Oxidative stress-mediated induction of pulmonary oncogenes, inflammatory, and apoptotic markers following time-course exposure to ethylene glycol monomethyl ether in rats.

Autor:	Somade OT; Department of Biochemistry, College of Biosciences, Federal University of Agriculture, Abeokuta, Nigeria., Ajayi BO; Department of Chemical Sciences, Faculty of Natural Sciences, Ajayi Crowther University, Oyo, Nigeria., Adeyi OE; Department of Biochemistry, College of Biosciences, Federal University of Agriculture, Abeokuta, Nigeria., Adeshina AA; School of Medicine, All Saints University, Roseau, Dominica., Adekoya MO; Department of Biochemistry, College of Biosciences, Federal University of Agriculture, Abeokuta, Nigeria., Abdulhameed RO; Department of Biochemistry, College of Biosciences, Federal University of Agriculture, Abeokuta, Nigeria.
Jazyk:	angličtina
Zdroj:	Metabolism open [Metabol Open] 2020 Dec 15; Vol. 9, pp. 100075. Date of Electronic Publication: 2020 Dec 15 (Print Publication: 2021).
DOI:	10.1016/j.metop.2020.100075
Abstrakt:	Ethylene glycol monomethyl ether (EGME) has been used in many products usually handled by humans including inks, paints, polishes, brake fluids and so on. This present study therefore, investigated its effect on lung, in a time-course study in male Wistar rats. Animals were orally administered 50 mg/kg body weight of EGME for a period of 7, 14, and 21 days. Following 7 days of oral exposure to EGME, activities of GPx and SOD were significantly increased, as well as levels of K-Ras, c-Myc, p53, caspase-3, TNF-α and, IL-6, while NO level and GST activity were significantly reduced compared with control. At the end of 14 days exposure, GSH level was significantly decreased, while levels of K-Ras, c-Myc, p53, caspase-3, TNF-α, IL-6, NO and the activities of SOD and GPx were significantly elevated with respect to control. After 21 days of EGME administration, levels of Bcl-2, IL-10, GSH and NO as well as GST activity were significantly decreased, while levels of K-Ras, c-Myc, p53, Bax, caspase-3, IL-6, IL-1β, TNF-α, as well as GPx, CAT, and SOD activities were significantly elevated compared with control. Lung histopathology revealed chronic disseminated alveolar inflammation, bronchiolitis, severe alveolar and bronchi hyperplasia, severe disseminated inflammation, thrombosis, and thickened vessels as a result of EGME exposures. Exposures to EGME could trigger lung damage via the disorganization of the antioxidant system, eliciting the up-regulation of inflammatory, apoptotic, and oncogenic markers in rats. Competing Interests: None to declare. (© 2020 Published by Elsevier Inc.)
Databáze:	MEDLINE
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