Acrylamide is a commonly used industrial chemical that is known to be neurotoxic to mammals. However, its developmental toxicity is rarely assessed in mammalian models because of the cost and complexity involved. We used zebrafish to assess the neurotoxicity, developmental and behavioral toxicity of acrylamide. At 6 h post fertilization, zebrafish embryos were exposed to four concentrations of acrylamide (10, 30, 100, or 300 mg/L) in a medium for 114 h. Acrylamide caused developmental toxicity characterized by yolk retention, scoliosis, swim bladder deficiency, and curvature of the body. Acrylamide also impaired locomotor activity, which was measured as swimming speed and distance traveled. In addition, treatment with 100 mg/L acrylamide shortened the width of the brain and spinal cord, indicating neuronal toxicity. In summary, acrylamide induces developmental toxicity and neurotoxicity in zebrafish. This can be used to study acrylamide neurotoxicity in a rapid and cost-efficient manner.

Veterinary pharmaceuticals may cause unexpected adverse effects on non-target aquatic species. While these pharmaceuticals were previously identified as priority compounds in ambient water, their ecological risks are relatively unknown. In this study, a series of chronic toxicity tests were conducted for these pharmaceuticals using algae, two cladocerans, and a fish. After a 21-d exposure to amoxicillin, enrofloxacin, and neomycin, no observed effect concentration (NOEC) for the reproduction of Daphnia magna was detected at 27.2, 3.3, and 0.15 mg/L, respectively. For the survival of juvenile Oryzias latipes following the 40-d exposure, NOEC was found at 21.8, 3.2, and 0.87 mg/L, respectively. Based on the results of the chronic toxicity tests and those reported in the literature, predicted no-effect concentrations (PNECs) were determined at 0.078, 4.9, and 3.0 µg/L for amoxicillin, enrofloxacin, and neomycin, respectively. Their hazard quotients (HQs) were less than 1 at their average levels of occurrence in ambient freshwater. However, HQs based on the maximum detected levels of amoxicillin and enrofloxacin were determined at 21.2 and 6.1, respectively, suggesting potential ecological risks. As the potential ecological risks of these veterinary pharmaceuticals at heavily contaminated sites cannot be ignored, hotspot delineation and its management are required.

Bifenthrin, a third-generation synthetic pyrethroid, is widely used as an agricultural insecticide. However, it can flow into surface and groundwater, leading to adverse consequences such as immunotoxicity, hepatotoxicity, hormone dysregulation, or neurotoxicity. Nevertheless, the entire range of its neurotoxic consequences, particularly in aquatic organisms, remains unclear. In this study, we conducted an extensive examination of how exposure to bifenthrin affects the behavior and nervous system function of aquatic vertebrates, using a zebrafish model and multiple-layered assays. We exposed wild-type and transgenic lines [tg(elavl3:eGFP) and tg(mbp:mGFP)] to bifenthrin from <3 h post-fertilization (hpf) to 120 hpf. Our findings indicate that bifenthrin exposure concentrations of 103.9 and 362.1 μg/L significantly affects the tail-coiling response at 24 hpf and the touch-evoked responses at 72 hpf. Moreover, it has a significant effect on various aspects of behavior such as body contact, distance between subjects, distance moved, and turn angle. We attribute these effects to changes in acetylcholinesterase and dopamine levels, which decrease in a concentration-dependent manner. Furthermore, neuroimaging revealed neurogenesis defects, e.g., shortened brain and axon widths, and demyelination of oligodendrocytes and Schwann cells. Additionally, the transcription of genes related to neurodevelopment (e.g., gap43, manf, gfap, nestin, sox2) were significantly upregulated and neurotransmitters (e.g., nlgn1, drd1, slc6a4a, ache) was significantly downregulated. In summary, our data shows that bifenthrin exposure has detrimental effects on neurodevelopmental and neurotransmission systems in the zebrafish embryo/larvae model.

Parabens can potentially disrupt the hormonal regulation of energy metabolism, leading to issues related to obesity, metabolic health, and the cardiovascular and nervous systems. However, the health effects of parabens have yielded conflicting research results. The impact of these substances on aquatic organisms, specifically their neuro- and cardio-toxic effects, has been insufficiently investigated. Hence, the primary goal of our research was to investigate and comprehensively assess the neuro- and cardio-toxic effects of four distinct parabens using the Daphnia magna model. After 48 h of exposure to various concentrations (0.1, 1, and 10 mg/L) of four parabens (methyl-, ethyl-, propyl-, and butyl-paraben), along with a solvent control, we conducted a series of physiological tests, behavioral observations, and gene transcription analyses, focusing on cardiomyopathy, serotonin, glutamate, dopamine, GABA, acetylcholine receptors, and ion flux. From a physiological perspective, the heart rate and thoracic limb activity of the exposed daphnids showed substantial time- and dose-dependent inhibitions. Notably, among the parabens tested, butylparaben exhibited the most potent inhibition, with significant alterations in cardiomyopathy-related gene transcription. In the context of neurotoxicity, all the parabens had a significant impact on gene expression, with methylparaben having the most pronounced effect. Additionally, significant changes were observed in parameters such as distance moved, the distance between individuals, and the extent of body contact among the daphnids. In summary, our findings indicate that each paraben has the capacity to induce neurobehavioral and cardiotoxic disorders in Daphnia magna. The effects of butylparaben on the cardiovascular and nervous systems were found to be the most pronounced. These discoveries showed the potential ecological implications of paraben exposure in aquatic ecosystems, particularly regarding the predator avoidance abilities of Daphnia magna.

The genotoxicity, development toxicity, carcinogenicity, and acute or chronic toxic effects of glutaraldehyde (GA), particularly during occupational exposure through its use as a fixative, disinfectant, and preservative, are well-documented but its effects on neurotoxicity have not been investigated. We performed in vitro and in vivo studies to examine the developmental neurotoxicity (DNT) of GA. Neurite outgrowth was examined in an in vitro co-culture model consisting of SH-SY5Y human neuroblastoma cells and human astrocytes. Cell Counting Kit-8, lactate dehydrogenase assay, and high-content screening revealed that GA significantly inhibited neurite outgrowth at non-cytotoxic concentration. Further studies showed that GA upregulated the mRNA expression of the astrocyte markers GFAP and S100β and downregulated the expression of the neurodevelopmental genes Nestin, βIII-tubulin, GAP43, and MAP2. Furthermore, in vivo zebrafish embryo toxicity tests explored the effects of GA on neural morphogenesis. GA adversely affected the early development of zebrafish embryos, resulting in decreased survival, irregular hatching, and reduced heart rate in a time- and concentration-dependent manner. Furthermore, the width of the brain and spinal cord was reduced, and the myelination of Schwann cells and oligodendrocytes was decreased by GA in transgenic zebrafish lines. These data suggest that GAs have potential DNT in vitro and in vivo, highlighting the need for caution regarding the neurotoxicity of GA.

Acrylamide has neurotoxic and/or cardiotoxic effects on humans however available information regarding the neuro- and cardiotoxicity currently is very limited for freshwater organism models. Using three distinct techniques, thus, we investigated the neuro- and cardiotoxic effects of acrylamide in the freshwater invertebrate model, Daphnia magna. We exposed D. magna to acrylamide at concentrations of 0.3, 2.7, and 11.1 mg/L for 48 h alongside a control group. We then conducted physiological (thoracic limb activity and heart rate) and behavioral tests (including distance moved, velocity, turn angle, moving duration, the distance between subjects, and body contact frequency), as well as gene transcription analyses (related to cardiomyopathy, the serotonergic synapse, neuroactive ligand-receptor interactions, the GABAergic synapse, and acetylcholine receptors). After acrylamide exposure, the thoracic limb activity and heart rates of D. magna showed time- and dose dependent inhibition. From low to high exposure concentrations, both heart rates and thoracic limb activity were decreased. Additionally, the distance between subjects and body contact frequencies was significantly reduced. At the gene transcription level, acrylamide significantly altered the transcription of five genes related to cardiomyopathy and eight genes related to the serotonergic synapse, neuroactive ligand-receptor interactions, and the GABAergic synapse. The signs of hindered neural and cardiac functions were shown in D. magna. This suggests that acrylamide exposure leads to cardiotoxicity and neurobehavior defects in D. magna. Because cardiotoxicity and neurobehavioral changes may cause an ecological imbalance via predation of D. magna, acrylamide may also be considered a threat to freshwater ecosystem.