Vascular Oxidative Stress Induced by Diesel Exhaust Microparticles

Labranche, Nathalie; Khattabi, Charaf El; Dewachter, Laurence; Dreyfuss, Céline; Fontaine, Jeanine; Borne, Philippe van de; Berkenboom, Guy; Pochet, Stéphanie

doi:10.1097/fjc.0b013e318270f1a8

Cited by 12 publications

(10 citation statements)

References 34 publications

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“…In Wistar rats exposed to SRM 2975 by intra-tracheal instillation, vasomotor function was unaffected although the rats had extensive lung inflammation [159]. However, SRM 2975 disturbed vasomotor function of hypertensive rats [160]. Furthermore, SRM 2975 has been reported to increase both lung inflammation as well as plaque formation in ApoE −/− mice [60].…”

Section: The Role Of Organic Chemicals and Pah In Mediating Cvdmentioning

confidence: 99%

Potential role of polycyclic aromatic hydrocarbons as mediators of cardiovascular effects from combustion particles

et al. 2019

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Air pollution is the most important environmental risk factor for disease and premature death, and exposure to combustion particles from vehicles is a major contributor. Human epidemiological studies combined with experimental studies strongly suggest that exposure to combustion particles may enhance the risk of cardiovascular disease (CVD), including atherosclerosis, hypertension, thrombosis and myocardial infarction. In this review we hypothesize that adhered organic chemicals like polycyclic aromatic hydrocarbons (PAHs), contribute to development or exacerbation of CVD from combustion particles exposure. We summarize present knowledge from existing human epidemiological and clinical studies as well as experimental studies in animals and relevant in vitro studies. The available evidence suggests that organic compounds attached to these particles are significant triggers of CVD. Furthermore, their effects seem to be mediated at least in part by the aryl hydrocarbon receptor (AhR). The mechanisms include AhR-induced changes in gene expression as well as formation of reactive oxygen species (ROS) and/or reactive electrophilic metabolites. This is in accordance with a role of PAHs, as they seem to be the major chemical group on combustion particles, which bind AhR and/or is metabolically activated by CYP-enzymes. In some experimental models however, it seems as PAHs may induce an inflammatory atherosclerotic plaque phenotype irrespective of DNA- and/or AhR-ligand binding properties. Thus, various components and several signalling mechanisms/pathways are likely involved in CVD induced by combustion particles. We still need to expand our knowledge about the role of PAHs in CVD and in particular the relative importance of the different PAH species. This warrants further studies as enhanced knowledge on this issue may amend risk assessment of CVD caused by combustion particles and selection of efficient measures to reduce the health effects of particular matters (PM).

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Section: The Role Of Organic Chemicals and Pah In Mediating Cvdmentioning

confidence: 99%

Potential role of polycyclic aromatic hydrocarbons as mediators of cardiovascular effects from combustion particles

et al. 2019

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“…DEP suspensions were prepared as previously described. 21 In short, DEP (2 mg/mL) were suspended in PBS, vortexed, and sonicated for 2 min by probe sonication. They were sonicated for 15 min in a bath sonicator just before use.…”

Section: Methodsmentioning

confidence: 99%

“…DEP concentrations were chosen according to previous studies. 10,21 We also exposed M1 and M2 macrophages for an additional 24 h with DEP suspensions or DEP extracts.…”

Section: Dep Exposurementioning

confidence: 99%

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Effects of diesel exhaust particles on macrophage polarization

et al. 2016

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Background: Exposure to diesel exhaust particles (DEP) has long been associated with increased cardiovascular morbidity and mortality. The development of DEP toxicity seems to be linked to inflammation in which macrophages play a critical role. Macrophages can be polarized into proinflammatory M1 or anti-inflammatory M2 macrophages. The aim of this study was to identify the role of inflammation in DEP-induced toxicity by assessing the effects of DEP on macrophage polarization. Methods: Monocyte-derived macrophages (Mϕ) were stimulated with interferon γ and lipopolysaccharide or interleukin (IL)-4 to obtain M1 and M2 subtypes, respectively. To test the polarization capacity of DEP, Mϕ cells were exposed to DEP and compared to Mϕ, M1, and M2. We also studied the effects of DEP on already-polarized M1 or M2. The M1 markers assessed were tumor necrosis factor α (TNF-α) and IL-1β, while the M2 markers were the mannose receptor C type 1 (MRC-1) and transglutaminase 2 (TGM2). Results: Western blots revealed a 31 kDa band corresponding to pro-IL-1β, but only in M1-polarized macrophages. In M1, we also observed an upregulation of TNF-α messenger RNA (mRNA) expression. MRC-1 and TGM2 mRNA expression were only significantly enhanced in M2. DEP had no effect on any of the M1/M2 markers assessed. Moreover, DEP were not able to modify the phenotype of already-polarized M1 or M2. Conclusion: Mϕ incubation with DEP did not have any effect on macrophage polarization, at least on the markers assessed in this study, namely, TNF-α/IL-1β for M1, and MRC-1/TGM2 for M2. Hence, these data argue against an important role of inflammation in DEP-induced vascular toxicity.

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“…Consequently, a multi-pollutant perspective should be the focus of air quality management, rather than adhering to a single-pollutant viewpoint (Huang et al, 2012). Furthermore, although several recent studies have investigated the combined toxicity of complex mixtures of chemicals (Labranche et al, 2012), detailed investigations into synergistic toxicity and the possible mechanisms involved in biological responses to complex exposures remain scarce (Ku et al, 2017). Therefore, in the present study, we performed a chemical analysis of mineral coals from two different Colombian mines to identify the main compounds present.…”

Section: Introductionmentioning

confidence: 99%

Systems chemo-biology analysis of DNA damage response and cell cycle effects induced by coal exposure

et al. 2020

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Cell cycle alterations are among the principle hallmarks of cancer. Consequently, the study of cell cycle regulators has emerged as an important topic in cancer research, particularly in relation to environmental exposure. Particulate matter and coal dust around coal mines have the potential to induce cell cycle alterations. Therefore, in the present study, we performed chemical analyses to identify the main compounds present in two mineral coal samples from Colombian mines and performed systems chemo-biology analysis to elucidate the interactions between these chemical compounds and proteins associated with the cell cycle. Our results highlight the role of oxidative stress generated by the exposure to the residues of coal extraction, such as major inorganic oxides (MIOs), inorganic elements (IEs) and polycyclic aromatic hydrocarbons (PAH) on DNA damage and alterations in the progression of the cell cycle (blockage and/or delay), as well as structural dysfunction in several proteins. In particular, IEs such as Cr, Ni, and S and PAHs such as benzo[a]pyrene may have influential roles in the regulation of the cell cycle through DNA damage and oxidative stress. In this process, cyclins, cyclin-dependent kinases, zinc finger proteins such as TP53, and protein kinases may play a central role.

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Vascular Oxidative Stress Induced by Diesel Exhaust Microparticles

Abstract: Although in vitro exposure to DEP produces a vascular oxidative stress, repeated in vivo exposures to DEP only impair vascular function in SHR, via an upregulation of p22phox. This suggests a synergistic effect on endothelial dysfunction between particulate air pollution and hypertension.

Cited by 12 publications

References 34 publications

Potential role of polycyclic aromatic hydrocarbons as mediators of cardiovascular effects from combustion particles

Potential role of polycyclic aromatic hydrocarbons as mediators of cardiovascular effects from combustion particles

Effects of diesel exhaust particles on macrophage polarization

Systems chemo-biology analysis of DNA damage response and cell cycle effects induced by coal exposure

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