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Nanomaterials have attracted much attention in the biomedical field. Black phosphorus quantum dots (BPQDs) have shown great potential in biomedical applications, but their potential risks to biosafety and environmental stability have not been fully evaluated. In the present study, zebrafish (Danio rerio) embryos were exposed to 0, 2.5, 5 and 10 mg/L BPQDs from 2 to 144 h post-fertilization (hpf) to explore developmental toxicity. The results showed that exposure to BPQDs for 96 h induced developmental malformations (tail deformation, yolk sac edema, pericardial edema, and spinal curvature) in zebrafish embryos. ROS and antioxidant enzyme activities (CAT, SOD, MDA and T-AOC) were substantially altered and the acetylcholinesterase (AChE) enzyme activity was significantly decreased in the BPQDs exposed groups. Locomotor behavior was inhibited after BPQDs exposure for 144 h in zebrafish larvae. A significant increase in 8-OHdG content indicates DNA oxidative damage in embryos. In addition, obvious apoptotic fluorescence signals were detected in the brain, spine, yolk sac and heart. At the molecular level, the mRNA transcript levels of key genes related to skeletal development (igf1, gh, MyoD and LOX), neurodevelopment (gfap, pomca, bdnf and Mbpa), cardiovascular development (Myh6, Nkx2.5, Myl7, Tbx2b, Tbx5 and Gata4) and apoptosis (p53, Bax, Bcl-2, apaf1, caspase-3 and caspase-9) were abnormal after BPQDs exposure. In conclusion, BPQDs induced morphological malformations, oxidative stress, locomotor behavior disorders, DNA oxidative damage and apoptosis in zebrafish embryos. This study provides a basis for further study on the toxic effects of BPQDs. [Display omitted] • BPQDs caused developmental toxicity in the zebrafish embryos. • BPQDs induced oxidative stress, oxidative DNA damage and apoptosis in zebrafish embryos. • BPQDs induced developmental neurotoxicity and decreased locomotor behavior. [ABSTRACT FROM AUTHOR]

Dechlorane Plus (DP) is a widely used chlorinated flame retardant, which has been extensively detected in the environment. Although DP content in the surface water is low, it can pose a continuous exposure risk to aquatic organisms due to its strong bioaccumulation. Considering that the related studies on the toxicity mechanism of DP exposure are limited, the effect of DP on carp embryo development was evaluated. In the present work, carp embryos were exposed to different concentrations (0, 30, 60, and 120 μg/L) of DP at 3 h post-fertilization (hpf). The expression levels of neural and skeletal development-associated genes, such as sox2, sox19a, Mef2c and BMP4 , were detected with quantitative PCR, and the changes in different developmental toxicity endpoints were observed. Our results demonstrated that the expression levels of sox2, sox19a, Mef2c and BMP4 were significantly altered and several developmental abnormalities were found in DP-exposed carp embryos, such as DNA damage, increased mortality rate, delayed hatching time, reduced hatching rate, decreased body length, and increased morphological deformities. In addition, the activities of reactive oxygen species and malondialdehyde were remarkably higher in 60 and 120 μg/L DP exposure groups than in control group. These results suggest that DP can exhibit a unique modes of action, which lead to aberration occurrence in the early development stage of common carps, which may be related to some gene damage and oxidative stress. Besides, the parameters evaluated here can be used as tools to access the environmental risk for biota and humans exposed to DP. Image 1 • DP has embryotoxic effects on common carp. • DP could delay embryo development and even cause embryo death. • DP exposure could induce DNA damage and oxidative stress. • ROS and MDA may play an important role in DP-induced developmental deformity. [ABSTRACT FROM AUTHOR]