Teratogenic response and bioaccumulation to zebrafish embryos by decabromodiphenyl ether (BDE-209) in the suspension of nano-SiO2 particles

• Main Authors: Chao, Shu-Ju, 趙淑如
• Other Authors: Huang, Chih-Pin
• Format: Others
• Language: en_US
• Published: 2017
• Online Access: http://ndltd.ncl.edu.tw/handle/974n4y

博士 === 國立交通大學 === 環境工程系所 === 105 === The rapidly growing and widespread application of nanotechnology in high-tech industries such as semiconductor manufacturing and biomedical engineering result in release of manufactured nanoparticles (NPs) into the aquatic environment, especially nano-SiO2 particle (nSiO2). Decabromodiphenyl ether (BDE-209), an emerging contaminant, is a flame retardant used in consumer electronic equipment. The interaction between NPs and BDE-209 in aquatic environment is getting much concern since the co-existence of NPs and BDE-209 can strengthen the transport of these contaminants into aquatic organisms, thus promoting potential toxic impacts. Therefore, we investigate the teratogenic effects and uptake mechanism of the interactions between BDE-209 and zebrafish in the presence of nSiO2. The first part of this thesis was to investigate the influence of nSiO2 on the teratogenic responses of zebrafish embryo to BDE-209. Zebrafish embryo was exposed to BDE-209 in the absence and presence of nSiO2 for 96 hours post fertilization (hpf). Results also show that embryo temporarily delayed hatching when co-exposure to BDE-209 and nSiO2 at 60 hpf. Furthermore, there was heartbeat decline (28.3 beats/10s) and increase in irregular heartbeat (45.8%) in zebrafish larvae at 96 hpf, compared to the sole exposure to BDE-209 (32.7 beats/10s and 0%). Malformation in terms of spinal curvature (SC), pericardial edema (PE) and yolk sac edema (YSE) were observed on zebrafish larvae at 33.9, 23.4, and 18%, respectively. Overall, abnormal development of zebrafish was apparent at the co-existence of BDE-209 and nSiO2. Besides, the segmentation stage of the embryo was the most sensitive to BDE-209. As a result, nSiO2 could facilitate the transport of BDE-209 towards zebrafish embryos and negatively impact the development of zebrafish. The second part of this thesis investigated the influence of nSiO2 on the uptake behavior of BDE-209 by zebrafish embryo. The amount of BDE-209 on the outside chorion and inside embryo (dechorionated embryo) were measured. For single exposure of nSiO2, results show that nSiO2 accumulation on the chorion surface was higher than that of the dechorionated embryo. Clearly, nSiO2 accumulation on the chorion surface increased (129-200 mg nSiO2/g) with increasing exposure time (48 hpf), while the equilibrium adsorption of nSiO2 on the dechorionated embryo was approximately 0.42-0.54 mg nSiO2/g at 6 hpf. Results show that the formation of nSiO2-BDE-209 associates promoted both extracellular and intracellular uptake of BDE-209 by zebrafish embryo, thereby increasing the bioconcentration of BDE-209 on the chorion surface and embryo. The results also reveal that the accumulative amount of BDE-209 on the chorion was remarkably greater than that on dechorionated embryo at 48 hpf. Clearly, the uptake of BDE-209 was 17.2±0.45 mg/g chorion (or 86 ng BDE-209/chorion/embryo) and 0.37±0.01 mg/g embryos (or 18.6 ng BDE-209/dechorionated embryo/embryo), respectively under the co-exposure of BDE-209 and nSiO2. Results from the SEM and EDS analysis revealed that nSiO2 already passed through the chorion and adhered to the inside embryo. The third part of this thesis was to evaluate the 14-day long-term exposure of BDE-209 and nSiO2 on swimming performance and bioaccumulation of zebrafish larvae. Results showed that the degree of swimming bladder disorder was 35.6-57.8% after co-exposure to BDE-209 and nSiO2 compared to single exposure (< 8%). Also, the area of swimming bladder was significantly smaller than that of BDE-209 alone. The above results were consistent with the change in swimming behavior. Exposure to BDE-209 and nSiO2 caused a significant effect on swimming speed (1.55-1.91 mm/s) in comparison with the control larvae (2.94-3.41 mm/s). Furthermore, BDE-209 accumulation under co-exposure of BDE-209 and nSiO2 was 3-7 folds that of single exposure at 7 dpf. Interestingly, both BDE-183 and BDE-153 was observed in larvae due to the metabolic debromination of BDE-209. Results suggested that the presence of nSiO2 facilitated the debromination of BDE-209 and produced more toxic lower-brominated PBDEs. All relevant evidences suggested that nSiO2 aggregate acted as a carrier of the accumulation of BDE-209 on the chorion surface and accelerate the penetration of BDE-209 into embryo, thereby the bioconcentration of BDE-209 was significantly enhanced in zebrafish, and increased the ecotoxicity of BDE-209. Moreover, the decline of swimming speed and enhancement bioaccumulation of BDE-209 in zebrafish larvae were induced after long-term exposure. The toxicity enhancement of BDE-209 may be due to the synergy effects of BDE-209 adsorption by nSiO2 aggregates. Interactions between nanoparticles and hazardous chemicals can have far-reaching implications on ecological health.