Air pollution particulate matter (PM2.5)-induced gene expression of volatile organic compound and/or polycyclic aromatic hydrocarbon-metabolizing enzymes in an in vitro coculture lung model

Abbas, Imane; Saint-Georges, Françoise; Billet, Sylvain; Verdin, Anthony; Mulliez, P.; Shirali, Pirouz; Garçon, Guillaume

doi:10.1016/j.tiv.2008.09.020

Cited by 55 publications

(36 citation statements)

References 58 publications

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“…On one hand, PAHs have an important contribution to PM 2.5 -induced lung toxicity. 62 Some studies have shown that exposure to PAHs is associated with mitochondrial damage via decreasing mitochondrial DNA (mtDNA) content, reducing mitochondrial membrane potential, and modulating the metabolic machinery inside the cells, accompanied by oxidative stress. 63−65 This evidence suggests and important connection between PM 2.5 -bound PAHs and lung damage or mitochondrial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ambient PM_2.5 on Lung Mitochondrial Damage and Fusion/Fission Gene Expression in Rats

Kou

Geng

et al. 2015

Chem. Res. Toxicol.

143

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Exposure to ambient fine particulate matter (PM2.5) increases the risk of respiratory disease. Although previous mitochondrial research has provided new information about PM toxicity in the lung, the exact mechanism of PM2.5-mediated structural and functional damage of lung mitochondria remains unclear. In this study, changes in lung mitochondrial morphology, expression of mitochondrial fission/fusion markers, lipid peroxidation, and transport ATPase activity in SD rats exposed to ambient PM2.5 at different dosages were investigated. Also, the release of reactive oxygen species (ROS) via the respiratory burst in rat alveolar macrophages (AMs) exposed to PM2.5 was examined by luminol-dependent chemiluminescence (CL). The results showed that (1) PM2.5 deposited in the lung and induced pathological damage, particularly causing abnormal alterations of mitochondrial structure, including mitochondrial swelling and cristae disorder or even fragmentation in the presence of higher doses of PM2.5; (2) PM2.5 significantly affected the expression of specific mitochondrial fission/fusion markers (OPA1, Mfn1, Mfn2, Fis1, and Drp1) in rat lung; (3) PM2.5 inhibited Mn superoxide dismutase (MnSOD), Na(+)K(+)-ATPase, and Ca(2+)-ATPase activities and elevated malondialdehyde (MDA) content in rat lung mitochondria; and (4) PM2.5 induced rat AMs to produce ROS, which was inhibited by about 84.1% by diphenyleneiodonium chloride (DPI), an important ROS generation inhibitor. It is suggested that the pathological injury observed in rat lung exposed to PM2.5 is associated with mitochondrial fusion-fission dysfunction, ROS generation, mitochondrial lipid peroxidation, and cellular homeostasis imbalance. Damage to lung mitochondria may be one of the important mechanisms by which PM2.5 induces lung injury, contributing to respiratory diseases.

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Section: Discussionmentioning

confidence: 99%

Effect of Ambient PM_2.5 on Lung Mitochondrial Damage and Fusion/Fission Gene Expression in Rats

Kou

Geng

et al. 2015

Chem. Res. Toxicol.

143

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“…A wealth of literature has identified nonmethane hydrocarbon (NMHC) oxidation as a major influence upon climate change [1], environmental damage [2], and health effects [3]. The photochemical processing of NMHCs affects the ozone budget [4].…”

Section: Introductionmentioning

confidence: 99%

Temperature‐dependent kinetics for the ozonolysis of selected chlorinated alkenes in the gas phase

Leather

McGillen

Ghalaieny

et al. 2010

Int J of Chemical Kinetics

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The ozonolysis of olefinic species is an important tropospheric process impacting on climate and human health. However, few studies have investigated these reactions as a function of temperature and even less information is available upon the effects of alkene heteroatomic substitution on the Arrhenius parameters. The electron-withdrawing capacity of substituents about the olefinic bond strongly influences the rate of alkene ozonolysis. To understand better the effect of these substitutions, the temperature-dependence of a series of ozonechloroalkene reactions is investigated. Experiments were conducted in the EXTreme RAnge (EXTRA) chamber, over the range of 292-409 K and 760 Torr. The experimentally determined rate coefficients were fitted using an Arrhenius-type analysis to yield the following activation energies: 30.80 ± 0.79, 23.18 ± 0.59, 65.2 ± 2.8, 116.9 ± 5.6, 29.5 ± 1.8, and 18.67 ± 0.96 kJ mol −1 and preexponential A-factors 1.22

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“…Furthermore, Clara cell does not contain CYP2E1, but, when rats are exposed to ozone, the CYP2E1 is induced in the bronchiolar epithelium (Ioannides, 2008). In general Particulate Matter induces gene expression of CYP1A1 and CYP2E1 (Abbas et al, 2009 …”

Section: Air Pollution Modification Of Cypsmentioning

confidence: 99%

Air Pollution and Its Effects in the Respiratory System

Fortoul¹,

Rojas-Lemus²,

Rodríguez-Lara³

et al. 2011

The Impact of Air Pollution on Health, Economy, Environment and Agricultural Sources

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Air pollution particulate matter (PM2.5)-induced gene expression of volatile organic compound and/or polycyclic aromatic hydrocarbon-metabolizing enzymes in an in vitro coculture lung model

Cited by 55 publications

References 58 publications

Effect of Ambient PM_2.5 on Lung Mitochondrial Damage and Fusion/Fission Gene Expression in Rats

Effect of Ambient PM_2.5 on Lung Mitochondrial Damage and Fusion/Fission Gene Expression in Rats

Temperature‐dependent kinetics for the ozonolysis of selected chlorinated alkenes in the gas phase

Air Pollution and Its Effects in the Respiratory System

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Air pollution particulate matter (PM2.5)-induced gene expression of volatile organic compound and/or polycyclic aromatic hydrocarbon-metabolizing enzymes in an in vitro coculture lung model

Cited by 55 publications

References 58 publications

Effect of Ambient PM2.5 on Lung Mitochondrial Damage and Fusion/Fission Gene Expression in Rats

Effect of Ambient PM2.5 on Lung Mitochondrial Damage and Fusion/Fission Gene Expression in Rats

Temperature‐dependent kinetics for the ozonolysis of selected chlorinated alkenes in the gas phase

Air Pollution and Its Effects in the Respiratory System

Contact Info

Product

Resources

About

Effect of Ambient PM_2.5 on Lung Mitochondrial Damage and Fusion/Fission Gene Expression in Rats

Effect of Ambient PM_2.5 on Lung Mitochondrial Damage and Fusion/Fission Gene Expression in Rats