RESUMO
Given the commercial proliferation of silicon quantum dots (SiQDs) and their inevitable environmental dispersal, this study critically examines their biological and public health implications, specifically regarding Parkinson's disease. The study investigated the toxicological impact of SiQDs on the onset and development of PD-like symptoms through the induction of ferroptosis, utilizing both in vivo [Caenorhabditis elegans (C. elegans)] and in vitro (SH-SY5Y neuroblastoma cell line) models. Our findings demonstrated that SiQDs, characterized by their stable and water-soluble physicochemical properties, tended to accumulate in neuronal tissues. This accumulation precipitated dopaminergic neurodegeneration, manifested as diminished dopamine-dependent behaviors, and escalated the expression of PD-specific genes in C. elegans. Importantly, the results revealed that SiQDs induced ferritinophagy, a selective autophagy pathway that triggered ferroptosis and resulted in PD-like symptoms, even exacerbating disease progression in biological models. These insights were incorporated into a putatively qualitative and quantitative adverse outcome pathway framework, highlighting the serious neurodegenerative risks posed by SiQDs through ferroptosis pathways. This study provides a multidisciplinary analysis critical for informing policy on the regulation of SiQDs exposure to safeguard susceptible populations and guiding the responsible development of nanotechnologies impacting environmental and public health.