Assessment of oxidative DNA damage formation by organic complex mixtures from airborne particles PM10

Gábelová, Alena; Valovičová, Zuzana; Lábaj, Juraj; Bacová, G; Binková, Blanka; Farmer, Peter B.

doi:10.1016/j.mrfmmm.2007.03.003

Cited by 22 publications

(17 citation statements)

References 50 publications

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“…The oxidative effect observed at the highest dose for station 1 in both seasonal samplings could be due to the presence in this site of other oxidant species. These results confirm the role of oxidative stress in PM 10 -induced biological effects as demonstrated in several in vitro and in vivo studies (Claxton et al 2004;Donaldson et al 2002;Dybdahl et al 2004;Singh et al 2004;Gábelová et al 2007). It should be pointed out that the DNA damage showed in our study even at low doses, represents the final biological effect of exposure to urban PM 10 , consisting of a complex mixture of compounds including PAHs, methyl-PAHs, and nitro-PAHs, which represent only the 0.01% of the organic fraction.…”

Section: Discussionsupporting

confidence: 89%

Evaluation of Direct-Oxidative DNA Damage on Human Lung Epithelial Cells Exposed to Urban Airborne Particulate Matter

Cavallo¹,

Ursini²,

Filippo³

et al. 2008

Water Air Soil Pollut: Focus

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Airborne particulate matter (PM) extracts were investigated for their content of organic compounds and for the direct and oxidative DNA damage induced on lung epithelial cells A549. PM 10 was seasonally collected at two monitoring sites (Stations 1 and 2), characterized by different traffic loads. The cells were exposed for 30 min to extracts of PM 10 diluted at 0.025%, 0.05%, and 0.1% for summer samples, and at 0.05%, 0.1%, and 0.15% for winter samples. Oxidative and direct DNA damage were evaluated by formamidopyrimidine glycosylase (fpg) comet assay analyzing tail moment (TM) values from fpg-enzyme-treated cells (TMenz) and enzyme untreated cells (TM) respectively and by comet percentage analysis. Measurements relating to Station 2 showed higher levels of polycyclic aromatic hydrocarbons (PAHs), and their methyl-(methyl-PAHs) and nitro-(nitro-PAHs) derivatives in both the seasons. Nitro-PAH concentrations were higher in summer than in winter at both the stations. We found a significant increase of comet percentages at the highest dose of extract from both stations in summer and from Station 2 in winter. The TM and TMenz values relative to the summer sampling showed an early oxidative DNA damage induction also followed by direct DNA damage more evident at Station 2, that seems to correlate with the presence of higher nitro-PAH concentrations during the warm season. At both monitoring stations, the results from winter sampling campaign showed a direct DNA damage induction at 0.1% of extract and oxidative-direct DNA damage at the highest dose (0.15%).

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Section: Discussionsupporting

confidence: 89%

Evaluation of Direct-Oxidative DNA Damage on Human Lung Epithelial Cells Exposed to Urban Airborne Particulate Matter

Cavallo¹,

Ursini²,

Filippo³

et al. 2008

Water Air Soil Pollut: Focus

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“…In particular the high level of oxidative damage in the IN site with respect to the HW site could be ascribed to the concentration of Cu, Zn e Cd that is 3-10 fold higher then in the PM sampled in the HW site. This finding supports the results obtained in other studies that showed the role of transition metals in reactive oxygen specie production and in oxidative stress induction [11,12]. In different studies the genotoxic and oxidative activity of Cu and Zn are reported [13].…”

Section: Genotoxic Damage and Oxidative Stress Of Pm Extractssupporting

confidence: 92%

Genotoxic and oxidative damage related to PM_2.5chemical fraction

Gianotti¹,

Scozia²,

Bonetta³

et al. 2008

WIT Transactions on Ecology and the Environment

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Many studies have pointed out a correlation between airborne PM quantitative exposure and health effects. The aim of this research is the investigation of the role of the PM 2.5 chemical fraction in the DNA damage induction in human cells (A549). Air samples (PM 2.5 ) were collected in different sites (urban, industrial and highway) using a high-volume sampler. Organic and water-soluble extracts of PM 2.5 were tested on A549 cells to evaluate genotoxic and oxidative damage using the Comet assay without and with formamido-pyrimidine-glycosylase (Fpg). Organic and water extracts were analysed for determination of PAHs by GC-MS methods and metals by the ICP-MS technique respectively. The PM 2.5 organic extract of all the samples caused a significant dose-dependent increase of the A549 DNA damage. The genotoxic effect was related to IPA PM 2.5 content and the highest effect was observed for the motorway site sample (65.03 CL/10m3 ) while the oxidative damage was observed in PM 2.5 water extract of the industrial and motorway sites. The extent of the oxidative damage seems to be related to the type and concentration of metals present in these samples. The results of this study emphasize the importance of evaluating the PM chemical composition for the biological effect determination. This concern highlights the need for considering its qualitative composition in addition to its size and air concentration for PM health effect evaluation and exposure management.

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“…The physicochemical characteristics of nanoparticles enable them to absorb compounds and can easily cross various biological barriers without a specific transporter [Wamer et al, 1997;Li et al, 2003;Xia et al, 2006;Gabelova et al, 2007]. Therefore, the interactions among nanoparticles and other pollutants are complex.…”

mentioning

confidence: 99%

“…Therefore, the interactions among nanoparticles and other pollutants are complex. For example, adsorbed organic compounds can undergo various interactions (additive or synergistic) with other particulate components or physical factors (UV-irradiation) to enhance/multiply the adverse health effects of particulate air pollution [Gabelova et al, 2007]. Additive as well as synergistic effects on early pulmonary inflammation were observed when 14 nm or 95 nm ultrafine carbon black particles and staphylococcal lipoteichoic acid was administrated intratracheally in male BALB/c mice [Yamamoto et al, 2006].…”

mentioning

confidence: 99%

Synergistic genotoxicity caused by low concentration of titanium dioxide nanoparticles and p,p′‐DDT in human hepatocytes

Shi

Zhang

Jiang

et al. 2009

Environ and Mol Mutagen

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The use of titanium dioxide nanoparticles (nano-TiO(2)) for the degradation of dichlorodiphenyltrichloroethane (p,p'-DDT) increases the risk of exposure to trace nano-TiO(2) and p,p'-DDT mixtures. The interaction of p,p'-DDT and nano-TiO(2) at low concentrations may alter toxic response relative to nano-TiO(2) or p,p'-DDT alone. In this work, the combined genotoxicity of trace nano-TiO(2) and p,p'-DDT on human embryo L-02 hepatocytes without photoactivation was studied. Nano-TiO(2) (0.1 g/L) was mixed with 0.01-1 mmol/L p,p'-DDT to determine adsorption isotherms. L-02 cells were exposed to different levels of p,p'-DDT (0, 0.001, 0.01, and 0.1 mumol/L) and nano-TiO(2) (0, 0.01, 0.1, and 1 microg/mL) respectively. The adsorption of p,p'-DDT by nano-TiO(2) was approximately 0.3 mmol/g. Cell viability, apoptosis, and DNA double strand breaks were similar among all test groups. Nano-TiO(2) alone (0.01-1 microg/mL) increased the levels of oxidative stress and oxidative DNA adducts (8-OHdG), but it did not induce DNA breaks or chromosome damage. Addition of trace nano-TiO(2) with trace p,p'-DDT synergistically enhanced genotoxicity via increasing oxidative stress, oxidative DNA adducts, DNA breaks, and chromosome damage in L-02 cells. Low concentrations of nano-TiO(2) and p,p'-DDT increased oxidativestress by reactive oxygen species (ROS) formation and lipid oxidation. Oxidative stress is a major pathway for DNA and chromosome damage. Dose-dependent synergistic genotoxicity induced by combined exposure of trace p,p'-DDT and nano-TiO(2) suggests a potential environmental risk of nano-TiO(2) assisted photocatalysis.

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Assessment of oxidative DNA damage formation by organic complex mixtures from airborne particles PM10

Cited by 22 publications

References 50 publications

Evaluation of Direct-Oxidative DNA Damage on Human Lung Epithelial Cells Exposed to Urban Airborne Particulate Matter

Evaluation of Direct-Oxidative DNA Damage on Human Lung Epithelial Cells Exposed to Urban Airborne Particulate Matter

Genotoxic and oxidative damage related to PM_2.5chemical fraction

Synergistic genotoxicity caused by low concentration of titanium dioxide nanoparticles and p,p′‐DDT in human hepatocytes

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Assessment of oxidative DNA damage formation by organic complex mixtures from airborne particles PM10

Cited by 22 publications

References 50 publications

Evaluation of Direct-Oxidative DNA Damage on Human Lung Epithelial Cells Exposed to Urban Airborne Particulate Matter

Evaluation of Direct-Oxidative DNA Damage on Human Lung Epithelial Cells Exposed to Urban Airborne Particulate Matter

Genotoxic and oxidative damage related to PM2.5chemical fraction

Synergistic genotoxicity caused by low concentration of titanium dioxide nanoparticles and p,p′‐DDT in human hepatocytes

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Product

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Genotoxic and oxidative damage related to PM_2.5chemical fraction