Developmental toxicity in marine medaka (Oryzias melastigma) embryos and larvae exposed to nickel

As an important trace metal, nickel (Ni) has been reported extensively in the studies on freshwater animals. However, the toxic effects of Ni on marine organisms are not clearly understood. Therefore, in order to investigate the toxic effects of Ni on the early development of marine fish, the marine medaka (Oryzias melastigma) embryos and larvae were immersed in 0.13-65.80 mg/L Ni solution. The results showed that Ni exposure changed the egg size and heart rate of the embryos, lowered the hatchability, increased the deformity rate, and shortened the total body length of newly hatched larvae. Besides, it was found that before organogenesis and post-hatching periods were the sensitive periods of embryos to Ni. The 25 d LC50 value of embryos was 49.28 mg/L, and the 5 d LC50 of larvae was 55.92 mg/L, indicating that the embryos were more sensitive to Ni than the larvae. Furthermore, the expressions of the metallothionein (MT) gene, the skeletal development-related gene (Cyp26b1) and the cardiac development-related genes (ATPase, smyd1, cox2 and bmp4) were determined, and the results showed that the expressions of ATPase and smyd1 were up-regulated, while MT, Cyp26b1 and cox2 were significantly down-regulated at 9 days post-fertilization (dpf). Overall, Ni exposure caused a significant toxic effect on the early development of the O. melastigma embryos and larvae. Our findings could provide an important supplement to the toxicity data of tropical Ni and provide a reference for the exploration of the molecular mechanisms of Ni toxicity.

Automated summary

The study found that nickel exposure had significant toxic effects on the early development of marine fish, affecting egg size, heart rate, hatchability, deformity rate, and total body length of newly hatched larvae. Embryos were more sensitive to nickel than larvae, with specific genes showing altered expressions in response to nickel exposure.