Disruption of Nrf2 signaling underlies oxidative stress and inflammatory injury induced by nitenpyram in Hyriopsis cumingii.

Authors

Qinglin Yang, Zhenzhen Feng, Huan Tang, Shaoyu Hu, Xiaobo Yu, Yanhong Li, Zhengli Wu

Published in

Journal of hazardous materials. Volume 515. Pages 143088. Jul 24, 2026. Epub Jul 24, 2026.

Abstract

Neonicotinoid pesticides (NNIs) are emerging aquatic contaminants, yet their toxicological mechanisms in bivalves remain insufficiently understood. In this study, the effects of nitenpyram (NTP) on Hyriopsis cumingii were investigated using integrated biochemical, metabolomic, and molecular approaches. Hemocyte assays revealed dose-dependent cytotoxicity, mitochondrial dysfunction, oxidative stress, and genotoxicity, while hepatopancreatic analyses demonstrated metabolic activation, sustained elevation of transaminase activities, and incomplete recovery following exposure. Metabolomic profiling further identified concentration-dependent alterations in amino acid, fatty acid, and antioxidant metabolism, with depletion of glutathione and L-acetylcarnitine highlighting mitochondrial vulnerability. Molecular docking suggested weak affinity of NTP for the examined nicotinic acetylcholine receptor subunits but stronger binding to HcKeap1, implying potential interference with HcNrf2-mediated antioxidant signaling. In line with this prediction, high-dose NTP exposure was associated with reduced HcNrf2 transcription, enhanced NF-κB-related inflammatory responses, and delayed recovery from hepatopancreatic injury. Pharmacological activation of HcNrf2 by tert-butylhydroquinone partially restored antioxidant capacity and mitigated inflammatory responses, suggesting a potential protective role of Nrf2 pathway modulation. Collectively, these findings suggest that oxidative stress, mitochondrial dysfunction, and metabolic disruption are prominent toxic responses to NTP in H. cumingii, while the measured endpoints provide limited evidence for classical cholinergic neurotoxicity and do not exclude other neurotoxic mechanisms. This work provides mechanistic insight into the ecological risks of NNIs and suggests potential strategies for mitigating pesticide-induced impacts in freshwater aquaculture.

PMID:
42508075
Bibliographic data and abstract were imported from PubMed on 28 Jul 2026.

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