We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Co-exposure to PFOA, PFBA and nanoplastics synergistically exacerbates neurotoxicity by impairing PINK1/Parkin-mediated mitophagy
AI summary Read the abstract
Researchers investigated the combined neurotoxic effects of two PFAS chemicals (PFOA and PFBA) with nanoplastics using zebrafish and human neuronal cells. They found that co-exposure synergistically worsened neurodevelopmental impairments and behavioral abnormalities by disrupting a key cellular cleanup pathway called PINK1/Parkin-mediated mitophagy. The study suggests that nanoplastics can amplify the neurotoxicity of PFAS compounds by impairing the cells' ability to clear damaged mitochondria.
Perfluorooctanoic acid (PFOA) and perfluorobutyric acid (PFBA), as representative long-chain and short-chain per- and polyfluoroalkyl substances (PFAS), are widely distributed in the environment. These compounds can interact with nanoplastics (NPs) to form complex mixed pollutants, posing potential threats to aquatic organisms and human health. The nervous system, characterized by high sensitivity and energy dependence, is particularly vulnerable to such pollutants. However, the mechanisms underlying neurological toxicity induced by co-exposure to PFOA, PFBA, and NPs remain largely unclear. In this study, zebrafish larvae and human neuroblastoma SH-SY5Y cells were employed as model systems to systematically evaluate the effects of PFOA and PFBA, alone or in combination with NPs, on neural development, behavior, cell viability, mitochondrial function, and autophagy. The results demonstrated that NPs exhibited a significantly higher adsorption capacity for PFOA than for PFBA, and that co-exposure exacerbated neurodevelopmental impairments, behavioral abnormalities, and reductions in cell viability. At the molecular level, co-exposure markedly inhibited the PINK1/Parkin-mediated mitophagy pathway, resulting in mitochondrial damage accumulation, disruption of energy metabolism, and blockade of autophagic flux. Through PINK1 overexpression and pharmacological activation experiments, the pivotal role of the PINK1/Parkin-mediated mitophagy pathway in mitigating neurotoxicity was functionally validated. Collectively, this study elucidates the molecular mechanism by which co-exposure to PFOA, PFBA, and NPs induces neurotoxicity via suppression of mitophagy. These findings identify a potential molecular target for the prevention and treatment of PFAS- and NPs-induced neurological injury and provide valuable theoretical and experimental evidence for evaluating the neurotoxic risks of mixed environmental pollutants.
More Papers Like This
The mitochondrial fission-mitophagy axis drives neuronal S-phase arrest and hippocampal damage in co-exposure to polystyrene nanoplastics and lead
AI summary Read the abstract
Researchers found that polystyrene nanoplastics facilitated lead accumulation in hippocampal neurons via clathrin-mediated endocytosis, and that co-exposure — but not either stressor alone — synergistically triggered S-phase cell cycle arrest, oxidative stress, and memory deficits in mice by driving excessive mitochondrial fission and activating the PINK1/Parkin mitophagy pathway.
Adverse effects of polystyrene nanoplastic and its binary mixtures with nonylphenol on zebrafish nervous system: From oxidative stress to impaired neurotransmitter system
AI summary Read the abstract
Researchers investigated the individual and combined effects of polystyrene nanoplastics and the industrial chemical nonylphenol on the zebrafish nervous system over 45 days. Both substances induced oxidative stress and disrupted neurotransmitter systems, with combined exposure generally producing more severe effects on glutamate metabolism and brain tissue damage. The study suggests that the interaction between nanoplastics and co-occurring environmental pollutants can amplify neurotoxic effects in fish.
Nanoplastics drive toxicity under co-exposure with perfluorooctanesulfonic acid in human intestinal cells
AI summary Read the abstract
Researchers exposed human intestinal cells to nanoplastics, the industrial chemical PFOS, and their combination, and found that co-exposure caused more severe cellular disruption than either substance alone. Nanoplastics primarily damaged mitochondria while PFOS affected cell membranes and internal structures, and their combination triggered broader metabolic changes including disrupted amino acid and lipid metabolism. The study suggests that the interaction between nanoplastics and common environmental chemicals may pose compounding risks to gut health.
Enhanced neurotoxic effect of PCB-153 when co-exposed with polystyrene nanoplastics in zebrafish larvae
AI summary Read the abstract
Researchers found that when zebrafish larvae were exposed to both polystyrene nanoplastics and the toxic chemical PCB-153 together, the neurological damage was significantly worse than from either pollutant alone. The combined exposure caused hyperactive swimming behavior and suppressed immune, brain, and detoxification pathways at the genetic level. This is concerning because nanoplastics and persistent organic pollutants frequently co-exist in the environment, meaning their real-world health effects on aquatic life and humans may be greater than studies of single pollutants suggest.
Combined toxicity of polyethylene micro/nanoplastics and PFOA in zebrafish (Danio rerio): Impacts on antioxidant, neurotransmission, and gut microbiota
AI summary Read the abstract
Researchers exposed zebrafish to polyethylene micro/nanoplastics and the industrial pollutant PFOA individually and in combination, assessing antioxidant capacity, neurotransmission, and gut microbiome composition. Combined exposure caused greater oxidative stress, more severe neurotransmitter disruption, and larger gut microbiome shifts than either contaminant alone, highlighting synergistic risks of co-occurring plastic and PFAS pollution.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.