scholarly journals Salivary Leucocytes as In Vitro Model to Evaluate Nanoparticle-Induced DNA Damage

Nanomaterials ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1930
Author(s):  
Vanessa Valdiglesias ◽  
Natalia Fernández-Bertólez ◽  
Carlota Lema-Arranz ◽  
Raquel Rodríguez-Fernández ◽  
Eduardo Pásaro ◽  
...  
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
Metal Oxide ◽  
Oxidative Dna Damage ◽  
Metal Oxide Nanoparticles ◽  
Consumer Products ◽  
Specific Regulation ◽  
Vitro Model ◽  
The Impact

Metal oxide nanoparticles (NPs) have a wide variety of applications in many consumer products and biomedical practices. As a result, human exposure to these nanomaterials is highly frequent, becoming an issue of concern to public health. Recently, human salivary leucocytes have been proposed as an adequate non-invasive alternative to peripheral blood leucocytes to evaluate genotoxicity in vitro. The present study focused on proving the suitability of salivary leucocytes as a biomatrix in the comet assay for in vitro nanogenotoxicity studies, by testing some of the metal oxide NPs most frequently present in consumer products, namely, titanium dioxide (TiO2), zinc oxide (ZnO), and cerium dioxide (CeO2) NPs. Primary and oxidative DNA damage were evaluated by alkaline and hOGG1-modified comet assay, respectively. Any possible interference of the NPs with the methodological procedure or the hOGG1 activity was addressed before performing genotoxicity evaluation. Results obtained showed an increase of both primary and oxidative damage after NPs treatments. These data support the use of salivary leucocytes as a proper and sensitive biological sample for in vitro nanogenotoxicity studies, and contribute to increase the knowledge on the impact of metal oxide NPs on human health, reinforcing the need for a specific regulation of the nanomaterials use.

scholarly journals Molecular Mechanisms of Zinc Oxide Nanoparticle-Induced Genotoxicity

Materials ◽  
2017 ◽  
Vol 10 (12) ◽  
pp. 1427 ◽  
Author(s):  
Agmal Scherzad ◽  
Till Meyer ◽  
Norbert Kleinsasser ◽  
Stephan Hackenberg
Keyword(s):  
Dna Damage ◽  
Zinc Oxide ◽  
Mammalian Cells ◽  
Oxidative Dna Damage ◽  
Molecular Mechanisms ◽  
Consumer Products ◽  
Zno Nps ◽  
Cytotoxic Effects

Background: Zinc oxide nanoparticles (ZnO NPs) are among the most frequently applied nanomaterials in consumer products. Evidence exists regarding the cytotoxic effects of ZnO NPs in mammalian cells; however, knowledge about the potential genotoxicity of ZnO NPs is rare, and results presented in the current literature are inconsistent. Objectives: The aim of this review is to summarize the existing data regarding the DNA damage that ZnO NPs induce, and focus on the possible molecular mechanisms underlying genotoxic events. Methods: Electronic literature databases were systematically searched for studies that report on the genotoxicity of ZnO NPs. Results: Several methods and different endpoints demonstrate the genotoxic potential of ZnO NPs. Most publications describe in vitro assessments of the oxidative DNA damage triggered by dissoluted Zn2+ ions. Most genotoxicological investigations of ZnO NPs address acute exposure situations. Conclusion: Existing evidence indicates that ZnO NPs possibly have the potential to damage DNA. However, there is a lack of long-term exposure experiments that clarify the intracellular bioaccumulation of ZnO NPs and the possible mechanisms of DNA repair and cell survival.

scholarly journals Genotoxic Impact of Aluminum-containing Nanomaterials in Human Intestinal and Hepatic Cells.

2020 ◽  
Author(s):  
Pégah Jalili ◽  
Sylvie HUET ◽  
Agnès Burel ◽  
Benjamin-Christoph Krause ◽  
Caroline Fontana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Comet Assay ◽  
Oxidative Dna Damage ◽  
Cell Transformation ◽  
Oral Exposure ◽  
No Production ◽  
Ionic Form ◽  
Ion Release

Abstract Background: Exposure of consumers to aluminum-containing nanomaterials (Al NMs) through numerous products is an area of concern for public health agencies since human health risks are not completely elucidated. In addition, the available data on the genotoxicity of Al2O3 and Al0 NMs are inconclusive or rare. In order to provide further information, the present study investigated the in vitro genotoxic potential of Al0 and Al2O3 NMs in intestinal and liver cell models since these tissues represent organs which would be in direct contact or could experience potential accumulation following oral exposure. Methods: Differentiated human intestinal Caco-2 and hepatic HepaRG cells were exposed to Al0 and Al2O3 NMs (0.03 to 80 µg/cm2) and the results were compared with those obtained with the ionic form AlCl3. Several methods, including H2AX labelling, the alkaline comet assay and micronucleus (MN) assays were used. Oxidative stress and oxidative DNA damage were assessed using High Content Analysis (HCA) and the formamidopyrimidine DNA-glycosylase -modified comet assay respectively. Moreover, carcinogenic properties of Al NMs were investigated through the cell transforming assay (CTA) in Bhas 42 cells.Results: The three forms of Al did not induce chromosomal damage when tested in the MN assay. Furthermore, no cell transformation was observed in Bhas 42 cells. However, although no production of oxidative stress was detected in HCA assays, Al2O3 NMs induced oxidative DNA damage in Caco-2 cells in the comet assay following a 24 h treatment. Considerable DNA damage was observed with Al0 NMs in both cell lines in the comet assay, although this was likely due to interference with these NMs. Finally, no genotoxic effects were observed with AlCl3. Conclusion: The slight effects observed with Al NMs are therefore not likely to be related to ion release in the cell media.

Basal damage and oxidative DNA damage in children with chronic kidney disease measured by use of the comet assay

2011 ◽  
Vol 725 (1-2) ◽  
pp. 22-28 ◽  
Author(s):  
Banu Aykanat ◽  
Gonca Cakmak Demircigil ◽  
Kibriya Fidan ◽  
Necla Buyan ◽  
Kaan Gulleroglu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Dna Damage ◽  
Kidney Disease ◽  
Comet Assay ◽  
Oxidative Dna Damage

DNA damage induced by coal dust, fly and bottom ash from coal combustion evaluated using the micronucleus test and comet assay in vitro

2017 ◽  
Vol 324 ◽  
pp. 781-788 ◽  
Author(s):  
Cristina Araujo Matzenbacher ◽  
Ana Letícia Hilario Garcia ◽  
Marcela Silva dos Santos ◽  
Caroline Cardoso Nicolau ◽  
Suziane Premoli ◽  
...  
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
Coal Combustion ◽  
Micronucleus Test ◽  
Coal Dust ◽  
Bottom Ash

Effect of phytoestrogen and antioxidant supplementation on oxidative DNA damage assessed using the comet assay

2001 ◽  
Vol 485 (2) ◽  
pp. 169-176 ◽  
Author(s):  
Jayne Sierens ◽  
John A. Hartley ◽  
Maeli J. Campbell ◽  
Anthony J.C. Leathem ◽  
Jayne V. Woodside
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
Oxidative Dna Damage ◽  
Antioxidant Supplementation

scholarly journals ATM-dependent pathways of chromatin remodelling and oxidative DNA damage responses

2017 ◽  
Vol 372 (1731) ◽  
pp. 20160283 ◽  
Author(s):  
N. Daniel Berger ◽  
Fintan K. T. Stanley ◽  
Shaun Moore ◽  
Aaron A. Goodarzi
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Strand Break ◽  
Chromatin Remodelling ◽  
Double Strand Breaks ◽  
Biochemical Network ◽  
Regulatory Function ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
The Impact

Ataxia-telangiectasia mutated (ATM) is a serine/threonine protein kinase with a master regulatory function in the DNA damage response. In this role, ATM commands a complex biochemical network that signals the presence of oxidative DNA damage, including the dangerous DNA double-strand break, and facilitates subsequent repair. Here, we review the current state of knowledge regarding ATM-dependent chromatin remodelling and epigenomic alterations that are required to maintain genomic integrity in the presence of DNA double-strand breaks and/or oxidative stress. We will focus particularly on the roles of ATM in adjusting nucleosome spacing at sites of unresolved DNA double-strand breaks within complex chromatin environments, and the impact of ATM on preserving the health of cells within the mammalian central nervous system. This article is part of the themed issue ‘Chromatin modifiers and remodellers in DNA repair and signalling’.

scholarly journals Corrigendum to: Standardisation of the in vitro comet assay: influence of lysis time and lysis solution composition on the detection of DNA damage induced by X-rays

Mutagenesis ◽  
2019 ◽  
Vol 34 (5-6) ◽  
pp. 431-431
Author(s):  
José M Enciso ◽  
Kristine B Gutzkow ◽  
Gunnar Brunborg ◽  
Ann-Karin Olsen ◽  
Adela López de Cerain ◽  
...  
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
X Rays ◽  
Solution Composition ◽  
Lysis Time

scholarly journals Potential role of oxidative DNA damage in the impact of PNPLA3 variant (rs 738409 C>G) in hepatocellular carcinoma risk

Hepatology ◽  
2014 ◽  
Vol 60 (3) ◽  
pp. 1110-1111 ◽  
Author(s):  
Emeric Limagne ◽  
Vanessa Cottet ◽  
Alexia Karen Cotte ◽  
Samia Hamza ◽  
Patrick Hillon ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Potential Role ◽  
The Impact ◽  
Carcinoma Risk

scholarly journals Beta-carotene enhances the recovery of lymphocytes from oxidative DNA damage.

1998 ◽  
Vol 45 (1) ◽  
pp. 183-190 ◽  
Author(s):  
L Fillion ◽  
A Collins ◽  
S Southon
Keyword(s):  
Dna Damage ◽  
Oxidative Damage ◽  
Oxidative Dna Damage ◽  
Enhanced Recovery ◽  
Beta Carotene ◽  
Epidemiological Studies ◽  
Dietary Factors ◽  
Causal Mechanism ◽  
Strand Breaks

Epidemiological studies have revealed a strong correlation between high intake of fruit and vegetables and low incidence of certain cancers. Micronutrients present in these foods are thought to decrease free radical attack on DNA and hence protect against mutations that cause cancer, but the fine details of the causal mechanism have still to be elucidated. Whether dietary factors can modulate DNA repair--a crucial element in the avoidance of carcinogenesis--is an intriguing question that has not yet been satisfactorily answered. In order to investigate the effects of beta-carotene on oxidative damage and its repair, volunteers were given a single 45 mg dose and lymphocytes taken before and after the supplement were treated in vitro with H2O2. DNA strand breaks and oxidised pyrimidines were measured at intervals, to monitor the removal of oxidative DNA damage. We found inter-individual variations in response. In cases where the baseline plasma beta-carotene concentration was high, or where supplementation increased the plasma concentration, recovery from oxidative damage (i.e. removal of both oxidised pyrimidines and strand breaks) was relatively rapid. However, what seems to be an enhancement of repair might in fact represent an amelioration of the continuing oxidative stress encountered by the lymphocytes under in vitro culture conditions. We found that culture in a 5% oxygen atmosphere enhanced recovery of lymphocytes from H2O2 damage.

Sign in / Sign up

Export Citation Format

Share Document