Toxic Effects and Mechanisms of Silver and Zinc Oxide Nanoparticles on Zebrafish Embryos in Aquatic Ecosystems.
Yen-Ling LeeYung-Sheng ShihZi-Yu ChenFong-Yu ChengJing-Yu LuYuan-Hua WuYing-Jang WangPublished in: Nanomaterials (Basel, Switzerland) (2022)
The global application of engineered nanomaterials and nanoparticles (ENPs) in commercial products, industry, and medical fields has raised some concerns about their safety. These nanoparticles may gain access into rivers and marine environments through industrial or household wastewater discharge and thereby affect the ecosystem. In this study, we investigated the effects of silver nanoparticles (AgNPs) and zinc oxide nanoparticles (ZnONPs) on zebrafish embryos in aquatic environments. We aimed to characterize the AgNP and ZnONP aggregates in natural waters, such as lakes, reservoirs, and rivers, and to determine whether they are toxic to developing zebrafish embryos. Different toxic effects and mechanisms were investigated by measuring the survival rate, hatching rate, body length, reactive oxidative stress (ROS) level, apoptosis, and autophagy. Spiking AgNPs or ZnONPs into natural water samples led to significant acute toxicity to zebrafish embryos, whereas the level of acute toxicity was relatively low when compared to Milli-Q (MQ) water, indicating the interaction and transformation of AgNPs or ZnONPs with complex components in a water environment that led to reduced toxicity. ZnONPs, but not AgNPs, triggered a significant delay of embryo hatching. Zebrafish embryos exposed to filtered natural water spiked with AgNPs or ZnONPs exhibited increased ROS levels, apoptosis, and lysosomal activity, an indicator of autophagy. Since autophagy is considered as an early indicator of ENP interactions with cells and has been recognized as an important mechanism of ENP-induced toxicity, developing a transgenic zebrafish system to detect ENP-induced autophagy may be an ideal strategy for predicting possible ecotoxicity that can be applied in the future for the risk assessment of ENPs.
Keyphrases
- oxide nanoparticles
- silver nanoparticles
- oxidative stress
- cell death
- diabetic rats
- endoplasmic reticulum stress
- cell cycle arrest
- induced apoptosis
- risk assessment
- dna damage
- signaling pathway
- drug induced
- liver failure
- ischemia reperfusion injury
- heavy metals
- healthcare
- human health
- wastewater treatment
- respiratory failure
- magnetic resonance imaging
- reactive oxygen species
- pi k akt
- pregnant women
- endothelial cells
- acute respiratory distress syndrome
- current status
- cell proliferation
- magnetic resonance
- high resolution