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Nanoplastics amplify ciprofloxacin-induced immunotoxicity: Oxidative stress in splenocytes and conformational and functional changes in lysozyme
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In lab tests on mouse spleen cells, nanoplastics combined with the antibiotic ciprofloxacin caused more oxidative stress, cell damage, and inflammation than ciprofloxacin alone. The combination also caused greater structural and functional changes to the immune protein lysozyme, suggesting nanoplastics may worsen ciprofloxacin's harmful effects on immune cells.
Nanoplastics (NPs) and ciprofloxacin (CIP), as emerging contaminants, widely coexist in the environment. Both NPs and CIP can accumulate in the spleen, suggesting a potential risk of immunotoxicity. However, studies on the mechanisms of immunotoxicity induced by combined exposure to NPs@CIP remain limited. The study found that NPs amplified the immunotoxic effects induced by CIP, manifested as splenocyte damage and conformational and functional changes in the immune factor lysozyme (LZM). At the cellular level, NPs exacerbated CIP-induced oxidative stress damage in splenocytes, as indicated by a burst in intracellular reactive oxygen species (ROS) levels (205.43% → 247.82%, +42.39%), increased consumption of superoxide dismutase (SOD) (52.20% → 48.77%, -3.44%), and greater accumulation of malondialdehyde (MDA) (179.95% → 190.25%, +10.30%), a final product of lipid peroxidation. This oxidative damage led to a further decrease in cell viability (54.05% → 48.09%, -5.96%), and exacerbated secretion of inflammatory cytokines TNF-α, IL-6, and IL-1β (+279.07, +25.28, +162.05 pg/mg prot), suggesting that oxidative stress not only induced splenocyte damage but triggered inflammatory responses. At the molecular level, we hypothesize that CIP adsorbed on the NP surface interacts with LZM, potentially forming an NPs-CIP-LZM ternary complex. This putative complex could exacerbate conformational and functional damage to LZM, manifesting as backbone denaturation, loosening of secondary structure, perturbation of the Trp microenvironment, and decreased enzymatic activity. This study provides mechanistic insights into the dual pathways through which NPs may amplify CIP-induced immunotoxicity, offering a theoretical basis for the mechanistic understanding of NPs toxicity and for risk evaluation strategies.
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