Polystyrene Nanoplastic Exposure Induces Developmental Toxicity by Activating the Oxidative Stress Response and Base Excision Repair Pathway in Zebrafish (Danio rerio)

Abstract

The widespread accumulation of nanoplastics is a growing concern for the environmental and human health. However, studies on the mechanisms of nanoplastic-induced developmental toxicity are still limited. Here, we systematically investigated the potential biological roles of nanoplastic exposure in zebrafish during the early developmental stage. The zebrafish embryos were subjected to exposure to 100 nm polystyrene nanoplastics with different concentrations (0, 100, 200, and 400 mg/L). The results indicated that nanoplastic exposure could decrease the hatching and survival rates of zebrafish embryos. In addition, the developmental toxicity test indicated that nanoplastic exposure exhibits developmental toxicity via the inhibition of the heart rate and body length in zebrafish embryos. Besides, behavioral activity was also significantly suppressed after 96 h of nanoplastic exposure in zebrafish larvae. Further biochemical assays revealed that nanoplastic-induced activation of the oxidative stress responses, including reactive oxygen species accumulation and enhanced superoxide dismutase and catalase activities, might affect developmental toxicity in zebrafish embryos. Furthermore, a quantitative polymerase chain reaction assay demonstrated that the mRNA levels of the base excision repair (BER) pathway-related genes, including lig1 , lig3 , polb , parp1 , pold , fen1 , nthl1 , apex , xrcc1 , and ogg1 , were altered in zebrafish embryos for 24 h after nanoplastic exposure, indicating that the activation of the BER pathway would be stimulated after nanoplastic exposure in zebrafish embryos. Therefore, our findings illustrated that nanoplastics could induce developmental toxicity through activation of the oxidative stress response and BER pathways in zebrafish.

Nanoplastic Exposure Mediates Neurodevelopmental Toxicity by Activating the Oxidative Stress Response in Zebrafish (Danio rerio)

“…Cells produce antioxidant enzymes in response to oxidative stress in vivo, and SOD is the most dominant component of antioxidant enzymes. In our study, various concentrations of 20 nm-NPs significantly reduced the activity of SOD (Figure B), which is similar to previous study that 100 nm-NPs significantly reduced the activity of SOD . Moreover, the expression level of the Cu/Zn-SOD gene showed a compensatory increase (Figure C), also illustrating that exposure to NPs causes abnormal SOD activity in oxidative stress.…”

“…In our study, various concentrations of 20 nm-NPs significantly reduced the activity of SOD ( Figure 5 B), which is similar to previous study that 100 nm-NPs significantly reduced the activity of SOD. 45 Moreover, the expression level of the Cu/Zn-SOD gene showed a compensatory increase ( Figure 5 C), also illustrating that exposure to NPs causes abnormal SOD activity in oxidative stress. Several studies have shown that MPs and NPs can cause ROS metabolism and oxidative stress in zebrafish by regulating the antioxidants of SOD.…”

Nanoplastics induces Arrhythmia in Human Stem-cells derived Cardiomyocytes

“…Quantitative polymerase chain reaction (qPCR) revealed a dose-dependent upregulation of endoplasmic reticulum (ER) stress starting from day 5 onwards (Figure 2a). Consistent with Feng et al, upregulation of catalase (CAT) was observed in cells treated with 20 and 40 µg/ml NPs, suggesting an increase in oxidative stress independent of the superoxide dismutase (SOD)pathway (Figure 2a) (Feng et al, 2022). Complementing the qPCR ndings, MitoSOX assay revealed an increase in oxidative stress in a dose-dependent manner on day 5 and 7 (Figure 2b).…”

The use of zebrafish to assess water quality and remediation efforts.

“…In accordance to these outcomes, the ecotoxicity of untreated tannery, hospital and whole tin mining effluent have been reported to cause loss in fish motility, decrease in total distance travelled and an alerting increase in frozen time (Affandi et al,2019;Chagas et al,2019;Rosales-Pérez et al,2022). These behavioural alterations were attributed to the presence of various substances explained to interfere with locomotion in aquatic species, such as heavy metals, nanoplastics, CECs such as anti-depressants (e.g., diazepam), pesticides (e.g., fenvalerate and tebuconazole), endocrine-disrupting chemicals (e.g., bisphenol A) (Ogungbemi et al,2019;Chen et al,2021;Rao et al,2022;Yao et al,2022;Feng et al,2022).…”