Difenoconazole is a type of triazole fungicide that is widely used in the treatment of plant diseases. Triazole fungicides have been shown in several studies to impair the development of the nervous system in zebrafish embryos. There is still little known about difenoconazole-induced neurotoxicity in fish. In this study, zebrafish embryos were exposed to 0.25, 0.5, and 1 mg/L of difenoconazole solution until 120 h post-fertilization (hpf). The difenoconazole-exposed groups showed concentration-dependent inhibitory tendencies in heart rate and body length. Malformation rate and spontaneous movement of zebrafish embryos increased, and the locomotor activity decreased in the highest exposure group. The content of dopamine and acetylcholine was reduced significantly in difenoconazole treatment groups. The activity of acetylcholinesterase (AChE) was also increased after treatment with difenoconazole. Furthermore, the expression of genes involved in neurodevelopment was remarkably altered, which corresponded with the alterations of neurotransmitter content and AChE activity. These results indicated that difenoconazole might affect the development of the nervous system through influencing neurotransmitter levels, enzyme activity, and the expression of neural-related genes, ultimately leading to abnormal locomotor activity in the early stages of zebrafish.

During early vertebrate development, various small non-coding RNAs (sRNAs) such as MicroRNAs (miRNAs) and Piwi-interacting RNAs (piRNAs) are dynamically expressed for orchestrating the maternal-to-zygotic transition (MZT). Systematic analysis of expression profiles of zebrafish small RNAome will be greatly helpful for understanding the sRNA regulation during embryonic development.

Bacterioplankton communities are closely related to river alterations and biogeochemical processes in freshwater reservoirs. Affected by reservoir regulation and hydrological variation, regulated rivers can create distinctive patterns in bacterioplankton communities. In this study, we conducted 16S rRNA V4 amplicon high-throughput sequencing to investigate compositional changes in the bacterioplankton community and its environmental responses to damming effects in the Pengxi River, the largest tributary on the northern bank of the Three Gorges Reservoir (TGR). The bacterial community was dominated by the phyla Proteobacteria and Actinobacteria, accounting for 51.0% and 13.1% of all sequences, respectively. Distinct differences in the bacterioplankton community composition were observed between the backwater and riverine areas, and the dominant taxa showed clear shifts at the class level between the upper stream and backwater area sites along the Pengxi River. Conductivity, transparency and temperature were considered the major environmental factors driving the bacterioplankton composition variation. Additionally, the functional profiles of the bacterioplankton community corresponded with compositional changes in reservoir regulation by TGR. Therefore, these results provide insights into dam effects on the bacterioplankton community in the Pengxi River, and further research should focus on the potential ecological processes of river regulation by dams or reservoirs.

Total ammonia nitrogen (TAN) is a common and potent neurotoxic pollutant in aquatic environments. Due to their strong adsorption capacity, titanium dioxide nanoparticles (n-TiO₂), a widely used engineered material, can induce combined toxicity with multiple pollutants. However, the combined neurotoxicity of n-TiO₂ and TAN and its underlying mechanisms remain unclear. In this study, zebrafish embryos were exposed to TAN (0, 0.1, 1, 10 mg/L) and n-TiO₂ (100 µg/L) individually or in combination for 120 h. The results indicated that co-exposure to n-TiO₂ and TAN significantly increased the bioaccumulation of TAN in zebrafish embryos compared to TAN alone. Consequently, this led to exacerbated neurotoxicity, manifested as developmental impairments and abnormal motor behavior. Mechanistic investigations revealed that the co-exposure aggravated developmental neurotoxicity by triggering neuronal apoptosis and oxidative stress, disrupting the cholinergic and dopaminergic systems, and impairing neural and retinal development. Transcriptomic analysis further indicated that the co-exposure predominantly perturbed neurodevelopment, oxidative stress, and apoptosis. In conclusion, this study confirms that n-TiO₂ significantly amplifies TAN-induced neurodevelopmental toxicity by promoting its bioaccumulation and synergistically disrupting multiple neurophysiological processes. These findings provide crucial scientific evidence for assessing the combined ecological risks of nanomaterials and conventional pollutants.