We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Brain lipidomics identifies mitochondrial redox dysfunction and metabolic trade-offs associated with Parkinson’s disease-like pathology induced by Nanoplastics exposure
Summary
Using high-resolution lipidomics in Drosophila chronically exposed to polystyrene nanoplastics, researchers found dose-dependent remodeling of mitochondrial membrane lipids—particularly cardiolipins—along with increased fat storage molecules and signs of Parkinson's disease-like metabolic dysfunction.
Abstract Growing nanoplastics exposure raises concern for neurotoxicity, particularly given recent evidence of plastic accumulation within human brain tissue-a highly lipid enriched organ, yet effects on brain lipid metabolism remains poorly understood. Here, we employed high-resolution untargeted lipidomics to map brain lipid perturbations in Drosophila melanogaster chronically exposed to environmentally relevant levels of polystyrene nanoplastics (NPs). Polystyrene NPs accumulated in fly brains and induced dose-dependent remodeling of mitochondrial membrane lipids, notably cardiolipins and phosphatidylethanolamines, accompanied by increased diacylglycerols/triacylglycerols and monounsaturated fatty acids and by lipid droplet expansion. Guided by these lipidomic signatures, targeted biochemical assays demonstrated depolarized mitochondrial membrane potential, elevated mitochondrial reactive-oxygen species, inhibition of respiratory-chain complexes I and IV, and a shift in NAD(H) and NADP(H) redox couples toward a reduced state and increasing lipid peroxidation. This redox imbalance was accompanied by decreased tyrosine-hydroxylase expression, dopamine depletion, and impaired locomotor behavior, hallmarks of PD-like neurodegeneration. Dopaminergic neurochemistry was impaired (tyrosine hydroxylase and dopamine decreased), with concomitant reduction of GABA, and locomotor and circadian deficits emerged. Remarkbly, co-treatment with the antioxidant N-acetylcysteine (NAC) restored mitochondrial membrane potential, reduced mitochondrial ROS and lipid peroxidation, normalized neutral lipid and MUFA accumulation, and rescued neurotransmitter levels and behavior. Stable-isotope tracing confirmed disrupted TCA cycle flux after NP exposure that was rescued by NAC. Collectively, these findings reveal lipidomic remodeling as a critical link between environmental nanoplastic exposure and PD-like pathology, highlighting mitochondrial redox–lipid interactions as early determinants and support redox-directed interventions to mitigate risk.
Sign in to start a discussion.
More Papers Like This
Brain single-nucleus transcriptomics highlights that polystyrene nanoplastics potentially induce Parkinson’s disease-like neurodegeneration by causing energy metabolism disorders in mice
In a mouse study, oral exposure to polystyrene nanoplastics caused brain changes resembling Parkinson's disease, including loss of dopamine-producing neurons and movement problems. Advanced single-cell brain analysis revealed that the nanoplastics disrupted energy production in brain cells, particularly in the brain regions most affected by Parkinson's disease. This research raises the alarming possibility that chronic nanoplastic exposure through food and water could contribute to neurodegenerative diseases.
Environmentally relevant concentrations of polystyrene nanoplastics induce Parkinson’s-like neurotoxicity in C. elegans via oxidative stress
Researchers exposed roundworms to environmentally realistic concentrations of polystyrene nanoplastics and observed movement problems and brain changes resembling Parkinson's disease. The nanoplastics selectively damaged dopamine-producing neurons and increased toxic protein clumping through oxidative stress, and when an antioxidant treatment was applied, it partially reversed the harmful effects.
Size-Dependent Disruption of Lipid Metabolism by Polystyrene Micro- and Nanoplastics in Caenorhabditis elegans Revealed Through Multi-Omics and Functional Genetic Validation
Researchers used the model organism C. elegans to study how polystyrene particles of different sizes affect lipid metabolism, finding that both 100-nanometer and 1-micrometer particles disrupted fat storage and lipid processing. Multi-omics analysis identified four core genes governing the size-dependent metabolic disruption, and elevated levels of specific lipid metabolites confirmed that microplastics can meaningfully interfere with lipid homeostasis.
Metabolic effects of dietary exposure to polystyrene microplastic and nanoplastic in fruit flies
Researchers used fruit flies as a model organism to study the metabolic effects of ingesting polystyrene microplastic and nanoplastic particles at environmentally relevant doses. They found that both particle sizes disrupted metabolic processes, with nanoplastics causing more pronounced changes in energy storage and lipid metabolism. The study suggests that dietary exposure to plastic particles, even at levels found in the environment, can meaningfully alter metabolic physiology.
Micro-nanoplastics and Parkinson’s disease: evidence and perspectives
Researchers reviewed growing evidence linking micro- and nanoplastic exposure to Parkinson's disease, a degenerative brain condition. Lab studies suggest these particles may accelerate disease by promoting the misfolding of a key brain protein (alpha-synuclein), triggering inflammation, and damaging mitochondria — though large-scale human studies are still needed to establish causation and define safe exposure thresholds.