Glutamate synaptic pathway plays an important role in neodymium oxide-incduced oxidative stress and inflammation of the brain

Introduction Rare earth elements (REEs) are increasingly used across various industries, raising concerns regarding their potential health impacts. Exposure to REEs has been linked to systemic diseases affecting the respiratory, nervous, and immune systems. We aimed to explore the effects of REE exposure on neurological health. Methods We performed high-throughput sequencing to identify differentially expressed proteins in the plasma of REE-exposed patients compared to healthy individuals. Additionally, in the mouse model, we employed western blotting, quantitative real-time PCR (qRT-PCR), and kits to verify the association between REE exposure and brain damage. Results We identified 144 differentially expressed proteins in the plasma of REE-exposed patients. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated that these proteins were primarily related to synaptic functions and the glutamate synaptic pathway. A protein–protein interaction network constructed using the STRING database revealed strong interactions among brain injury-related proteins following REE exposure. In animal experiments, western blot analysis showed that exposure to Nd 2 O 3 significantly increased protein levels of calcium channel voltage-dependent P/Q-type alpha 1A subunit, phospholipase A2 group IVA, and SH3 and multiple ankyrin repeat domains 1. qRT-PCR results confirmed increased expression of corresponding genes. Concurrently, elevated levels of malondialdehyde and nitric oxide and decreased total antioxidant capacity were observed. Discussion Overall, our findings suggest that Nd 2 O 3 exposure is closely associated with brain damage, and the glutamate synaptic pathway plays a significant role. Our study provides novel insights into the molecular mechanisms underlying Nd 2 O 3 -induced neurotoxicity.