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Unveiling the underlying mechanism: Metabolic reprogramming and oxidative stress mediate nanoplastic-induced hepatotoxicity in a freshwater fish (Pseudorasbora parva)
Summary
Scientists studied how tiny plastic particles (nanoplastics) affect fish livers and found that the smallest particles (80 nanometers) caused the most damage by disrupting the body's ability to fight harmful chemicals and process energy. The smallest plastic particles were especially harmful because they damaged the fish's natural defense systems and changed how their cells make energy. While this study was done in fish, it raises concerns about how these tiny plastic particles in our environment might also harm human health.
In this study, the toxic effects of nanoplastics with different particle sizes (80 nm, 200 nm, 500 nm) were systematically investigated using Pseudorasbora parva as a model. By integrating physiological and biochemical indicators, transcriptomics and metabolomics analysis, it was found that the toxic effects of nanoplastics were significantly particle size-dependent. Among them, 80 nm particles showed the strongest oxidative damage effect, which significantly inhibited SOD and CAT activities and induced metabolic reprogramming, manifested as the up-regulation of key glycolysis genes (LDHA, HK1) and significant disturbance of organic acid and amino acid metabolic pathways. The 200 nm particles mainly affect immune-related functions and may induce ferroptosis through the GPx4/PKM2 pathway, while the 500 nm particles cause extensive immunosuppression and inflammatory response. The results showed that 80 nm NPs caused the most serious primary physiological damage to the body by destroying the oxidative defense system and energy metabolism homeostasis, highlighting its special risks in the ecological risk assessment of NPs.
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