Polyethylene terephthalate (PET) micro- and nanoplastic particles affect the mitochondrial efficiency of human brain vascular pericytes without inducing oxidative stress

Tools

Gettings, Sean M. and Timbury, William and Dmochowska, Anna and Sharma, Riddhi and McGonigle, Rebecca and MacKenzie, Lewis E. and Miquelard-Garnier, Guillaume and Bourbia, Nora (2024) Polyethylene terephthalate (PET) micro- and nanoplastic particles affect the mitochondrial efficiency of human brain vascular pericytes without inducing oxidative stress. NanoImpact, 34. 100508. ISSN 2452-0748 (https://doi.org/10.1016/j.impact.2024.100508)

[thumbnail of Gettings-etal-NanoImpact-2024-micro-and-nanoplastic-particles-affect-the-mitochondrial-efficiency-of-human-brain-vascular-pericytes]
Preview
 Text. Filename: Gettings-etal-NanoImpact-2024-micro-and-nanoplastic-particles-affect-the-mitochondrial-efficiency-of-human-brain-vascular-pericytes.pdf
Final Published Version
License: Creative Commons Attribution 4.0 logo
Download (6MB)| Preview

Abstract

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.

ORCID iDs

Gettings, Sean M., Timbury, William, Dmochowska, Anna, Sharma, Riddhi, McGonigle, Rebecca, MacKenzie, Lewis E. ORCID logoORCID: https://orcid.org/0000-0002-8151-0525, Miquelard-Garnier, Guillaume and Bourbia, Nora;
CORE (COnnecting REpositories)