Gibberellic acid (GA) induces developmental toxicity in zebrafish (Danio rerio) embryos via oxidative stress.

Gibberellic acid (GA) is a plant growth regulator that stimulates the growth of leaves and increases yield in agricultural production. However, GA is also regarded as an environmental endocrine disruptor, and its effect on aquatic life remains unclear. In this study, the toxic effects of GA on the development of zebrafish (Danio rerio) embryos were evaluated, and the mechanisms were revealed. The expression of genes related to development and function in zebrafish embryos at 96 h post fertilization (96 hpf) were detected by RT-qPCR method. Furthermore, the level of reactive oxygen species (ROS) and the expression of genes related to oxidative stress were detected. The results showed that the hatching and survival rates of zebrafish embryos were inhibited by 25 and 50 μmol/L GA, and the phenotype of pericardial edema was observed, indicating that GA may have cardiotoxicity on zebrafish embryos. Further RT-qPCR experiments showed that the above results may attributed to the down-regulation of Myl7 and Vmhc genes. Besides, the phenotypes of liver degeneration, and the decrease of eye size were led by 10-50 μmol/L GA, along with the alteration of Fabp10a, Gclc, Gsr, Gnat1, and Gnat2 genes, suggesting that GA may exhibit toxicities on liver and eye in zebrafish embryos. In addition, the phenotype of kidney edema and the up-regulation of Kim1, Plce1, and Pkd2 genes were triggered by 50 μmol/L GA, indicating that GA may have toxic effect on kidney in zebrafish embryos. The level of ROS and the expression of genes related to oxidative stress were up-regulated under 10-50 μmol/L GA exposure, which may contribute to the developmental toxicity in zebrafish embryos. In summary, GA may affect the ecological environment of aquatic life, and its harm to aquatic ecology should be given special attention in the future.