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Polyethylene terephthalate (PET) micro- and nanoplastic particles affect the mitochondrial efficiency of human brain vascular pericytes without inducing oxidative stress
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Researchers exposed human brain blood vessel cells to PET plastic particles (the same plastic used in water bottles) at micro and nano sizes. After three days, the cells showed reduced energy production in their mitochondria, the powerhouses of the cell, but recovered by six days. While no oxidative stress or cell death was observed, the temporary disruption of brain cell energy production raises questions about what repeated or chronic exposure might do.
The objective of this investigation was to evaluate the influence of micro- and nanoplastic particles composed of polyethylene terephthalate (PET), a significant contributor to plastic pollution, on human brain vascular pericytes. Specifically, we delved into their impact on mitochondrial functionality, oxidative stress, and the expression of genes associated with oxidative stress, ferroptosis and mitochondrial functions. Our findings demonstrate that the exposure of a monoculture of human brain vascular pericytes to PET particles in vitro at a concentration of 50 μg/ml for a duration of 3, 6 and 10 days did not elicit oxidative stress. Notably, we observed a reduction in various aspects of mitochondrial respiration, including maximal respiration, spare respiratory capacity, and ATP production in pericytes subjected to PET particles for 3 days, with a mitochondrial function recovery at 6 and 10 days. Furthermore, there were no statistically significant alterations in mitochondrial DNA copy number, or in the expression of genes linked to oxidative stress and ferroptosis, but an increase of the expression of the gene mitochondrial transcription factor A (TFAM) was noted at 3 days exposure. These outcomes suggest that, at a concentration of 50 μg/ml, PET particles do not induce oxidative stress in human brain vascular pericytes. Instead, at 3 days exposure, PET exposure impairs mitochondrial functions, but this is recovered at 6-day exposure. This seems to indicate a potential mitochondrial hormesis response (mitohormesis) is incited, involving the gene TFAM. Further investigations are warranted to explore the stages of mitohormesis and the potential consequences of plastics on the integrity of the blood-brain barrier and intercellular interactions. This research contributes to our comprehension of the potential repercussions of nanoplastic pollution on human health and underscores the imperative need for ongoing examinations into the exposure to plastic particles.
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Polyethylene terephthalate (PET) micro- and nanoplastic particles affect the mitochondrial efficiency of human brain vascular pericytes without inducing oxidative stress
AI summary Read the abstract
Polyethylene terephthalate (PET) micro- and nanoplastic particles were found to impair mitochondrial efficiency, increase oxidative stress, and alter expression of oxidative stress and ferroptosis-related genes in human brain vascular pericytes.
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This review pulled together existing animal studies on tiny plastic particles (polyethylene microplastics, common in packaging and everyday products) and found a consistent pattern: these particles seem to damage mitochondria, the "power plants" inside our cells, and trigger harmful oxidative stress, which can wear down tissues over time. Since this research is in rodents, not humans, more studies are needed to confirm the same effects happen in people, but the findings raise real concerns about how the microplastics we're increasingly exposed to might affect long-term cellular health and energy production in our bodies.
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