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Nanoplastics and Benzo[a]pyrene Co-pollution aggravates pulmonary ferroptosis via endoplasmic reticulum stress-triggered IRE1α liquid-liquid phase separation
Original title: Nanoplastics and Benzo[a]pyrene Co-pollution aggravates pulmonary ferroptosis via endoplasmic reticulum stress-triggered IRE1α liquid-liquid phase separation
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Tiny plastic particles floating in the air can act like tiny taxis, ferrying a harmful chemical found in car exhaust and smoke (benzo[a]pyrene) deeper into our lung cells than it could get on its own. Once inside, this combo triggers a chain reaction of cell stress that damages lung cells' natural defenses and pushes them toward a harmful type of cell death. This matters because it suggests that breathing in plastic pollution alongside common air pollutants like exhaust fumes could be more damaging to our lungs than either one alone.
Nanoplastics (NPs) and polycyclic aromatic hydrocarbons (PAHs), owing to strong hydrophobic interactions, commonly coexist as complex pollutants in atmospheric environments. Despite their widespread presence, the mechanisms underlying the inhalation toxicity of NP-PAH complexes remain poorly understood. This study investigates the cooperative effects of environmentally relevant concentrations of polyethylene terephthalate (PET) NPs and Benzo[a]pyrene (BaP) on pulmonary toxicity. The results show that NPs act as carriers that enhance cellular internalization and accumulation of BaP, thereby intensifying lung injury through synergistic effects. Mechanistic analyses indicate that NPs promote BaP translocation into the endoplasmic reticulum (ER), aggravating the unfolded protein response (UPR) within the ER lumen and worsening ER dysfunction. ER stress induces the formation of inositol-requiring enzyme 1α (IRE1α) condensates via liquid-liquid phase separation (LLPS), a process markedly enhanced by BaP through direct interaction with IRE1α. Co-condensation of BaP and IRE1α significantly increases IRE1α activity toward X-box binding protein 1 (XBP1) splicing. This activation leads to transcriptional upregulation of E3 ubiquitin-protein ligase synoviolin (SYVN1). Further evidence indicates that SYVN1-mediated ubiquitination of nuclear factor erythroid 2-related factor 2 (Nrf2) suppresses its cytoprotective function, thereby increasing cellular susceptibility to ferroptosis. Collectively, these findings provide insight into the compound toxicity of BaP and NPs and explain how combined pollutants induce lung injury through ER stress-triggered ferroptosis.
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