Gasoline fume inhalation induces apoptosis, inflammation, and favors Th2 polarization in C57BL/6 mice.

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Tytuł:: Gasoline fume inhalation induces apoptosis, inflammation, and favors Th2 polarization in C57BL/6 mice.
Autorzy:: Nour-Eldine W; Gilbert and Rose-Marie Chagoury School of Medicine, Lebanese American University, Byblos, Lebanon.
Sayyed K; School of Arts and Sciences, Department of Natural Sciences, Lebanese American University, Byblos, Lebanon.
Harhous Z; Gilbert and Rose-Marie Chagoury School of Medicine, Lebanese American University, Byblos, Lebanon.
Dagher-Hamalian C; Gilbert and Rose-Marie Chagoury School of Medicine, Lebanese American University, Byblos, Lebanon.
Mehanna S; Department of Natural Sciences, Lebanese American University, Beirut, Lebanon.
Achkouti D; Gilbert and Rose-Marie Chagoury School of Medicine, Lebanese American University, Byblos, Lebanon.
ElKazzaz H; Gilbert and Rose-Marie Chagoury School of Medicine, Lebanese American University, Byblos, Lebanon.
Khnayzer RS; Department of Natural Sciences, Lebanese American University, Beirut, Lebanon.
Kobeissy F; Faculty of Medicine, Department of Biochemistry and Molecular Genetics, American University of Beirut, Beirut, Lebanon.
Khalil C; School of Arts and Sciences, Department of Natural Sciences, Lebanese American University, Byblos, Lebanon.
Abi-Gerges A; Gilbert and Rose-Marie Chagoury School of Medicine, Lebanese American University, Byblos, Lebanon.
Źródło:: Journal of applied toxicology : JAT [J Appl Toxicol] 2022 Jul; Vol. 42 (7), pp. 1178-1191. Date of Electronic Publication: 2022 Jan 25.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: : Chichester : John Wiley And Sons
Original Publication: [Philadelphia, Pa. : Heyden & Son, c1981-
MeSH Terms:: Gasoline*/toxicity
Inflammation*/chemically induced
Animals ; Apoptosis ; Female ; Inhalation Exposure/adverse effects ; Lung ; Mice ; Mice, Inbred C57BL
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Grant Information:: CNRS-L/LAU No. 858 to A.A-G National Council for Scientific Research (CNRS-L) in Lebanon and the Lebanese American University; post-doctoral fellowship program (WN-E, KS, ZH, and SM); SRRC-R-2019-109 to A.A-G Lebanese American University (LAU), through the office of the Graduate Studies and Research office (GSR); 2/SPRG15 to C.K. Lebanese American University (LAU), through the office of the Graduate Studies and Research office (GSR)
Contributed Indexing:: Keywords: Th2 polarization; antioxidant enzymes; apoptosis; gasoline inhalation; inflammation
Substance Nomenclature:: 0 (Gasoline)
Entry Date(s):: Date Created: 20220110 Date Completed: 20220614 Latest Revision: 20220713
Update Code:: 20240105
DOI:: 10.1002/jat.4286
PMID:: 35001415
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Gasoline exposure has been widely reported in the literature as being toxic to human health. However, the exact underlying molecular mechanisms triggered by its inhalation have not been thoroughly investigated. We herein present a model of sub-chronic, static gasoline vapor inhalation in adult female C57BL/6 mice. Animals were exposed daily to either gasoline vapors (0.86 g/animal/90 min) or ambient air for 5 days/week over 7 consecutive weeks. At the end of the study period, toxic and molecular mechanisms underlying the inflammatory, oxidative, and apoptotic effects triggered by gasoline vapors, were examined in the lungs and liver of gasoline-exposed (GE) mice. Static gasoline exposure induced a significant increase (+21%) in lungs/body weight (BW) ratio in GE versus control (CON) mice along with a pulmonary inflammation attested by histological staining. The latter was consistent with increases in the transcript levels of proinflammatory cytokines [Interleukins (ILs) 4 and 6], respectively by ~ 6- and 4-fold in the lungs of GE mice compared to CON. Interestingly, IL-10 expression was also increased by ~ 10-fold in the lungs of GE mice suggesting an attempt to counterbalance the established inflammation. Moreover, the pulmonary expression of IL-12 and TNF-α was downregulated by 2- and 4-fold, respectively, suggesting the skewing toward Th2 phenotype. Additionally, GE mice showed a significant upregulation in Bax/Bcl-2 ratio, caspases 3, 8, and 9 with no change in JNK expression in the lungs, suggesting the activation of both intrinsic and extrinsic apoptotic pathways. Static gasoline exposure over seven consecutive weeks had a minor hepatic portal inflammation attested by H&E staining along with an increase in the hepatic expression of the mitochondrial complexes in GE mice. Therefore, tissue damage biomarkers highlight the health risks associated with vapor exposure and may present potential therapeutic targets for recovery from gasoline intoxication.
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