Determination of Genotoxicity Attributed to Diesel Exhaust Particles in Normal Human Embryonic Lung Cell (WI-38) Line

Lee, Hee Jae; Lee, Young Joo; Lim, Yong Beom; Sim, Woo Jong; Jang, Ji Hye; Heo, Hye Ryeon; Lim, Hyunwoo; Jung, Ji Won; Kim, Jin Sik

doi:10.3390/biom11020291

Cited by 6 publications

(3 citation statements)

References 69 publications

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“…Both environmental and engineered NMs have been shown to induce adverse health effects, such as pulmonary, cardiovascular, neurological, and reproductive disorders [ 6 , 7 , 8 ]. A direct association between exposure to diesel exhaust particles (DEPs) in exhaust fumes and lung cancer has been demonstrated [ 9 , 10 , 11 , 12 ]. Engineered NMs, (e.g., metallic nanoparticles, quantum dots, carbon nanotubes) have also been shown to cause toxicity after inhalation exposure [ 13 , 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

Advanced Respiratory Models for Hazard Assessment of Nanomaterials—Performance of Mono-, Co- and Tricultures

et al. 2022

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Advanced in vitro models are needed to support next-generation risk assessment (NGRA), moving from hazard assessment based mainly on animal studies to the application of new alternative methods (NAMs). Advanced models must be tested for hazard assessment of nanomaterials (NMs). The aim of this study was to perform an interlaboratory trial across two laboratories to test the robustness of and optimize a 3D lung model of human epithelial A549 cells cultivated at the air–liquid interface (ALI). Potential change in sensitivity in hazard identification when adding complexity, going from monocultures to co- and tricultures, was tested by including human endothelial cells EA.hy926 and differentiated monocytes dTHP-1. All models were exposed to NM-300K in an aerosol exposure system (VITROCELL® cloud-chamber). Cyto- and genotoxicity were measured by AlamarBlue and comet assay. Cellular uptake was investigated with transmission electron microscopy. The models were characterized by confocal microscopy and barrier function tested. We demonstrated that this advanced lung model is applicable for hazard assessment of NMs. The results point to a change in sensitivity of the model by adding complexity and to the importance of detailed protocols for robustness and reproducibility of advanced in vitro models.

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Section: Introductionmentioning

confidence: 99%

Advanced Respiratory Models for Hazard Assessment of Nanomaterials—Performance of Mono-, Co- and Tricultures

et al. 2022

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“…Based on previous reports, DEPs induce genotoxicity in normal human embryonic lung cells, and its potential inhibitory effects on cell cycle progression through RNA expression have been noted [40,41]. First, to confirm the cytotoxicity of 9,10-PQ in HeLa cells, we treated the cells with 1, 2, 4, or 8 µM 9,10-PQ for up to 24 h, in agreement with the methods of a previous study [16], and examined the cell morphology, viability, and protein expression (Figure S1A-C).…”

Section: Exposure To 910-pq Disturbs Mitotic Progressionmentioning

confidence: 99%

Cytotoxicity of 9,10-Phenanthrenequinone Impairs Mitotic Progression and Spindle Assembly Independent of ROS Production in HeLa Cells

Kim

Leem

et al. 2022

Toxics

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The polycyclic aromatic hydrocarbon quinone derivative 9,10-phenanthrenequinone (9,10-PQ) is one of the most abundant and toxic components found in diesel exhaust particles (DEPs). These DEPs are created during diesel fuel combustion and are considered the main source of urban air pollution. As 9,10-PQ can produce excessive reactive oxygen species (ROS) through redox cycling, it has been shown to exert potent cytotoxic effects against various cell types. However, the mechanisms underlying this cytotoxicity remain unclear. In this study, we showed that 9,10-PQ exerts cytotoxicity by impairing mitotic progression and spindle assembly in HeLa cells. Exposure to 9,10-PQ impaired spindle assembly and chromosome alignment, resulting in delayed mitotic entry and progression in HeLa cells. Furthermore, 9,10-PQ exposure decreased the CEP192 and p-Aurora A levels at the spindle poles. Notably, these mitotic defects induced by 9,10-PQ were not rescued by scavenging ROS, implying the ROS-independent activity of 9,10-PQ. Therefore, our results provide the first evidence that 9,10-PQ exerts its cytotoxicity through specific inhibition of mitotic progression and spindle assembly, independent of ROS.

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“…Based on epidemiological evidence indicating DEP’s association with an increase in the relative risk of lung cancer, Lee et al [ 3 ] attempted to study the genotoxic effects of DEP at the chromosomal level using normal embryonic human lung fibroblast cells with micronuclei (MN) and comet assays. They found that DEP exposure induced DNA damage at the chromosomal level in normal human lung cells and provided information on the expression of genes associated with genotoxic stress.…”

mentioning

confidence: 99%

Health and Environmental Effect of Advanced Materials and Fine Particles

Yu¹

2022

Biomolecules

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Determination of Genotoxicity Attributed to Diesel Exhaust Particles in Normal Human Embryonic Lung Cell (WI-38) Line

Cited by 6 publications

References 69 publications

Advanced Respiratory Models for Hazard Assessment of Nanomaterials—Performance of Mono-, Co- and Tricultures

Advanced Respiratory Models for Hazard Assessment of Nanomaterials—Performance of Mono-, Co- and Tricultures

Cytotoxicity of 9,10-Phenanthrenequinone Impairs Mitotic Progression and Spindle Assembly Independent of ROS Production in HeLa Cells

Health and Environmental Effect of Advanced Materials and Fine Particles

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