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Impact of polystyrene nanoplastics on apoptosis and inflammation in zebrafish larvae: Insights from reactive oxygen species perspective
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Researchers showed that polystyrene nanoplastics accumulate in zebrafish larvae and trigger excessive reactive oxygen species production via NADPH oxidase upregulation, causing mitochondrial dysfunction, apoptosis, and NF-κB-driven inflammation — with inhibiting ROS generation effectively blocking downstream cell death and inflammatory responses.
In recent years, there has been a growing focus on the toxicity and mortality induced by nanoplastics (NPs) in aquatic organisms. However, studies investigating mechanisms underlying oxidative stress (OS), apoptosis, and inflammation induced by NPs in fish remain limited. This study observed that polystyrene NPs (PS-NPs) were accumulated into zebrafish larvae and zebrafish embryonic fibroblast (ZF4 cells), accompanied by the occurrence of pathological damage both at the cellular and tissue-organ level. Additionally, the transcriptional up-regulation of NADPH oxidases (NOXs) and subsequent excessive generation of reactive oxygen species (ROS) resulted in notable changes in the relative mRNA and protein expression levels associated with antioxidant oxidase systems in larvae. Furthermore, the study identified the impact of NPs on mitochondrial ultrastructural, resulting in mitochondrial depolarization and downregulation of mRNA expression related to the electron transport chain due to excessive ROS generation. Short-term exposure to NPs also triggered apoptosis and inflammation in zebrafish larvae, evident from significant up-regulation in mRNA expressions of proapoptotic factors and NF-κB proinflammatory signaling pathway, as well as increased transcription and protein levels of pro-inflammatory factors in larvae. Inhibition of intracellular excessive ROS effectively reduced the induction of apoptosis, NF-κB P65 nuclear migration levels, and cytokine secretion, underscoring OS as a pivotal factor throughout the process of apoptosis and inflammatory responses induced by NPs. This research significantly advances our comprehension of biological effects and underlying mechanisms of NPs in freshwater fish.
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ROS-driven crosstalk between ferroptosis and necroptosis mediates neurotoxicity induced by maternal exposure to polystyrene nanoplastics in zebrafish
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Adult female zebrafish were exposed to polystyrene nanoplastics for 28 days. The particles passed to their embryos and larvae, which had lower hatching rates, more malformations, reduced movement and fewer neurons in part of the brain. The damage was driven by oxidative stress and two cell-death pathways, and antioxidant treatment partly reversed it.
Immune response to polystyrene microplastics: Regulation of inflammatory response via the ROS-driven NF-κB pathway in zebrafish (Danio rerio)
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Researchers found that polystyrene microplastics triggered immune system inflammation in zebrafish by generating reactive oxygen species (ROS) that activated the NF-kB signaling pathway. The microplastics accumulated mainly in the intestines, causing tissue damage and behavioral changes in the fish. This study identifies a specific molecular mechanism by which microplastics cause immune dysfunction, which could be relevant to understanding inflammation in humans exposed to microplastics.
Polystyrene microplastics induce apoptosis via ROS-mediated p53 signaling pathway in zebrafish
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Researchers discovered that polystyrene microplastics trigger programmed cell death in zebrafish gills through a molecular pathway involving reactive oxygen species and the p53 gene. The microplastics caused dose- and time-dependent oxidative damage, inflammation, and physical injury to gill tissue at concentrations as low as 10 micrograms per liter. The study provides molecular-level evidence explaining how microplastic exposure can harm aquatic organisms.
Polystyrene nanoplastics induced cardiomyocyte apoptosis and myocardial inflammation in carp by promoting ROS production
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Researchers exposed carp to polystyrene nanoplastics of different sizes and found that the particles caused heart muscle cell death and cardiac inflammation. Smaller nanoplastics penetrated deeper into heart tissue and caused more severe damage by promoting the production of reactive oxygen species. The study provides evidence that nanoplastic pollution in aquatic environments can directly harm fish cardiovascular health.
Toxicological impacts of nanopolystyrene on zebrafish oocyte with insight into the mechanism of action: An expression-based analysis
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Researchers investigated the mechanism by which nanopolystyrene causes toxicity in zebrafish oocytes, finding it triggers oxidative stress, immune disruption, and mitochondrial dysfunction through changes in key gene expression pathways.
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