽  
Risk Of Cancer ◽  
Oxidative Damage To Dna

Oxidative-stress-induced damage to DNA includes a multitude of lesions, many of which are mutagenic and have multiple roles in cancer and aging. Many lesions have been characterized by MS-based methods after extraction and digestion of DNA. These preparation steps may cause spurious base oxidation, which is less likely to occur with methods such as the comet assay, which are based on nicking of the DNA strand at modified bases, but offer less specificity. The European Standards Committee on Oxidative DNA Damage has concluded that the true levels of the most widely studied lesion, 8-oxodG (8-oxo-7,8-dihydro-2′-deoxyguanosine), in cellular DNA is between 0.5 and 5 lesions per 106 dG bases. Base excision repair of oxidative damage to DNA can be assessed by nicking assays based on oligonucleotides with lesions or the comet assay, by mRNA expression levels or, in the case of, e.g., OGG1 (8-oxoguanine DNA glycosylase 1), responsible for repair of 8-oxodG, by genotyping. Products of repair in DNA or the nucleotide pool, such as 8-oxodG, excreted into the urine can be assessed by MS-based methods and generally reflects the rate of damage. Experimental and population-based studies indicate that many environmental factors, including particulate air pollution, cause oxidative damage to DNA, whereas diets rich in fruit and vegetables or antioxidant supplements may reduce the levels and enhance repair. Urinary excretion of 8-oxodG, genotype and expression of OGG1 have been associated with risk of cancer in cohort settings, whereas altered levels of damage, repair or urinary excretion in case-control settings may be a consequence rather than the cause of the disease.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

scholarly journals Oxidative damage to DNA: Inhibition of guanine damage

2006 ◽  
Vol 78 (12) ◽  
pp. 2297-2304 ◽  
Author(s):  
Sriram Kanvah ◽  
Gary B. Schuster
Keyword(s):  
Oxidative Damage ◽  
Structural Changes ◽  
Global Structure ◽  
Chemical Damage ◽  
Oxidation Of Dna ◽  
Anthraquinone Derivatives ◽  
Covalently Linked ◽  
The One ◽  
Oxidative Damage To Dna ◽  
Dna Inhibition

One-electron oxidation of DNA results in chemical damage to nucleobases, particularly guanine in multiple G sequences. Oxidation may be triggered by numerous events, including photosensitization. We describe studies of photoinduced oxidations of DNA triggered by irradiation of covalently linked anthraquinone derivatives under various conditions that affect the global structure of the DNA. These structural changes have subtle effects on the result of the one-electron oxidation.

scholarly journals Oxidative damage to DNA: do we have a reliable biomarker?

1996 ◽  
Vol 104 (suppl 3) ◽  
pp. 465-469 ◽  
Author(s):  
A R Collins ◽  
M Dusinská ◽  
C M Gedik ◽  
R Stĕtina
Keyword(s):  
Oxidative Damage ◽  
Oxidative Damage To Dna
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