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Zinc oxide nanoparticles damage the prefrontal lobe in mouse: Behavioral impacts and key mechanisms
Dan Zhang1, Zhiyuan Wang2, Hongmei Deng2
1Key Laboratory of Medical Electrophysiology, Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, and Collaborative Innovation Center for Prevention of Cardiovascular Diseases, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, China; Department of Rehabilitation Medicine, Southwest Medical University, Luzhou, China.
Abstract:
Zinc Oxide nanoparticles (ZnO NPs) have dualistic properties due to their advantage and toxicity. However, the impact and mechanisms of ZnO NPs on the prefrontal lobe have limited research. This study investigates the behavioral changes following exposure to ZnO NPs (34 mg/kg, 30 days), integrating multiple behaviors and bioinformatics analysis to identify critical factors and regulatory mechanisms. The essential differentially expressed genes (DEGs) were identified, including ORC1, DSP, AADAT, SLITRK6, and STEAP1. Analysis of the DEGs based on fold change reveals that ZnO NPs primarily regulate cell survival, proliferation, and apoptosis in neural cells, damaging the prefrontal lobe. Moreover, disruption of cell communication, mineral absorption, and immune pathways occurs. Gene set enrichment analysis (GSEA) further shows enrichment of behavior, neuromuscular process, signal transduction in function, synapses-related, cAMP signaling, and immune pathways. Furthermore, alternative splicing (AS) genes highlight synaptic structure/function, synaptic signal transduction, immune responses, cell proliferation, and communication.
