Comparing different surface modifications of zinc oxide nanoparticles in the developmental toxicity of zebrafish embryos and larvae

• Published in: Ecotoxicology and environmental safety 2022-09, Vol.243, p.113967-113967, Article 113967
• Main Authors: Chen, Zi-Yu, Yang, Yi-Chun, Wang, Bour-Jr, Cheng, Fong-Yu, Lee, Yen-Ling, Lee, Yu-Hsuan, Wang, Ying-Jan
• Format: Article
• Language: English
• Subjects: Autophagy; Danio rerio; Developmental changes; Liver toxicity; Surface modification; Zinc oxide nanoparticles (ZnONPs)
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2022.113967

Nanotechnology allows for a greater quality of life, but may also cause environmental and organismic harm. Zinc oxide nanoparticles (ZnONPs) are one of the most commonly used metal oxide nanoparticles for commercial and industrial products. Due to its extensive use in various fields, there has already been much concern raised about the environmental health risks of ZnONPs. Many studies have investigated the toxicological profile of ZnONPs in zebrafish embryonic development; however, the specific characteristics of ZnONPs in zebrafish embryonic/larval developmental damage and their molecular toxic mechanisms of liver development are yet to be fully elucidated. This study aimed to reveal the hazard ranking of different surface modifications of ZnONPs on developing zebrafish and the toxicological mechanisms of these modified ZnONPs in liver tissue. The ~30 nm ZnONPs with amino- (NH2- ZnONPs) or carboxyl- (COOH-ZnONPs) modification were incorporated during the embryonic/larval stage of zebrafish. Severe toxicity was observed in both ZnONP groups, especially NH2-ZnONPs, which presented a higher toxicity in the low concentration groups. After prolonging the exposure time, the long-term toxicity assay showed a greater retardation in body length of zebrafish in the NH2-ZnONP group. Response data from multiple toxicity studies was integrated for the calculation of the EC50 values of bulk ZnO and ZnONPs, and the hazard levels were found to be decreasing in the order of NH2-, COOH-ZnONPs and bulk ZnO. Notably, NH2-ZnONPs induced ROS burden in the developing liver tissue, which activated autophagy-related gene and protein expression and finally induced liver cell apoptosis to reduce liver size. In conclusion, our findings are conducive to understanding the hazard risks of different surface modifications of ZnONPs in aquatic environments and will also be helpful for choosing the type of ZnONPs in future industrial applications. [Display omitted] •NH2- and COOH-modified ZnONPs induce acute, developmental and chronic toxicity.•NH2- and COOH ZnONPs result in a higher hazard risk than bulk ZnO, especially the NH2-ZnONPs.•ZnONPs trigger hepatotoxicity, and NH2-ZnONPs induce more severe toxicity than COOH- ZnONPs.•NH2-ZnONPs cause multiple responses, such as ROS burden, autophagy and apoptosis in the liver.