Maternal exposure to dietary uranium causes oxidative stress and thyroid disruption in zebrafish offspring.

The contamination of uranium in aquatic ecosystems has raised growing global concern. However, the understanding of its chronic effects on aquatic organisms is limited, particularly with regards to transgenerational toxicity. In this study, we evaluated the maternal transfer risk of uranium using zebrafish. Sexually mature female zebrafish were exposed to 2 and 20 ng/g of uranium-spiked food for 28 days. The induced bioconcentration, thyroid disruption, and oxidative stress in both the adults (F0) and their embryos (F1) were further investigated. Element analysis showed that uranium was present in both F0 and F1, with higher concentrations observed in F1, indicating significant maternal offloading to the offspring. Meanwhile, an increased malformation and decreased swim speed were observed in the F1. Thyroid hormone analysis revealed significant decreases in the levels of triiodothyronine (T3) in both the F0 adults and F1 embryos, but thyroxine (T4) was not significantly affected. Additionally, the activities of antioxidant defenses, including catalase (CAT) and superoxide dismutase (SOD), and the expression of glutathione (GSH) and malondialdehyde (MDA) were significantly altered in the F0 and F1 larvae at 120 hpf. The hypothalamic-pituitary-thyroid (HPT) axis, oxidative stress, and apoptosis-related gene transcription expression were also significantly affected in both generations. Taken together, these findings highlight the importance of considering maternal transfer in uranium risk assessments.

Accumulation and Distribution of Fluorescent Microplastics in the Early Life Stages of Zebrafish.

As a new type of environmental pollutant, microplastic has been widely found in the aquatic environment and poses a high threat to aquatic organisms. The bioaccumulation of microplastics plays a key role in their toxic effects; however, as a particulate, their bioaccumulations are different from many other pollutants. Described here is a feasible method to visually determine the accumulation and distribution of microplastics in zebrafish embryos or larvae using fluorescent microplastics. Embryos are exposed to different concentrations (0.1, 1, and 10 mg/L) of fluorescent microplastics with a diameter of 500 nm for 120 h. It is shown in the results that microplastics can bioaccumulate in zebrafish embryos/larvae in a concentration-dependent manner. Before hatching, strong fluorescence is found around the embryonic chorion; while in zebrafish larvae, the yolk sac, pericardium, and gastrointestinal tract are the main accumulated sites of microplastics. The results demonstrate the uptake and internalization of microplastics in zebrafish at early life stages, which will provide basis for better understanding the impact of microplastics on aquatic animals.

Waterborne uranium causes toxic effect and thyroid disruption in zebrafish larvae.

Uranium is a radioactive element that is widely present in aquatic environment. However, limited knowledge is available about the effect of uranium on thyroid system, which plays a key role in the development of animals. In this study, zebrafish embryos were exposed to different environmentally relevant concentrations of uranium (2, 20 and 100 µg/L) for 120 h. The bioaccumulation, developmental toxicities, changes of thyroid hormones (THs) and key genes related to the hypothalamic-pituitary-thyroid (HPT) axis in larvae were analyzed after exposure. Results showed that uranium could bioaccumulate in zebrafish larvae, with the bioconcentration factors ranging from 49.6 to 523. Consequently, significant developmental toxicities and changes in locomotor activities were observed with a concentration-dependent manner. The levels of triiodothyronine (T3) levels in larvae were substantially decreased, whereas those of thyroxine (T4) were increased in fish bodies. The levels of THs were regulated by the negative feedback loops through HPT axis related genes, most of which (NIS, Deio1, Deio2, TRα, TSHß and UGT1ab) were significantly depressed after exposure to uranium. Our results suggest the potential toxicities and thyroid disruption of uranium on zebrafish, which would provide baseline data set for better understanding the impact of waterborne uranium on aquatic organisms and the associated mechanisms. This study also highlights the key role of thyroid disruption in the ecological risk assessment of uranium pollution.

Long-term exposure to the non-steroidal anti-inflammatory drug (NSAID) naproxen causes thyroid disruption in zebrafish at environmentally relevant concentrations.

The presence of trace levels of pharmaceuticals is an emerging issue impacting the aquatic ecosystem. Naproxen (NPX) is a nonsteroidal anti-inflammatory drug (NSAID) that has been frequently detected in aquatic environments worldwide. Recently, concerns regarding endocrine disruption by NSAIDs have increased; however, their effects on the thyroid system have yet to be understood. In this study, zebrafish were utilized to evaluate the thyroid-disrupting effects of NPX. After a 60-day exposure to various concentrations of NPX (0.1, 1, 10 and 100 µg/L), the body length and weight of the zebrafish were significantly decreased. The decrease of cytochrome P450 gene expression and enzyme activity might inhibit the metabolism of NPX, which might result in the significant bioconcentration in zebrafish. Thyroid hormone (TH) analysis showed that both triiodothyronine (T3) and thyroxine (T4) levels were substantially decreased. Gene transcription expressions along the hypothalamic-pituitary-thyroid (HPT) axis were also markedly affected. Significant downregulation of dio1, dio2, nis, nkx2.1, pax8, tg, tpo, trß and ttr levels, along with the stimulation of the tshß gene, were also observed in exposed fish compared to controls. Western blot analysis indicated that expression of the TTR protein was significantly decreased, which coincides with the results of the gene expression analysis. Collectively, our observations show that NPX increases the risk of bioconcentration and thyroid disruption in zebrafish. Given the continued increasing consumption and emission of pharmaceuticals, thyroid disruption should be considered when assessing the aquatic risk of long-term exposure to environmentally relevant concentrations of pharmaceuticals.