Aged polystyrene microplastics exposure affects apoptosis via inducing mitochondrial dysfunction and oxidative stress in early life of zebrafish.

In recent years, the toxic effects of microplastics (MPs) on aquatic organisms have been increasingly recognized. However, the developmental toxicity and underlying mechanisms of photoaged MPs at environmental concentrations remain unclear. Therefore, the photodegradation of pristine polystyrene (P-PS) under UV irradiation was used to investigate, as well as the developmental toxicity and underlying mechanisms of zebrafish (Danio rerio) exposed to P-PS and aged polystyrene (A-PS) at environmentally relevant concentrations (0.1-100 µg/L). Mortality, heart rate, body length, and tail coiling frequency of zebrafish larvae were the developmental toxicity endpoints. A-PS had increased crystallinity, the introduction of new functional groups, and higher oxygen content after UV-photoaging. The toxicity results showed that exposure to A-PS resulted in more adverse developmental toxicity than exposure to P-PS. Exposure to A-PS induced oxidative damage, as evidenced by elevated production of reactive oxygen species (ROS) and DNA damage, and led to decreased mitochondrial membrane potential (MMP) and causes the release of cytochrome c (cyt c) from the mitochondria. The caspase-3/-9 activation signaling pathways may cause developmental toxicity via mitochondrial apoptosis. Significant changes in the expression of genes were further explored linking with oxidative stress, mitochondria dysfunctions and apoptosis pathways following A-PS exposure. These findings underscore the importance of addressing the environmental applications of aged MPs and call for further research to mitigate their potential risks on aquatic ecosystems and human health.

Photoaged polystyrene microplastics result in neurotoxicity associated with neurotransmission and neurodevelopment in zebrafish larvae (Danio rerio).

Microplastics (MPs) are emerging pollutants widely distributed in the environment, inducing toxic effects in various organisms. However, the neurotoxicity and underlying mechanisms of simulated sunlight-aged MPs have rarely been investigated. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant concentrations (0, 0.1, 1, 10, and 100 µg/L) of virgin polystyrene (V-PS) and aged polystyrene (A-PS) for 120 hpf to evaluate the neurotoxicity. The results demonstrated that simulated sunlight irradiation altered the physicochemical properties (morphology, functional groups, and chemical composition) of V-PS. Exposure to A-PS causes greater toxicity on locomotor ability in larval zebrafish than V-PS. Motor neuron development was disrupted by transgenic (hb9-GFP) zebrafish larvae exposed to A-PS, with significant alterations in neurotransmitter levels (ACh, DA, 5-HT, and GABA) and enzyme activity (AChE, ChAT, and ChE). Further investigation found that exposure to A-PS had a significantly impact on the expression of neurotransmission and neurodevelopment-related genes in zebrafish. These findings suggest that A-PS induces neurotoxicity by its effects on neurotransmission and neurodevelopment. This study highlights the neurotoxic effects and mechanisms of simulated sunlight irradiation of MPs, providing new insights for assessing the ecological risks of photoaged MPs in the environment.

Photoaged microplastics induce neurotoxicity via oxidative stress and abnormal neurotransmission in zebrafish larvae (Danio rerio).

Microplastics (MPs) are ubiquitous environmental contaminants and cause neurotoxicity in various organisms. However, previous studies that analyzed the effects of MPs mainly focused on virgin polystyrene (V-PS) as representative models of MPs, and the mechanism underlying the neurotoxicity of photoaged polystyrene (P-PS) remains largely unknown. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant concentrations (0.1-100 µg/L) of V-PS and P-PS(10 µm). The results indicated that UV radiation accelerated the aging process and changed physical and chemical properties of PS. Whereas exposure to both V-PS and P-PS at low concentrations (100 µg/L) significantly reduced the locomotor behavior of zebrafish larvae, P-PS caused more severe neurotoxicity compared to V-PS. The activity of antioxidant enzymes (SOD, CAT, and GST) and MDA content were significantly altered in zebrafish exposed to 10-100 µg/L of P-PS. Similarly, exposure to P-PS significantly increased neurotransmitter (5-HT, GABA, DA, and ACh) levels and activity of AChE, ChAT, and ChE. Star plots based on integrated biomarker response (IBR) values showed more incline toward neurotransmitter biomarkers in response to increasing P-PS concentration, and the behavioral parameters negatively correlated with the neurotransmitter biomarkers. Further investigations revealed that the expression of neurotransmission- (e.g., ache, drd3, 5th2c, and gat1) and oxidative stress- (e.g., cat1, sod1, gpx1a, and gstrl) related genes was significantly affected by PS in larval zebrafish. Thus, this study provides new insights on the potential risks of MPs into the environment.

UV-aged microplastics induces neurotoxicity by affecting the neurotransmission in larval zebrafish.

Microplastics (MPs) are nearly ubiquitous in aquatic ecosystems and may affect aquatic organisms. In this study, virgin and aged polystyrene MPs (PS-MPs) of size 1 µm were selected to analyze their adverse effects on larvae zebrafish. Exposure to PS-MPs significantly reduced the average swimming speed of zebrafish, and the behavioral effects caused by aged PS-MPs on zebrafish were more pronounced. Fluorescence microscopy revealed that 10-100 µg/L of PS-MPs accumulated in tissues of zebrafish. As an endpoint of neurotransmitter concentration, exposure to aged PS-MPs at doses ranging from 0.1 to 100 µg/L significantly increased the dopamine (DA), 5-hydroxytryptamine (5-HT), γ-aminobutyric acid (GABA), and acetylcholine (ACh) levels in zebrafish. Similarly, exposure to aged PS-MPs significantly altered the expression of genes related to these neurotransmitters (e.g., dat, 5ht1aa, and gabral genes). According to Pearson correlation analyses, neurotransmissions was significantly correlated with neurotoxic effects of aged PS-MPs. Thus, aged PS-MPs cause neurotoxicity in zebrafish through their effects on DA, 5-HT, GABA, and ACh neurotransmissions. The results highlight the importance of the neurotoxicity of aged PS-MPs in zebrafish, which has important implications for the risk assessment of aged MPs and the conservation of aquatic ecosystems.

Bioaccumulation Behavior and Human Health Risk of Polybrominated Diphenyl Ethers in a Freshwater Food Web of Typical Shallow Lake, Yangtze River Delta.

BACKGROUND: Polybrominated diphenyl ethers (PBDEs) have been commonly found in aquatic ecosystems. Many studies have elucidated the bioaccumulation and biomagnification of PBDEs in seas and lakes, yet few have comprehensively evaluated the bioaccumulation, biomagnification, and health risks of PBDEs in shallow lakes, and there is still limited knowledge of the overall effects of biomagnification and the health risks to aquatic organisms. METHODS: In this study, a total of 154 samples of wild aquatic organism and environmental samples were collected from typical shallow lakes located in the Yangtze River Delta in January 2020. The concentrations of PBDEs were determined by an Agilent 7890 gas chromatograph coupled and an Agilent 5795 mass spectrometer (GC/MS) and the bioaccumulation behavior of PBDEs was evaluated in 23 aquatic organisms collected from typical shallow lakes of the Yangtze River Delta. Furthermore, their effects on human health were evaluated by the estimated daily intake (EDI), noncarcinogenic risk, and carcinogenic risk. RESULTS: The concentrations of ΣPBDE (defined as the sum of BDE-28, -47, -100, -99, -153, -154, -183, and -209) in biota samples ranged from 2.36 to 85.81 ng/g lipid weight. BDE-209, BDE-153 and BDE-47 were the major PBDE congeners. The factors affecting the concentration of PBDEs in aquatic organisms included dietary habits, species, and the metabolic debromination ability of the PBDE congeners. BDE-209 and BDE-47 were the strongest bioaccumulative PBDE congeners in aquatic organisms. Additionally, except for BDE-99, BDE-153 and BDE-154, the trophic magnification factor (TMF) values of PBDE congeners were significantly higher than 1. Moreover, the log Kow played a significant role in the biomagnification ability of PBDE congeners. The noncarcinogenic risk of PBDE congeners and carcinogenic risk of BDE-209 from aquatic products were lower than the thresholds. CONCLUSIONS: PBDE congeners were bioaccumulated and biomagnified to varying degrees in aquatic organisms from typical shallow lakes. Both the noncarcinogenic and carcinogenic risks assessment of edible aquatic products indicated that none of the PBDE congeners pose health risks to the localite. This study will provide a basis for a comprehensive assessment of PBDEs in aquatic ecosystems in shallow lakes and for environmental prevention measures for decision-makers.