Emamectin benzoate (EMB) is a widely used pesticide and feed additive in agriculture and aquaculture. It easily enters the aquatic environment through various pathways, thus causing adverse effects on aquatic organisms. However, there are no systematic studies regarding the effects of EMB on the developmental neurotoxicity of aquatic organisms. Therefore, the aim of this study was to evaluate the neurotoxic effects and mechanisms of EMB at different concentrations (0.1, 0.25, 0.5, 1, 2, 4 and 8 μg/mL) using zebrafish as a model. The results showed that EMB significantly inhibited the hatching rate, spontaneous movement, body length, and swim bladder development of zebrafish embryos, as well as significantly increased the malformation rate of zebrafish larvae. In addition, EMB adversely affected the axon length of motor neurons in Tg (hb9: eGFP) zebrafish and central nervous system (CNS) neurons in Tg (HuC: eGFP) zebrafish and significantly inhibited the locomotor behavior of zebrafish larvae. Meanwhile, EMB induced oxidative damage and was accompanied by increasing reactive oxygen species in the brains of zebrafish larvae. In addition, gene expression involvement in oxidative stress-related (cat, sod and Cu/Zn-sod), GABA neural pathway-related (gat1, gabra1, gad1b, abat and glsa), neurodevelopmental-related (syn2a, gfap, elavl3, shha, gap43 and Nrd) and swim bladder development-related (foxa3, pbxla, mnx1, has2 and elovlla) genes was significantly affected by EMB exposure. In conclusion, our study shows that exposure to EMB during the early life stages of zebrafish significantly increases oxidative damage and inhibits early central neuronal development, motor neuron axon growth and swim bladder development, ultimately leading to neurobehavioral changes in juvenile zebrafish.

Bisphenol analogues (BPs) have already attracted wide concern owing to the environmental and health risks they pose. The exposure pathways and health risk of preschool-aged children to BPs, however, are still poorly understood. In this study, we choose population survey with 184 preschool-age children from a suburb of Nanjing, eastern China, further reveal the internal and external exposures concentrations, distribution profiles, potential sources and eventually assess health risk of preschool-age children to eight kinds of BPs. The results verify that the 95th percentile (P95) concentrations of Ʃ₈BPs ranged from 0.27 to 41.6 ng/mL, with a median concentration of 7.83 ng/mL in the urine samples. BPA, and BPF were the predominant BPs in urine, accounting for 67.3%, and 18.0% of Ʃ₈BPs. The urine-based estimated daily intake (EDI) of Ʃ₈BPs was 187 ng/kg body weight/day. Similarly, BPA, and BPF were the main BPs in the environmental exposure sources, accounting for 80.8%, and 11.7% of the total BPs. Moreover, the total external exposure dose of Ʃ₈BPs via the environmental sources was 68.1 ng/kg body weight/day, including BPA (56 ng/kg body weight/day), BPF (7.68 ng/kg body weight/day) and BPB (2.62 ng/kg body weight/day). The oral intake of drinking water and food (vegetables and rice) was the main exposure pathways of BPs in preschool-age children. Furthermore, the hazard quotient (HQ) of BPs have been evaluated and the results show no occurrence of high risk. Additionally, the urine-based EDI was significantly higher than the total external exposure dose, suggesting the existence of other pathways of BP exposure to be further explored. To the best of our knowledge, this is the first study to conduct both an internal and external exposure assessment of BPs.

Lignin-carbohydrate complexes (LCCs) from different lignocellulosic biomass have shown biological qualities as antioxidant and immunostimulant. By contrast, the application of LCCs as protectant against neurotoxicity caused by different compounds is scarce. In this work, two kinds of LCCs with carbohydrate-rich and lignin-rich fractions were obtained from wheat stalk and used to protect against BPA-neurotoxicity in zebrafish. The results showed that BPA at a concentration of 500 µg/L results in neurotoxicity, including significant behavioral inhibition, and prevents the expression of central nervous system proteins in transgenic zebrafish models (Tg (HuC-GFP)). When the zebrafish was treated by LCCs, the reactive oxygen species of zebrafish decreased significantly with the change of antioxidant enzymes and lipid peroxidation, which was due to the LCCs’ ability to suppress the mRNA expression level of key genes related to nerves. This is essential in view of the neurotoxicity of BPA through oxidative stress. In addition, BPA exposure had negative effects on the exercise behavior, the catalase (CAT) and superoxide dismutase (SOD) activity, and the larval development and gene expression of zebrafish larvae, and LCC preparations could recover these negative effects by reducing oxidative stress. In zebrafish treated with BPA, carbohydrate-rich LCCs showed stronger antioxidant activity than lignin-rich LCCs, showing their potential as a neuroprotective agents.