Teratogenicity of Methyl Ethyl Ketone (2-Butanone) on the Development of Albino Rat Newborns

Document Type : Original Article

Author

Department of Biology, College of Science, Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia

Abstract

Several experimental studies reported the cellular toxicity of methyl ethyl ketone (MEK) in all organelles and increase in the rate of mortality at higher doses with long times. Thus, in this study, we have evaluated the effect of perinatal exposure to methyl ethyl ketone (MEK) on the histological, biochemical, and behavioral development of newborn mice. Experimental animals were divided into 2 groups, pregnant mice given 1 ml bottled drinking water daily by oral intubation and served as control and pregnant mice supplemented orally with 350 mg/kg body weight methyl ethyl ketone (MEK) dissolved in drinking water. The first-generation pups were examined during the lactation period. MEK induced a decrease in the postnatal body weights of newborn mice. Additionally, brain changes were seen in the pups of MEK-treated mice. A disturbance in the antioxidant defense system in the brain, liver, and kidney of newborn mice was evidenced by of the declined glutathione (GSH), and increased levels of peroxidase, superoxide dismutase (SOD), and lipid peroxidation. In addition, newborns of the MEK-supplemented mice exhibited significant expression of cellular apoptosis and fibrosis, liver and kidney in tissues which are significantly associated with cellar free radical initiation mechanisms. MEK at a dose of 350 mg/kg has teratogenicity, cytotoxicity, and deleterious effects on the development of newborn mice. Its cytotoxic logical effects proceeded via oxidative free radical, apoptotic, and fibrotic mechanisms.

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