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Influence of microplastics on bisphenol A and bisphenol AF toxicity in aquatic environments: Mechanistic insights for environmental risks
Summary
Researchers investigated how polyethylene microplastics interact with the industrial chemicals bisphenol A and bisphenol AF in zebrafish, finding that microplastics can either reduce or worsen the toxicity depending on the specific chemical and biological pathway involved. For bisphenol A, the microplastics partially absorbed the chemical and reduced its harmful effects, but for bisphenol AF, they worsened toxicity to certain organ systems. The study reveals that microplastics play a complicated dual role in modifying how other pollutants affect aquatic life.
Co-exposure to low-density polyethylene microplastics (LDPE-MPs) and plastic additives like bisphenol A (BPA) and bisphenol AF (BPAF) poses a growing concern in aquatic environments, yet the role of LDPE-MPs in modulating their toxicity remains debated. This study integrates transcriptome sequencing, adsorption/desorption kinetics, and computational toxicology to assess how LDPE-MPs influence BPA- and BPAF-induced toxicity in zebrafish. We found that BPAF is more toxic than BPA, with 96 h lethal concentration 50 % (LC) values of 1.659 mg/L for BPAF and 6.219 mg/L for BPA. LDPE-MPs act as dual modulators, alleviating or exacerbating toxicity in a chemical- and pathway-dependent manner. For BPA, LDPE-MPs mitigate its impact on phototransduction by adsorbing BPA, reducing its bioavailability, and preserving light signal conversion. In contrast, LDPE-MPs exacerbate BPA-induced nucleotide metabolism disruptions by enhancing inosine-5'-monophosphate dehydrogenase (IMPDH) activity, leading to increased gene transcription and accumulation of metabolic intermediates. For BPAF, LDPE-MPs alleviate glucose metabolism disruptions by enhancing ligand-receptor interactions, restoring glucose homeostasis. However, LDPE-MPs have little effect on BPAF-induced upregulation of steroid biosynthesis genes. These findings highlight the integration of multi-omics approaches (transcriptome sequencing, adsorption/desorption kinetics, and computational toxicology) to reveal the dual mechanisms of LDPE-MPs, addressing the knowledge gap in understanding pathway-specific toxicity mechanisms in existing studies. The results emphasize the necessity of prioritizing regulatory control of BPAF and integrating BPA/BPAF-MPs interactions into future pathway-based environmental risk assessment frameworks.