摘要
The toxicity of nano-materials has received increasing attention in recent years. Nevertheless, relatively few studies have focused on their oceanic distributions and toxicities. In this study, we assessed nano-ZnO toxicity in marine organisms using the yellowstriped goby （Mugilogobius chulae）. The relative differences in nano-ZnO dissolution and dispersal in seawater and fresh water were also investigated. The effects of nano-ZnO on embryonic development, deformity, hatching, mortality, and histopathology were analyzed. In addition, the effects of the Zn2＋ concentration on M. chulae hatching and mortality were compared. The results showed that nano-ZnO had higher solubility in seawater than in fresh water. Nano-ZnO significantly inhibited hatching. By the fifth day of exposure, the LC50 of nano-ZnO was 45.40 mg/L, and the mortality rate spiked. Hatching inhibition and lethality were dose-dependent over a range of 1-25 mg/L nano-ZnO. Zn2＋ inhibited hatching and increased lethality, but its effects were weaker than those of nano-ZnO at the same concentrations. Nano-ZnO also induced spinal bending, oedema, hypoplasia, and other deformities in M. chulae embryos and larvae. Histopathology revealed vacuolar degeneration, hepatocyte and enterocyte enlargement, and morphological abnormalities of the vertebrae. Therefore, nano-ZnO caused malformations in M. chulae by affecting embryonic growth and development. We conclude that nano-ZnO toxicity in seawater was significantly positively correlated with the associated Zn2＋ concentration and sedimentary behaviour. The toxicity of nano-ZnO was cumulative and showed a critical point, beyond which embryonic and developmental toxicity in marine fish was observed.
The toxicity of nano-materials has received increasing attention in recent years. Nevertheless, relatively few studies have focused on their oceanic distributions and toxicities. In this study, we assessed nano-ZnO toxicity in marine organisms using the yellowstriped goby （Mugilogobius chulae）. The relative differences in nano-ZnO dissolution and dispersal in seawater and fresh water were also investigated. The effects of nano-ZnO on embryonic development, deformity, hatching, mortality, and histopathology were analyzed. In addition, the effects of the Zn2＋ concentration on M. chulae hatching and mortality were compared. The results showed that nano-ZnO had higher solubility in seawater than in fresh water. Nano-ZnO significantly inhibited hatching. By the fifth day of exposure, the LC50 of nano-ZnO was 45.40 mg/L, and the mortality rate spiked. Hatching inhibition and lethality were dose-dependent over a range of 1-25 mg/L nano-ZnO. Zn2＋ inhibited hatching and increased lethality, but its effects were weaker than those of nano-ZnO at the same concentrations. Nano-ZnO also induced spinal bending, oedema, hypoplasia, and other deformities in M. chulae embryos and larvae. Histopathology revealed vacuolar degeneration, hepatocyte and enterocyte enlargement, and morphological abnormalities of the vertebrae. Therefore, nano-ZnO caused malformations in M. chulae by affecting embryonic growth and development. We conclude that nano-ZnO toxicity in seawater was significantly positively correlated with the associated Zn2＋ concentration and sedimentary behaviour. The toxicity of nano-ZnO was cumulative and showed a critical point, beyond which embryonic and developmental toxicity in marine fish was observed.
基金
supported by the Science and Technology Programs of Guangdong Province(Nos.2015A020215031,2013B020600007,and 2012B050200002)
supported by the National Key Technologies R&D Program of China(No.2015BAI09B05)
