The efficient capture of multi-pollutant residues in food is vital for food safety monitoring. In this study, in-situ-fabricated magnetic MIL-53(Al) metal organic frameworks (MOFs), with good magnetic responsiveness, were synthesized and applied for the magnetic solid-phase extraction (MSPE) of chloramphenicol, bisphenol A, estradiol, and diethylstilbestrol. Terephthalic acid (H₂BDC) organic ligands were pre-coupled on the surface of amino-Fe₃O₄ composites (H₂BDC@Fe₃O₄). Fe₃O₄@MIL-53(Al) MOF was fabricated by in-situ hydrothermal polymerization of H₂BDC, Al (NO₃)₃, and H₂BDC@Fe₃O₄. This approach highly increased the stability of the material. The magnetic Fe₃O₄@MIL-53(Al) MOF-based MSPE was combined with high-performance liquid chromatography-photo diode array detection, to establish a novel sensitive method for analyzing multi-pollutant residues in milk. This method showed good linear correlations, in the range of 0.05–5.00 μg/mL, with good reproducibility. The limit of detection was 0.004–0.108 μg/mL. The presented method was verified using a milk sample, spiked with four pollutants, which enabled high-throughput detection and the accuracies of 88.17–107.58% confirmed its applicability, in real sample analysis.

Bisphenol A (BPA) has emerged as a contaminant of concern because long-term exposure may affect the human endocrine system. Herein, a novel aptamer sensor based on magnetic separation and surface-enhanced Raman scattering (SERS) is proposed for the extremely sensitive and specific detection of trace BPA. Moreover, the capture unit was prepared by immobilizing thiolated (SH)-BPA aptamer complementary DNA on AuNP-coated magnetic halloysite nanotubes (MNTs@AuNPs), and SH-BPA aptamer-modified Au@4-MBA@Ag core–shell SERS nanotags acted as signal units. By the complementary pairing of the BPA aptamer and the corresponding DNA, MNTs@AuNPs and Au@4-MBA@AgCS were linked together through hybridization-ligation, which acted as the SERS substrate. In the absence of BPA, the constructed aptamer sensor generated electromagnetic enhancement and plasmon coupling to improve the sensitivity of SERS substrates. Owing to the high affinity between BPA and the aptamer, the aptamer probe bound to BPA was separated from the capture unit by an externally-induced magnetic field. Thus, the Raman intensity of the MNTs@AuNP-Ag@AuCS core–satellite assemblies was negatively correlated with the BPA concentration. High sensitivity measurements of BPA might be performed by determining the decline in SERS signal strength together with concentration variations. The proposed aptasensor is a promising biosensing platform for BPA detection.

Mycotoxins are secondary products produced primarily by fungi and are pathogens of animals and cereals, not only affecting agriculture and the food industry but also causing great economic losses. The development of rapid and sensitive methods for the detection of mycotoxins in food is of great significance for livelihood issues. This study employed an amino-functionalized zirconium luminescent metal–organic framework (LOF) (i.e., UiO-66-NH₂₎. Click chemistry was utilized to assemble UiO-66-NH₂ in a controlled manner, generating LOF assemblies to serve as probes for fluorescence-linked immunoassays. The proposed fluoroimmunoassay method for Zearalenone (ZEN) and Fumonisin B1 (FB1) detection based on the UiO-66-NH₂ assembled probe (CLICK-FLISA) afforded a linear response range of 1–20 μmol/L for ZEN, 20 μmol/L for FB1, and a very low detection limit (0.048–0.065 μmol/L for ZEN; 0.048–0.065 μmol/L for FB1). These satisfying results demonstrate promising applications for on-site quick testing in practical sample analysis. Moreover, the amino functionalization may also serve as a modification strategy to design luminescent sensors for other food contaminants.

Palytoxin (PTX), a toxin naturally synthesized by marine organisms like Palythoa, Ostreopsis and Trichodesmium spp. in tropical and temperate seas, bioaccumulates in fish and crustaceans, thereby exposing humans through the food chain. Although growing evidence highlights PTX's lethal hepatotoxicity, nephrotoxicity, and cardiotoxicity, its neurotoxic effects and the underlying mechanisms remain elusive. In this study, we assessed the cerebral neurotoxicity of PTX by using HT22 neuronal cells and a chronic mouse model, conducting a comprehensive analysis of phenotypic alterations and gene expression changes. Phenotypic analysis revealed significant damage to mitochondria, endoplasmic reticulum, and axons and disruptions in energy metabolism in PTX-treated neuronal cells and mouse brains. Transcriptome sequencing and real-time quantitative reverse transcription polymerase chain reaction indicated that key genes in the JNK/p38 MAPK signaling, mitochondrial stress, and endoplasmic reticulum stress pathways were significantly altered. Furthermore, pretreatment with JNK and p38 inhibitors significantly restored mitochondrial membrane potential, ATP content, and cell viability, while reducing the expression of pro-apoptotic genes in HT22 cells. These findings confirm that JNK/p38 MAPK signaling pathways activation, leading to mitochondrial stress, is a major contributor to PTX-induced neuronal cell death at the cellular level. Chronic exposure to PTX was shown to damage mammalian cerebral nerves, carrying a potential risk for neurodegenerative diseases. Our study provides insights into the environmental and health risks associated with PTX exposure and offers a foundation for risk assessment and intervention strategies.