Parthanatos is a caspase-independent form of programmed cell death triggered by PARP-1 overactivation and mitochondrial dysfunction, implicated in neurodegenerative diseases. In this study, we performed a proteomic analysis of SH-SY5Y neuronal cells undergoing parthanatos and evaluated the neuroprotective effects of sodium perborate tetrahydrate (SPT), an inorganic boron-containing compound. LC-MS/MS analysis revealed significant alterations in mitochondrial respiration, DNA repair, and inflammatory signaling pathways. Proteins such as MT-CO2, CYC1, POLR2L, and SLC25A5 -implicated in Parkinson's and Huntington's disease pathways- were found to be dysregulated. SPT pre-treatment led to reduced PARP-1 activation, decreased DNA fragmentation, and improved cell viability. These findings suggest that boron-containing inorganics, as metalloids, can modulate molecular targets involved in neuronal survival. Our study contributes novel experimental evidence on the biochemical effects of boron compounds in neurodegenerative processes, complementing current research in metalloid-biomolecule interactions and supporting their potential utility in therapeutic development for neurodegenerative diseases.
Keywords: Boron; Methylnitrosoguanidine (MNNG); Neurodegenerative diseases; Parthanatos; Proteomics; Sodium perborate tetrahydrate (SPT).
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