scholarly journals 8-oxoG DNA Glycosylase-1 Inhibition Sensitizes Neuro-2a Cells to Oxidative DNA Base Damage Induced by 900 MHz Radiofrequency Electromagnetic Radiation

2015 ◽  
Vol 37 (3) ◽  
pp. 1075-1088 ◽  
Author(s):  
Xiaoya Wang ◽  
Chuan Liu ◽  
Qinglong Ma ◽  
Wei Feng ◽  
Lingling Yang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Comet Assay ◽  
Cell Viability ◽  
Dna Glycosylase ◽  
Oxygen Species ◽  
Base Damage ◽  
Dna Base ◽  
Strand Breakage ◽  
Dna Strand ◽  
Dna Strand Breakage

Background/Aims: The purpose of this study was to explore the in vitro putative genotoxicity during exposure of Neuro-2a cells to radiofrequency electromagnetic fields (RF-EMFs) with or without silencing of 8-oxoG DNA glycosylase-1 (OGG1). Methods: Neuro-2a cells treated with or without OGG1 siRNA were exposed to 900 MHz Global System for Mobile Communication (GSM) Talk signals continuously at a specific absorption rate (SAR) of 0, 0.5, 1 or 2 W/kg for 24 h. DNA strand breakage and DNA base damage were measured by the alkaline comet assay and a modified comet assay using formamidopyrimidine DNA glycosylase (FPG), respectively. Reactive oxygen species (ROS) levels and cell viability were monitored using the non-fluorescent probe 2, 7-dichlorofluorescein diacetate (DCFH-DA) and CCK-8 assay. Results: Exposure to 900 MHz RF-EMFs with insufficient energy could induce oxidative DNA base damage in Neuro-2a cells. These increases were concomitant with similar increases in the generation of reactive oxygen species (ROS). Without OGG1 siRNA, 2 W/kg RF-EMFs induced oxidative DNA base damage in Neuro-2a cells. Interestingly, with OGG1 siRNA, RF-EMFs could cause DNA base damage in Neuro-2a cells as low as 1 W/kg. However, neither DNA strand breakage nor altered cell viability was observed. Conclusion: Even if further studies remain conducted we support the hypothesis that OGG1 is involved in the process of DNA base repair and may play a pivotal role in protecting DNA bases from RF-EMF induced oxidative damage.

Comet Assay: A Strong Tool for Evaluating DNA Damage and Comprehensive Guidelines for Plant Cells

2017 ◽  
Vol 3 (02) ◽  
pp. 65-72
Author(s):  
Ashish Agnihotri ◽  
Chandra Shekhar Seth
Keyword(s):  
Heavy Metals ◽  
Dna Damage ◽  
Comet Assay ◽  
Single Cells ◽  
Strand Breakage ◽  
Dna Strand ◽  
Environmental Genotoxicity ◽  
Genetic Ecotoxicology ◽  
Detailed Protocol ◽  
Dna Strand Breakage

Heavy metals affect plant system in various toxic ways including morphophysiological alterations and genotoxic damages inside a plant cell. The extent of DNA damage under any genotoxic agents can be effectively measured in single cells applying comet assay approach. Comet assay primarily measures DNA strand breakage in single cells and its use has increased in different areas: clinical applications, human monitoring, radiation biology and genetic ecotoxicology. This paper is a review of the detailed protocol and precautions to be taken while performing comet assay and may have been slightly modified from other original protocols according to the plant, organ, cell type, etc. In conclusion, the study reviewed in this paper demonstrate that the comet assay application in plants provides a reliable, sensitive and rapid system for the study of environmental genotoxicity caused by heavy metals.

Effect of methylated forms of selenium on cell viability and the induction of DNA strand breakage

1992 ◽  
Vol 43 (5) ◽  
pp. 1137-1141 ◽  
Author(s):  
Adrian C. Wilson ◽  
Henry J. Thompson ◽  
Pepper J. Schedin ◽  
Neil W. Gibson ◽  
Howard E. Ganther
Keyword(s):  
Cell Viability ◽  
Strand Breakage ◽  
Dna Strand ◽  
Dna Strand Breakage

scholarly journals MiR-4673 Modulates Paclitaxel-Induced Oxidative Stress and Loss of Mitochondrial Membrane Potential by Targeting 8-Oxoguanine-DNA Glycosylase-1

2017 ◽  
Vol 42 (3) ◽  
pp. 889-900 ◽  
Author(s):  
Hai-Li Huang ◽  
Ya-Peng Shi ◽  
Hui-Juan He ◽  
Ya-Hong Wang ◽  
Ting Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Membrane Potential ◽  
Cell Viability ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Bioinformatics Analysis ◽  
Dna Glycosylase ◽  
Ros Generation ◽  
Oxygen Species ◽  
Induced Apoptosis

Background: Our previous study identified a novel microRNA, miR-4673, which is upregulated in A549 cells exposed to paclitaxel (PTX). In this study, we investigated the role of miR-4673 in PTX-induced cytotoxicity. Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, apoptosis assay, 5,5’,6,6’-Tetrachloro-1,1’,3,3’-tetraethyl-imidacarbocyanine iodide (JC-1) staining and 2’,7’-Dichlorofluorescein (DCFH) staining were used to evaluate cell viability, apoptosis, mitochondrial membrane potential (MMP) loss and reactive oxygen species (ROS) generation in A549 and H1299 cells. Bioinformatics analysis and Luciferase reporter assay were used to explore whether 8-oxoguanine-DNA glycosylase-1 (OGG1) is a target gene of miR-4673. Results: Enforced expression of miR-4673 decreased cell viability and increased PTX-induced apoptosis, MMP loss and reactive oxygen species (ROS) generation in A549 and H1299 cells. Bioinformatics analysis, which was used to identify potential target of miR-4673, revealed a binding site of miR-4673 in 3’UTR of OGG1. Luciferase reporters assays showed that miR-4673 specifically binds to ‘CUGUUGA’ in 3’UTR of OGG1. Enforced expression of miR-4673 decreased accumulation of OGG1. In addition, silencing OGG1 enhanced inhibitory effects of PTX on apoptosis, MMP loss and ROS generation, which is similar to effects of miR-4673. Moreover, enforced expression of OGG1 compromised promoting effects of miR-4673 on PTX-induced apoptosis, MMP loss and ROS generation. Conclusion: miR-4673 modulates PTX-induced apoptosis, MMP loss and ROS generation by targeting OGG1.

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