Activated Toxicity of Diesel Particulate Extract by Ultraviolet A Radiation in Mammalian Cells: Role of Singlet Oxygen

Bao, Lingzhi; Xu, An; Tong, Liping; Chen, Shaopeng; Zhu, Lingyan; Zhao, Ye; Zhao, Guoping; Jiang, Erkang; Wang, Jun; Wu, Lijun

doi:10.1289/ehp.0800029

Cited by 32 publications

(33 citation statements)

References 68 publications

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“…However, to specifically reveal the potential carcinogenic effects of PAHs, application of organic extracts is more relevant. Although the genotoxicity of DEP extracts may be easily tested by standardized, well-established tests including cytotoxicity measurement [20], Ames test [20,21], analysis of double strand DNA breaks [21], apoptosis, frequency of micronuclei [22], bulky DNA adducts formation or oxidative DNA damage [12], for a comprehensive assessment of the biological processes induced by the DEP extracts the treatment of the whole genome gene expression analysis is a valuable tool.…”

Section: Introductionmentioning

confidence: 99%

Comparative Analysis of Toxic Responses of Organic Extracts from Diesel and Selected Alternative Fuels Engine Emissions in Human Lung BEAS-2B Cells

Líbalová

Rössner

Vrbová

et al. 2016

IJMS

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This study used toxicogenomics to identify the complex biological response of human lung BEAS-2B cells treated with organic components of particulate matter in the exhaust of a diesel engine. First, we characterized particles from standard diesel (B0), biodiesel (methylesters of rapeseed oil) in its neat form (B100) and 30% by volume blend with diesel fuel (B30), and neat hydrotreated vegetable oil (NEXBTL100). The concentration of polycyclic aromatic hydrocarbons (PAHs) and their derivatives in organic extracts was the lowest for NEXBTL100 and higher for biodiesel. We further analyzed global gene expression changes in BEAS-2B cells following 4 h and 24 h treatment with extracts. The concentrations of 50 µg extract/mL induced a similar molecular response. The common processes induced after 4 h treatment included antioxidant defense, metabolism of xenobiotics and lipids, suppression of pro-apoptotic stimuli, or induction of plasminogen activating cascade; 24 h treatment affected fewer processes, particularly those involved in detoxification of xenobiotics, including PAHs. The majority of distinctively deregulated genes detected after both 4 h and 24 h treatment were induced by NEXBTL100; the deregulated genes included, e.g., those involved in antioxidant defense and cell cycle regulation and proliferation. B100 extract, with the highest PAH concentrations, additionally affected several cell cycle regulatory genes and p38 signaling.

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Section: Introductionmentioning

confidence: 99%

Comparative Analysis of Toxic Responses of Organic Extracts from Diesel and Selected Alternative Fuels Engine Emissions in Human Lung BEAS-2B Cells

Líbalová

Rössner

Vrbová

et al. 2016

IJMS

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“…16 As shown in Figure 8D and E, 4-O-TEMPO triplet spectra and the relative signal intensity increased considerably in worms coexposed to DPE (20 μg/mL) plus UVA (0.5 J/cm 2 ) compared with those in the single treatment of DPE or UVA, or with the control worms, and NaN 3 (100 μM) significantly reduced this signal ( P < 0.05). Taken together, the results indicated that the ROS, especially 1 O 2 , played a pivotal role in the induction of germ cell apoptosis within C. elegans by coexposure to DPE plus UVA.…”

Section: Resultsmentioning

confidence: 78%

Synergistic Effects Induced by a Low Dose of Diesel Particulate Extract and Ultraviolet-A in Caenorhabditis elegans: DNA Damage-Triggered Germ Cell Apoptosis

Guo

Bian

Liang

et al. 2014

Chem. Res. Toxicol.

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Diesel exhaust has been classified as a potential carcinogen and is associated with various health effects. A previous study showed that the doses for manifesting the mutagenetic effects of diesel exhaust could be reduced when coexposed with ultraviolet-A (UVA) in a cellular system. However, the mechanisms underlying synergistic effects remain to be clarified, especially in an in vivo system. In the present study, using Caenorhabditis elegans (C. elegans) as an in vivo system we studied the synergistic effects of diesel particulate extract (DPE) plus UVA, and the underlying mechanisms were dissected genetically using related mutants. Our results demonstrated that though coexposure of wild type worms at young adult stage to low doses of DPE (20 μg/mL) plus UVA (0.2, 0.5, and 1.0 J/cm2) did not affect worm development (mitotic germ cells and brood size), it resulted in a significant induction of germ cell death. Using the strain of hus-1::gfp, distinct foci of HUS-1::GFP was observed in proliferating germ cells, indicating the DNA damage after worms were treated with DPE plus UVA. Moreover, the induction of germ cell death by DPE plus UVA was alleviated in single-gene loss-of-function mutations of core apoptotic, checkpoint HUS-1, CEP-1/p53, and MAPK dependent signaling pathways. Using a reactive oxygen species (ROS) probe, it was found that the production of ROS in worms coexposed to DPE plus UVA increased in a time-dependent manner. In addition, employing a singlet oxygen (1O2) trapping probe, 2,2,6,6-tetramethyl-4-piperidone, coupled with electron spin resonance analysis, we demonstrated the increased 1O2 production in worms coexposed to DPE plus UVA. These results indicated that UVA could enhance the apoptotic induction of DPE at low doses through a DNA damage-triggered pathway and that the production of ROS, especially 1O2, played a pivotal role in initiating the synergistic process.

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“…1 O 2 was distinctly detected as shown in Figure 5, and addition of NaN 3 to the medium concentration-dependently reduced formation of singlet oxygen ( Figure 6). Some investigators also reported generation of singlet oxygen induced in the presence of several photosensitizers following UV-A irradiation (Yin et al 2008;Bao et al 2009;Zhang et al 2011). Some nutrients also act as photosensitizers as noted by several investigators (for example, vitamins (riboflavin), porphyrins, nicotinamide (Baier et al 2006;Carbonare and Pathak 1992), lipids, free fatty acids (Regensburger et al 2012)).…”

Section: Discussionmentioning

confidence: 87%

“…ROS were induced by UV photo-irradiation of some photosensitizers in a medium containing fatty acids and vitamins (Regensburger et al 2012) and cytoplasmic urocanic acid, riboflavin, and b-nicotinamide adenine dinucleotide (NAD) (Baier et al 2006). Moreover, harmful chemical compounds such as crude coal tar, benzo[a]pyrene (Crallan, Ingham, and Routledge 2005), and diesel exhaust particles (Bao et al 2009;Guo et al 2014) also induced ROS associated with UV irradiation. However, some scavengers, such as glutathione (GSH), catalase (CAT), N-acetylcysteine (NAC), superoxide dismutase (SOD), and vitamin C, are contained in the cells or medium.…”

mentioning

confidence: 99%

Effects of UV-A LED light irradiation on growth of cultured RAW 264.7 cells

Ikehara

Nakahashi

et al. 2015

Toxicological & Environmental Chemistry

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The aim of this study was to examine the effects of ultraviolet A (UV-A) irradiationinduced damage on cultured macrophage RAW 264.7 cells and determine which components produced these manifestations. RAW 264.7 cells were irradiated with 365 nm UV-A using a light-emitting diode (LED). Cell viability and damage were determined using a calcein-AM and propidium iodide dual-staining assay and lactate dehydrogenase leakage, respectively. Intracellular reactive oxygen species (ROS) were measured by H 2 DCF-DA. The components of ROS in each medium were measured using an electron paramagnetic resonance (EPR) spectrometer in the presence of 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and 2,2,5,5-tetramethyl-3-pyrroline-3-carboxamide (TPC). While UV-A irradiation for 2 min significantly suppressed cell growth, LDH leakage did not occur. Addition of N-acetyl cysteine restored inhibition of cell proliferation, and reduced intracellular ROS levels. The EPR signal in the presence of TPC increased with time but was decreased by sodium azide. In addition, a typical EPR spectrum was obtained in the presence of DMPO, indicating the presence of a hydroxyradical. The spectrum was diminished by Lhistidine. Data suggest that ROS generated in cells or culture medium by UV-A irradiation is predominantly singlet oxygen, and this singlet oxygen suppressed cell proliferation.

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Activated Toxicity of Diesel Particulate Extract by Ultraviolet A Radiation in Mammalian Cells: Role of Singlet Oxygen

Cited by 32 publications

References 68 publications

Comparative Analysis of Toxic Responses of Organic Extracts from Diesel and Selected Alternative Fuels Engine Emissions in Human Lung BEAS-2B Cells

Comparative Analysis of Toxic Responses of Organic Extracts from Diesel and Selected Alternative Fuels Engine Emissions in Human Lung BEAS-2B Cells

Synergistic Effects Induced by a Low Dose of Diesel Particulate Extract and Ultraviolet-A in Caenorhabditis elegans: DNA Damage-Triggered Germ Cell Apoptosis

Effects of UV-A LED light irradiation on growth of cultured RAW 264.7 cells

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