Acute ZnO nanoparticles exposure induces developmental toxicity, oxidative stress and DNA damage in embryo-larval zebrafish
- Authors
- Zhao, X., Wang, S., Wu, Y., You, H., and Lv, L.
- ID
- ZDB-PUB-130607-3
- Date
- 2013
- Source
- Aquatic toxicology (Amsterdam, Netherlands) 136-137: 49-59 (Journal)
- Registered Authors
- Keywords
- Nano-ZnO, zebrafish, acute toxicity, oxidative stress, DNA damage, gene expression
- MeSH Terms
-
- Animals
- DNA Damage/drug effects*
- DNA Primers/genetics
- Embryo, Nonmammalian/drug effects
- Environmental Pollutants/toxicity*
- Gene Expression Regulation, Developmental/drug effects
- Growth and Development/drug effects*
- Larva/drug effects
- Nanoparticles/toxicity*
- Oxidative Stress/drug effects*
- Reactive Oxygen Species/metabolism
- Real-Time Polymerase Chain Reaction
- Statistics, Nonparametric
- Zebrafish/embryology*
- Zinc Oxide/toxicity*
- PubMed
- 23643724 Full text @ Aquat. Toxicol.
Nano-scale zinc oxide (nano-ZnO) is widely used in various industrial and commercial applications. However, the available toxicological information was inadequate to assess the potential ecological risk of nano-ZnO to aquatic organisms and the publics. In this study, the developmental toxicity, oxidative stress and DNA damage of nano-ZnO embryos were investigated in the embryo-larval zebrafish, the toxicity of Zn2+ releasing from nano-ZnO were also investigated to ascertain the relationship between the nano-ZnO and corresponding Zn2+. Zebrafish embryos were exposed to 1, 5, 10, 20, 50, and 100 mg/L nano-ZnO and 0.59, 2.15, 3.63, 4.07, 5.31, and 6.04 mg/L Zn2+ for 144 h post-fertilisation (hpf), respectively. Up to 144 hpf, activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), and malondialdehyde (MDA) contents, the genes related to oxidative damage, reactive oxygen species (ROS) generation and DNA damage in zebrafish embryos were measured. The nano-ZnO was found to exert a dose-dependent toxicity to zebrafish embryos and larvae, reducing the hatching rate and inducing malformation and the acute toxicity to zebrafish embryos was greater than that of the Zn2+ solution. The generation of ROS was significantly increased at 50 and 100 mg/L nano-ZnO. DNA damage of zebrafish embryo was evaluated by single-cell gel electrophoresis and was enhanced with increasing nano-ZnO concentration. Moreover, the transcriptional expression of mitochondrial inner membrane genes related to ROS production, such as Bcl-2, in response to oxidative damage, such as Nqo1, and related to antioxidant response element such as Gstp2 were significantly down-regulated in the nano-ZnO treatment groups. However, the nano-ZnO up-regulated the transcriptional expression of Ucp2-related to ROS production. In conclusion, nano-ZnO induces developmental toxicity, oxidative stress and DNA damage on zebrafish embryos and the dissolved Zn2+ only partially contributed to the toxicity of nano-ZnO. The adverse effects of nano-ZnO may be the important mechanisms of its toxicity to zebrafish embryos.