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Aromatic Surface Geometry as a Primary Mechanism of Nanoplastic Endocrine Disruption: A Cyclodextrin Competition Hypothesis
Summary
This research investigated selective colonization of microplastics by antimicrobial-resistant bacteria and mobile genetic elements, using culture-based and molecular methods to characterize resistance profiles. The study demonstrates that plastic surfaces can act as selective environments for antimicrobial resistance enrichment in aquatic ecosystems.
Microplastics and nanoplastics have been confirmed in human ovarian follicular fluid, seminal fluid, placental tissue, and reproductive organs, where they correlate with disrupted steroidogenesis and altered gonadotropin signaling. Established mechanistic pathways — mitochondrial dysfunction, PI3K/AKT inhibition, epigenetic modification, and disruption of the LH/cAMP/PKA/StAR axis — explain upstream steroidogenesis interference but do not account for the polymer-specific affinity between polystyrene particles and estrogen receptor α documented by surface plasmon resonance, in which polystyrene shows greater binding affinity than PVC or polyethylene. This polymer hierarchy is consistent with aromatic surface recognition: polystyrene has the highest density of pendant phenyl rings among common environmental plastics. This paper proposes a complementary receptor-level mechanism: polystyrene nanoplastic surface phenyl groups interact with the aromatic ligand-binding cavities of steroid hormone receptors through CH-π and hydrophobic contacts — the same mechanism class that governs steroid hormone recognition. This geometric surface mimicry may interfere with receptor access by steroid hormones without generating an activation signal. In vivo support comes from zebrafish studies showing that PS nanoplastic effects on neurotransmitter signaling and brain apoptosis are reversed by the ER antagonist ICI 182,720, confirming ER pathway dependence independent of additive leaching. β-cyclodextrin, whose hydrophobic cavity captures aromatic molecules through the same CH-π mechanism, is proposed as a competitive sequestrant of polystyrene aromatic surface groups. The cyclodextrin rescue experiment is presented as the critical distinguishing test between receptor-level geometric interference and upstream intracellular mechanisms, which would not be expected to respond to cyclodextrin competition. No clinical claims are made.