Genipin induces developmental toxicity through oxidative stress and apoptosis in zebrafish

Genipin, an iridoid substance, is mainly derived from Gardenia jasminoides Ellis of the traditional Chinese medicine and is widely used in raw materials for the food additive gardenia blue and biological materials. The developmental toxicity of genipin has not been investigated, and its underlying mechanism is unclear. Therefore, in this study we attempt to investigate the potential developmental toxicity of genipin in zebrafish embryos/ larvae. The results showed zebrafish embryos treated with 50 mu g/ml dose of genipin display inhibited hatching rates and body length. The pericardial edema was observed. It was also found that genipin could induce cardiotoxicity, hepatotoxicity and nephrotoxicity in zebrafish larvae. After genipin treatment, the suppression of antioxidant capacity and increase of oxidative stress were showed for the triggered generation of ROS and MDA, and decreased activity of SOD. Compared with the 0.5% DMSO group, a number of apoptotic cells in zebrafish were increased after genipin exposure. By measuring marker gene expression with the using of qRT-PCR, we proposed that developmental toxicity after genipin treatment might be associated with oxidative stress and apoptosis increase. Our research offers a better understanding for developmental toxicity of genipin.

Automated summary

The study demonstrated that genipin treatment inhibited hatching rates and body length, induced pericardial edema, cardiotoxicity, hepatotoxicity, and nephrotoxicity in zebrafish embryos/larvae. Genipin also increased oxidative stress and apoptosis in zebrafish, indicating a potential developmental toxicity mechanism associated with oxidative stress and apoptosis increase.