Nanoplastics possess the capacity for cellular internalization, and consequentially disrupt mitochondrial functionality, precipitating aberrations in energy metabolism. Given this, the potential accumulation of nanoplastics in alimentary sources presents a considerable hazard to the mammalian gastrointestinal system. While mitophagy serves as a cytoprotective mechanism that sustains redox homeostasis through the targeted removal of compromised mitochondria, the regulatory implications of mitophagy in nanoplastic-induced toxicity remain an underexplored domain. In the present investigation, polystyrene (PS) nanoparticles, with a diameter of 80 nm employed as a representative model to assess their toxicological impact and propensity to instigate mitophagy in intestinal cells both in vitro and in vivo. Data indicated that PS nanoparticles elicited BNIP3/NIX-mediated mitophagy within the intestinal milieu. Strikingly, the impediment of this degradation process at elevated concentrations was correlated with exacerbated pathological ramifications. In vitro assays corroborated that high-dosage cellular uptake of PS nanoparticles obstructed the mitophagy pathway. Furthermore, treatment with PS nanoparticles engendered alterations in gut microbiota composition and manifested a proclivity to modulate nutritional metabolism. Collectively, these findings elucidate that oral exposure to PS nanoparticles culminates in the inhibition of mitophagy and induces perturbations in the intestinal microbiota. This contributes valuable insights into the toxicological repercussions of nanoplastics on mammalian gastrointestinal health.
Keywords: Gut microbiota; Intestinal toxicity; Mitophagy; Polystyrene nanoparticles.
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