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Amitriptyline (AMI), the most commonly prescribed tricyclic antidepressant, is widely detected in water environments. Exposure to AMI may lead to diverse adverse effects on aquatic organisms, but little is known about the effect of short-term exposure to AMI on the gut microbiota of aquatic organisms and their recovery characteristics. In the present study, adult zebrafish (Danio rerio) were exposed to AMI (0, 2.5, 10, and 40 μg/L) for seven days, and then allowed to recover in AMI-free culture water for 21 days. The exposure caused gut damages in all the AMI treated groups of zebrafish, which became more severe after recovery compared to the control group. AMI exposure also disturbed the microbiota of zebrafish guts and rearing water even after the 21-day recovery period. Furthermore, AMI exposure affected microbes involved in the substance and energy metabolic functions in zebrafish guts and tended to increase the abundance of microbial genera associated with opportunistic pathogens. In addition, the microbial predicted metabolic functions in AMI-exposed guts of zebrafish were significantly altered after the 21-day recovery period, explaining the persistent effects of short-term exposure to AMI. The results of this study suggest that acute exposure to AMI may have persistent impacts on the gut histomorphology and the gut microbiota in aquatic organisms. [Display omitted] • AMI exposure caused gut damages in zebrafish and became more severe after recovery. • AMI exposure disturbed the bacterial communities of zebrafish guts and water. • Persistent impacts of AMI caused dysbiosis in zebrafish gut microbiota. • AMI exposure disordered the metabolic functions of gut microbiota after recovery. [ABSTRACT FROM AUTHOR]

Diazepam (DZP) residue has been frequently detected in wastewater, surface water, and groundwater due to its extensive use over the decades. In this study, we exposed female Japanese medaka (Oryzias latipes) to environmentally relevant doses of DZP (800 and 8000 ng/L) for 4 weeks, aimed to investigate their behavioral responses and possible links with ocular and brain oxidative stress homeostasis. As a result, DZP exposure could significantly reduce swimming activity (800 ng/L) and anxiety (800 and 8000 ng/L), indicating a sedative effect on medaka. The DZP exposure also significantly increased the social interaction in medaka at 8000 ng/L. Furthermore, exposure to DZP could alter the ocular and brain oxidative stress homeostasis in medaka. The ocular CAT activities significantly increased in the 800 ng/L-DZP groups, and the brain SOD, CAT, GST and MDA levels also significantly increased in both DZP exposure groups. Correlation analysis revealed that the ocular and brain oxidative stress induced by DZP exposure might play an important role in their behavioral toxicity to medaka. Our findings highlight the necessity to clarify the exact link between DZP exposure-induced oxidative stress in the neural and sensor systems and its behavioral toxicity to better assess the risks on nontarget aquatic species. [Display omitted] • Diazepam (DZP) significantly reduced swimming activity in medaka at 800 ng/L. • DZP exposure significantly reduced anxiety in medaka at 800 and 8000 ng/L. • DZP exposure significantly increased social interaction in medaka at 8000 ng/L. • DZP altered the ocular and brain oxidative stress homeostasis in medaka. • Ocular and brain oxidative stress was associated with behavioral toxicity of DZP. [ABSTRACT FROM AUTHOR]

Cetylpyridinium chloride (CPC) is a cationic surfactant that has been widely used as an antibacterial ingredient in pharmaceutical and personal care products. Due to its high residue in surface waters, there is increasing concern over the potential risk of CPC to aquatic ecosystems. However, knowledge of its impacts on fish is still limited. Therefore, this study exposed juvenile and adult zebrafish to CPC (0, 10, and 40 μg/L) for four days. Subsequently, changes in their behavioral traits and brain levels of several neurotransmitters were investigated. The behavioral assay showed that CPC exposure significantly decreased the locomotor activity and social interaction of zebrafish at both life stages, and juveniles were more sensitive to CPC exposure than adults. In the control groups, the brain neurotransmitters concentrations increased with age in zebrafish. However, CPC exposure tended to increase the brain neurotransmitter levels of juveniles but decreased their levels in adults. Correlation analysis revealed that the brain monoamine neurotransmitters and their turnover might play important roles in the life stage-dependent behavioral response to CPC. In particular, the DOPAC/DA ratio was significantly associated with CPC-induced hypoactivity and reduced social interactions in juveniles but not adults. Our findings demonstrated that CPC exposure could cause abnormal behavior in juvenile and adult zebrafish and disturb their brain neurotransmitters, even at environmentally relevant concentrations, and thus highlighted the necessity for further assessing its potential risks to aquatic ecosystems. [Display omitted] • CPC reduced locomotor activity and social behavior of juvenile and adult zebrafish. • Juveniles are more sensitive to CPC than adults in terms of behavioral responses. • Adults show higher brain neurotransmitters levels than juveniles in control groups. • CPC increased the neurotransmitter levels in juveniles but decreased them in adults. • DOPAC/DA ratio was associated with behaviors of juveniles but not those of adults. [ABSTRACT FROM AUTHOR]