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Nanoplastics amplify ciprofloxacin-induced immunotoxicity: Oxidative stress in splenocytes and conformational and functional changes in lysozyme.

Created on 29 Sep 2026

Authors

Qianyue Yin, Yuntao Qi, Xiangxiang Li, Shuqi Guo, Shaoyang Hu, Xingchen Zhao, Wansong Zong, Jixin Su, Rutao Liu

Published in

Environmental pollution (Barking, Essex : 1987). Pages 129256. Sep 28, 2026. Epub Sep 28, 2026.

Abstract

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.

PMID:
42805500
Bibliographic data and abstract were imported from PubMed on 29 Sep 2026.

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