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Abstract As an alternate of bisphenol A (BPA), bisphenol S (BPS) is now widely used to produce our daily consumer goods. Some studies have shown that BPS has the potential to disrupt the reproduction and glucose homeostasis. However, the impact of BPS on the nervous system remains unclear. The purpose of this study is to investigate the impact of BPS on the nervous systems of zebrafish in their early growing stages. The 96 h-LC 50 value of BPS to zebrafish larvae was 323 mg/L (95%CI: 308–339 mg/L). Zebrafish embryos were exposed to BPS at concentrations of 0, 0.03, 0.3 and 3.0 mg/L until 6 days postfertilization. Our results showed that 0.3 and 3.0 mg/L BPS exposure markedly decreased locomotor behavior, accompany by the increased oxidative stress, promoted apoptosis and altered retinal structure in zebrafish. In addition, the expression levels of six neurodevelopment genes (α1-tubuli n, elavl3 , gap43 , mbp , syn2a and gfap) were downregulated after 3.0 mg/L BPS treatment. In conclusion, BPS may affect locomotor behavior and alter retinal structure in zebrafish larvae partially by increasing oxidative stress, and by suppressing the expression levels of neurodevelopment genes. Graphical abstract Image Highlights • The developmental neurotoxicity of bisphenol S in zebrafish. • Bisphenol S exposure markedly decreased locomotor behavior. • Bisphenol S exposure promoted apoptosis and altered retinal structure in zebrafish. • Bisphenol S exposure downregulate the expression levels of neurodevelopment genes. [ABSTRACT FROM AUTHOR]

Synthetic organic insecticides, including pyrethroids, organophosphates, neonicotinoids and other types, have the potential to alter the ecosystems and many are harmful to humans. This study examines the developmental toxicity and neurotoxicity of three synthetic organic insecticides, including deltamethrin (DM), acephate (AP), and thiamethoxam (TM), using embryo-larval stages of zebrafish ( Danio rerio ). Results showed that DM exposure led to embryo development delay and a significant increase in embryo mortality at 24 and 48 h post-fertilization (hpf). DM and AP decreased embryo chorion surface tension at 24 hpf, along with the increase in hatching rate at 72 hpf. Moreover, DM caused ntl , shh, and krox20 misexpression in a dose-dependent manner with morphological deformities of shorter body length, smaller eyes, and larger head-body angles at 10 μg/L. TM did not show significant developmental toxicity. Furthermore, results of larval rest/wake assay indicated that DM (>0.1 μg/L) and AP (0.1 mg/L) increased activity behavior with different patterns. Interestingly, as an insect-specific pesticide, TM still could alter locomotor activity in zebrafish larvae at concentrations as low as 0.1 mg/L. Our results indicate that different types of synthetic organic insecticides could create different toxicity outcomes in zebrafish embryos and larvae. [ABSTRACT FROM AUTHOR]

The fungicide imazalil (IMZ) is used extensively to protect vegetable fields, fruit plantations and post-harvest crops from rot. Likely due to its wide-spread use, IMZ is frequently detected in vegetable, fruit, soil and even surface water samples. Even though several previous studies have reported on the neurotoxicity of IMZ, its effects on the neurobehavior of zebrafish have received little attention to date. In this study, we show that the heartbeat and hatchability of zebrafish were significantly influenced by IMZ concentrations of 300 μg L −1 or higher. Moreover, in zebrafish larvae, locomotor behaviors such as average swimming speed and swimming distance were significantly decreased after exposure to 300 μg L −1 IMZ for 96 h, and acetylcholinesterase (AChE) expression and activity were consistently inhibited in IMZ-treated fish. Our results further suggest that IMZ could act as a neuroendocrine disruptor by decreasing the expression of neurotoxicity-related genes such as Glial fibrillary acidic protein (Gfap) , Myelin basic protein (Mbp) and Sonic hedgehog a (Shha) during early developmental stages of zebrafish. In conclusion, we show that exposure to IMZ has the potential to induce developmental toxicity and locomotor behavior abnormalities during zebrafish development. [ABSTRACT FROM AUTHOR]

The widespread use of triclosan in personal care products as an antimicrobial agent is leading to its alarming tissue-bioaccumulation including human brain. However, knowledge of its potential effects on the vertebrate nervous system is still limited. Here, we hypothesized that sublethal triclosan concentrations are potent enough to alter motor neuron structure and function in zebrafish embryos exposed for prolonged duration. In this study, zebrafish embryos were used as vertebrate-animal model. Prolonged exposure (up to 4 days) of 0.6 mg/L (LC 50, 96 h) and 0.3 mg/L (

As a new protective and therapeutic fungicide, studies on famoxadone-cymoxanil are rare, and its toxicity to aquatic organisms has not been reported. In the present study, zabrafish embryos were exposed to several concentrations of famoxadone-cymoxanil at 10 hpf. Then, the changes of their shape, heart rate, development and function of innate and adaptive immune cells, oxidative stress, apoptosis, the expression of apoptosis-related genes and immune-related genes, the locomotor behavior were observed and detected in acute toxicity of famoxadone-cymoxanil. Our studies showed that, after exposure to famoxadone-cymoxanil, zebrafish embryos had decreased heart rate, shortened body length, swollen yolk sac. Secondly, the number of innate and adaptive immune cells was significantly reduced; and neutrophil migration and retention at the injury area were inhibited, indicating the developmental toxicity and immunotoxicity of famoxadone-cymoxanil on the zebrafish. We also found that the oxidative stress related indicators of embryos were changed significantly, and apoptosis were substantially increased. Further investigation of changes of some key genes in TLR signaling including TLR4 , MYD88 and NF-κB p65 revealed that the mRNA expression of these genes was up-regulated. Meanwhile, the mRNA expression of some proinflammatory cytokines such as TNF-α , IFN-γ , IL6 and IL-1β was also up-regulated. In addition, the activity, the total distance, time and average speed were decreased along with the increase of exposure concentration. The absolute turn angle, sinuosity and the enzymatic activity of acetylcholinesterase (AChE) were also increased. These results suggested that famoxadone-cymoxanil can induce developmental toxicity, immunotoxicity and neurobehavioral toxicity in zebrafish larvae. • Famoxadone-cymoxanil led to developmental toxicity and immunotoxicity of zebrafish embryos. • Famoxadone-cymoxanil induced oxidative stress and apoptosis of immune cells in zebrafish embryos. • TLR4 signaling pathway was involved in famoxadone-cymoxanil induced immunotoxicity in zebrafish embryos. • Famoxadone-cymoxanil caused neurobehavioral toxicity in zebrafish larvae. [ABSTRACT FROM AUTHOR]

Esfenvalerate is a pyrethroid insecticide used widely for agricultural and residential applications. This insecticide has been detected in aquatic environments at concentrations that can induce sub-lethal effects in organisms. In this study, zebrafish embryos were used to examine the effects of environmentally-relevant concentrations of esfenvalerate on development and behavior. It was hypothesized that esfenvalerate exposure would impair locomotion due to its effects on the central nervous system. We also measured mitochondrial bioenergetics and the expression of genes (dopamine system) as putative mechanisms of locomotor impairment. Concentrations of 0.02, 0.2 and 2 μg/L esfenvalerate did not induce significant mortality nor deformity in zebrafish, but there was an acceleration in hatching time for zebrafish exposed to 2 μg/L esfenvalerate. As an indicator of neurotoxicity, the Visual Motor Response (VMR) test was conducted with 5, 6, and 7 dpf zebrafish after continuous exposure, and higher concentrations were used (4 and 8 μg/L esfenvalerate) to better discern age-and dose dependent responses in behavior. Experiments revealed that, unlike the other stages, 6 dpf larvae showed evidence for hypo-activity with esfenvalerate, suggesting that different stages of larval development may show increased sensitivity to pyrethroid exposure. This may be related to age-dependent maturation of the central nervous system. We hypothesized that reduced larval activity may be associated with impaired production of ATP and the function of mitochondria at earlier life stages, however dramatic alterations in oxidative phosphorylation were not observed. Based on evidence that dopamine regulates behavior and studies showing that other pyrethroids affect dopamine system, we measured transcripts involved in dopaminergic signaling. We found that dopamine active transporter was down-regulated with 0.2 μg/L esfenvalerate. Lastly, we comprehensively summarize the current literature (>20 studies) regarding the toxicity of pyrethroids in zebrafish, which is a valuable resource to those studying these pesticides. This study demonstrates that esfenvalerate at environmentally-relevant levels induces hypoactivity that are dependent upon the age of the zebrafish, and these behavioral changes are hypothesized to be related to impaired dopamine signaling. • Esfenvalerate is a pyrethroid insecticide that affects zebrafish behaviors and is neurotoxic. • Dopamine active transporter mRNA was decreased by environmentally-relevant levels of esfenvalerate. • Esfenvalerate at environmentally-relevant levels induced hypoactivity, effects that were dependent upon age. • A comprehensive table summarizes data on pyrethroids in zebrafish as a resource for future experiments. [ABSTRACT FROM AUTHOR]