Oxidative Stress and DNA Damage Induced by 1-butyl-3-methylimidazolium Hydroxide ([Bmim]OH) Ionic Liquid in Mouse Liver

Abstract

Ionic liquids (ILs), particularly imidazolium-based compounds, are increasingly used in industrial and technological processes because of their distinctive physicochemical properties. However, concerns remain regarding their possible toxicological effects in biological systems. The present study investigated the acute hepatotoxic and genotoxic effects of 1-butyl-3-methylimidazolium hydroxide ([Bmim]OH) in female albino mice (Mus musculus). Acute toxicity testing was performed to determine the median lethal dose (LD50) of [Bmim]OH, and the calculated LD50 value of 18,197 mg/kg body weight was administered orally to experimental mice. Animals were divided into control and treatment groups, and liver tissues were collected after 12 and 24 h of exposure. Hepatic oxidative stress was assessed by measuring the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), while genotoxicity was evaluated using hepatic DNA damage analysis. The results showed that SOD activity increased slightly after 12 h and significantly after 24 h of exposure (75.30 ± 2.82 U/mg protein; p < 0.001) compared with the control group (66.98 ± 2.43 U/mg protein). In contrast, CAT activity decreased significantly after 24 h (17.69 ± 1.54 U/mg protein; p < 0.001), and GPx activity also declined significantly after 24 h (64.46 ± 2.31 U/mg protein; p < 0.001). No significant changes were observed after the shorter exposure period. The comet assay showed no significant DNA damage after 12 h of exposure, whereas the Olive tail moment increased significantly after 24 h (0.8050 ± 0.052; p < 0.05). These findings indicate that acute oral exposure to [Bmim]OH at its LD50 dose disturbed hepatic antioxidant enzyme activity and induced time-dependent DNA damage in mouse liver tissue.