Molecular Basis by Which PVC Nanoplastics Elicit Neurotoxic Outcomes

Polyvinyl chloride (PVC) nanoplastics (NPs) exposure in humans is neurotoxic. To underscore the possible mechanisms by which PVC NPs provoke neurotoxic outcomes, we have explored the interfacial interactions between PVC NPs and biological assemblies. Our results reveal that exposure to PVC NPs induces dose-dependent alterations in the spectroscopic signatures (UV-vis, fluorescence, and IR) of the model globular protein β-lactoglobulin (BLG). The nanoplastics-driven perturbations in BLG secondary and tertiary structure were accompanied by compromised retinol (Vitamin A) binding (necessary for neurological development). Furthermore, in the amyloidogenic model hen egg-white lysozyme (HEWL), PVC NPs exacerbated its rate of fibril formation. Exposure of PVC NPs to Caenorhabditis elegans (C. elegans) resulted in the ablation of dopaminergic (DA) neurons and compromised locomotion in a manner akin to that elicited by the neurotoxin paraquat. Collectively, the findings provide molecular- and systems-level evidence of the seqelae by which PVC NPs may initiate neurotoxic outcomes. The results may drive the development of more biocompatible NPs and shape public policy.