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Amplified toxic effects of nanoplastic composite norfloxacin on liver cells in mice: Mechanistic insights and multiscale evaluation
Summary
Researchers examined the combined toxic effects of nanoplastics and the antibiotic norfloxacin on mouse liver cells and found that co-exposure was significantly more harmful than either contaminant alone. The nanoplastics acted as carriers that increased antibiotic accumulation inside cells, amplifying oxidative damage and disrupting key protective enzymes. The study highlights that nanoplastics in the environment can worsen the toxicity of co-occurring pollutants like antibiotics.
The concomitant presence of nanoplastics (NPs) and antibiotics in environmental matrices demands urgent investigation into their combined toxicity, however, the underlying mechanisms remain poorly understood. Here, we employed a multiscale strategy to clarify the combined toxicity and mechanisms of NPs and norfloxacin (NOR) in primary murine hepatocytes. Specifically, co-exposure triggered a 59.0 % reduction in cell viability, exceeding individual treatments (NOR alone: 43.2 %), while amplifying intracellular reactive oxygen species (ROS) generation by 60.1 % compared to individual NOR treatment. NPs promoted NOR bioaccumulation via carrier-mediated transport, thereby aggravating oxidative imbalance through SOD suppression (24.3 % inhibition) and lipid peroxidation (48.3 % MDA elevation). Molecular analyses revealed NPs-NOR complexes destabilized the secondary structure of CAT, increasing α-Helix (2.2 %) content, and docking simulations identified NOR binding to residues. These findings mechanistically link NPs-antibiotic interactions to amplified toxicity via oxidative stress and conformational disruption, highlighting NPs as critical modulators of pollutant bioavailability. This work advances predictive frameworks for composite toxicity, underscores the need to prioritize risk assessment of co-contaminants in environmental and biomedical contexts.
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