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Propofol, one of the most widely used intravenous anesthetic in clinical practice, has been reported to impair cognitive and memory function. However, the toxicological effects of propofol on aquatic organisms are still poorly understood. This study explored the toxic effects of chronic propofol exposure (0.008, 0.04, and 0.2 mg L−1) on adult zebrafish from biochemical, transcriptional, and molecular level after 7, 14, 21 and 28 days of exposure. Results indicated that the reactive oxygen species (ROS) levels were significantly upregulated during the 28 days exposure period, and excessive ROS caused lipid peroxidation, resulting in increased malondialdehyde (MDA) contents in the zebrafish brain. In order to relieve the oxidative damage induced by the excessive ROS, the activities of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT)) were significantly activated, and detoxification enzyme (glutathione S-transferase, GST) activities showed an "activation-inhibition" trend. However, the antioxidant enzymes and detoxification enzyme system could not eliminate the excessive ROS in time and thus caused DNA damage in zebrafish brain. The olive tail moment (OTM) values displayed a "dose-response" relationship with propofol concentrations. Meanwhile, the transcription of related genes of Nrf2-Keap1 pathway was activated. Further molecular simulation experiments suggested that propofol could directly combine with SOD/CAT to change the activity of its biological enzyme. These findings indicated that zebrafish could regulate antioxidant capacity to combat oxidative stress at the early exposure stage, but the activity of antioxidant enzymes were significantly inhibited with the increase of propofol exposure time. Our results are of great importance for understanding toxicological effects of propofol on aquatic organisms. [Display omitted] • The activity of antioxidant enzymes in zebrafish brain was significantly inhibited. • Propofol triggered dose-dependent DNA damage and increased 8-OHdG content. • Nrf2/Keap1 signaling pathway was involved in the defense against oxidative damage. • Propofol preferentially interacted with SOD active center. • The environmental risks of propofol should be valued. [ABSTRACT FROM AUTHOR]

As an emerging environmental contaminant, di (2-ethylhexyl) phthalate (DEHP) is widely present in the aquatic environment, however, the effects and underlying mechanisms of DEHP on the aquatic organisms are poorly understood. This study systematically investigated the ecotoxicity induced by chronic exposure to environmental relevant concentrations of DEHP (0.03 mg/L, 0.1 mg/L, and 0.3 mg/L) on zebrafish brain. Results indicated that DEHP exposure significantly increased the levels of ROS and disturbance of the antioxidant enzymes activities in the brain, which may further enhance lipid peroxidation and DNA damage. Furthermore, acetylcholinesterase activity was first stimulated and inhibited by exposure to DEHP, and the antioxidant and apoptosis related genes were mainly upregulated. Risk assessment indicated that the ecotoxicity of DEHP on the zebrafish showed an "enhancement-reduction" trend as the exposure time was prolonged. Overall, these results provided new insights and useful information to ecological risk assessment and environmental management of DEHP pollution. • DEHP elevated the ROS levels and disturbed antioxidant homeostasis in zebrafish brain. • DEHP induced lipid peroxidation and DNA damage in brain of zebrafish. • DEHP caused hazardous effects on brain at the neural and genetic levels. • The ecotoxicological risk of DEHP to zebrafish brain first increased and then decreased with the increase of exposure time. [ABSTRACT FROM AUTHOR]

• DEHP presented low acute toxicity to adult zebrafish (Danio rerio) • DEHP induced oxidative stress, lipid peroxidation and DNA damage in zebrafish hepatic tissue. • Acetylcholinesterase (AChE) activity of zebrafish liver was significantly inhibited after DEHP exposure. • The ecotoxicological risk of adult zebrafish increased with increasing DEHP concentrations. Di-(2-ethylhexyl) phthalate (DEHP) has become a ubiquitous contaminant in aquatic environments due to its increasing utilization in recent years. Although its environmental risks to aquatic organisms have attracted widespread attention, the ecotoxicological effects and toxic mechanism of DEHP on zebrafish (Danio rerio) liver remain poorly understood. Herein, this study investigated the acute toxicity, oxidative damage, neurotoxicity, and DNA damage of DEHP on zebrafish at the individual, tissue, physiological and biochemical levels. Results showed that no evident lethal effects of DEHP on zebrafish were observed in all testing concentrations. But in the chronic toxicity test (28 days), superoxide dismutase (SOD) and catalase (CAT) activities in zebrafish liver mainly increased during the pre-and mid-exposure experiment and subsequently decreased after 28 days exposure, whereas the acetylcholinesterase (AChE) activities were always inhibited. By comparison, reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione S-transferase (GST) levels generally increased throughout the experiment, indicating that DEHP enhanced oxidative stress lipid peroxidation, and cytotoxicity of zebrafish liver. DEHP induced DNA damage in hepatocyte, which was positively correlated with changes in ROS levels (0.9874 ≥ R2 ≥ 0.7374). Based on the risk assessment results, the integrated biomarker response (IBR) values were positively correlated with the DHEP concentrations, suggesting that higher DHEP concentrations may cause much more serious detrimental effects to zebrafish liver. Overall, this study is of great significance for understanding the ecotoxicity and mechanism of DEHP on zebrafish. [ABSTRACT FROM AUTHOR]