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

Sean M Gettings; William Timbury; Anna Dmochowska; Riddhi Sharma; Rebecca McGonigle; Lewis E MacKenzie; Guillaume Miquelard-Garnier; Nora Bourbia

doi:10.1016/j.impact.2024.100508

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

NanoImpact. 2024 Apr 23:34:100508. doi: 10.1016/j.impact.2024.100508. Online ahead of print.

Authors

Sean M Gettings¹, William Timbury¹, Anna Dmochowska², Riddhi Sharma¹, Rebecca McGonigle³, Lewis E MacKenzie³, Guillaume Miquelard-Garnier², Nora Bourbia⁴

Affiliations

¹ UK Health Security Agency, Radiation Effects Department, Radiation Protection Science Division, Harwell Science Campus, Didcot, Oxfordshire OX11 0RQ, UK.
² Laboratoire PIMM, CNRS, Arts et Métiers Institute of Technology, Cnam, HESAM Universite, 75013 Paris, France.
³ Department of Pure and Applied Chemistry, University of Strathclyde, Glasgow G1 1RD, UK.
⁴ UK Health Security Agency, Radiation Effects Department, Radiation Protection Science Division, Harwell Science Campus, Didcot, Oxfordshire OX11 0RQ, UK. Electronic address: nora.bourbia@ukhsa.gov.uk.

PMID: 38663501
DOI: 10.1016/j.impact.2024.100508

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.

Keywords: Microplastic; Mitochondria; Nanoplastic; Oxidative stress; PET; Pericytes; Polyethylene terephthalate.