Nanoplastics Disrupt Energy Metabolism in Brain Cells

Scientists from the Trinity Biomedical Sciences Institute (TBSI) have discovered how nanoplastics – even smaller than microplastics – disrupt energy metabolism in brain cells. Their findings may have implications for better understanding neurodegenerative diseases characterised by declining neurological or brain function, and even shed new light on issues with learning and memory.

The study, led by Dr Gavin Davey and undergraduate Devin Seward from Trinity’s School of Biochemistry and Immunology, has revealed the specific mechanism by which these tiny nanoplastics can interfere with energy production in the brain in an animal model. The findings, recently published in the Journal of Hazardous Materials: Plastics, provide fresh insights into the potential health risks posed by environmental plastics.

Polystyrene nanoplastics (PS-NPs) are produced when larger plastics break down in the environment. These particles have been detected in multiple organs in the body, including the brain, sparking growing concerns about their possible role in neurological disease.

The Trinity team focused on mitochondria, the “powerhouses” of cells, which are critical for producing the energy needed for brain function. Mitochondrial dysfunction is a well-known feature of neurodegenerative diseases such as Parkinson’s and Alzheimer’s, as well as normal ageing.

By isolating mitochondria from brain cells, the researchers showed that exposure to PS-NPs specifically disrupted the “electron transport chain”, a simplified term for the set of protein complexes that work together to help generate cellular energy in the form of ATP. While individual mitochondrial complexes I and II were not directly impaired, electron transfer between complexes I–III and II–III, as well as the activity of complex IV, was significantly inhibited.

And although some of the concentrations of PS-NPs used in the study were higher than current estimates of human exposure the scientists found that electron transfer between complex I–III and complex II–III was potently inhibited at much lower concentrations, suggesting environmentally relevant exposures could also impair bioenergetic function over chronic timeframes.

Interestingly, the same broad effects were seen in synaptic mitochondria, which are essential for communication between brain cells. This suggests that nanoplastics could also interfere with synaptic plasticity, a process fundamental to learning and memory.

Dr Gavin Davey, who is based in the Trinity Biomedical Sciences Institute, said: “Importantly, the rise of synthetic plastics in the mid-20th century coincided with an increased global exposure to nanoplastics, so this newly discovered mitochondrial mechanism of nanoplastic-induced neurotoxicity may therefore help to explain why rates of neurodegenerative diseases have risen in recent decades, likely adding an environmental dimension to the known genetic and lifestyle risk factors.”