Developmental toxicity in rare minnow (Gobiocypris rarus) embryos exposed to Cu, Zn and Cd

• Developmental toxicity of Cu, Zn and Cd to fish embryos was investigated.
• Cu, Zn and Cd affects embryos in a dose–response relationship.
• Cu, Zn and Cd cause severe heart and body malformations.
• The vezf1, mt and hsp70 were involved in heavy metals caused heart and body defects.

Using rare minnow (Gobiocypris rarus) embryos as experimental model, the developmental toxicity of Cu, Zn and Cd were investigated following exposure to 0.001–1.000 mg/L for 72 h, and the toxicity effects were evaluated by larval malformation rate, heart rate, pericardial area, spontaneous movements, tail length, enzyme activities and biomarker genes. Our results revealed that increased malformation rate provide a gradual dose–response relationship, and the most pronounced morphological alteration was heart and body malformations. Values of 72 h EC50 with their 95 percent confidence intervals on G. rarus embryos were 0.103 (0.072–0.149) mg/L for Cu, 0.531 (0.330–1.060) mg/L for Zn, 0.219 (0.147–0.351) mg/L for Cd. Enzyme activities can be regard as a type of low-dose stimulation and high-dose inhibition. Stress and metabolism-related genes (hsp70, cyp1a and mt) were significantly up-regulated, development-related genes (wnt8a, vezf1 and mstn) were significantly down-regulated after the treatment by Cu, Zn and Cd. Overall, the present study points out Cu, Zn and Cd are highly toxic to G. rarus embryos. The information presented in this study will be helpful in fully understanding the toxicity induced by Cu, Zn and Cd in fish embryos.