Tissue-specific distribution and bioaccumulation of perfluoroalkyl acids, isomers, alternatives, and precursors in citrus trees of contaminated fields: Implication for risk assessment.

The ingestion of fruits containing perfluoroalkyl acids (PFAAs) presents potential hazards to human health. This study aimed to fill knowledge gaps concerning the tissue-specific distribution patterns and bioaccumulation behavior of PFAAs and their isomers, alternatives, and precursors (collectively as per-/polyfluoroalkyl substances, PFASs) within citrus trees growing in contaminated fields. It also assessed the potential contribution of precursor degradation to human exposure risk of PFASs. High concentrations of total target PFASs (∑PFASstarget, 92.45-7496.16 ng/g dw) and precursors measured through the total oxidizable precursor (TOP) assay (130.80-13979.21 ng/g dw) were found in citrus tree tissues, and short-chain PFASs constituted the primary components. The total PFASs concentrations followed the order of leaves > fruits > branches, bark > wood, and peel > pulp > seeds. The average contamination burden of peel (∑PFASstarget: 57.75%; precursors: 71.15%) was highest among fruit tissues. Bioaccumulation factors (BAFs) and translocation potentials of short-chain, branched, or carboxylate-based PFASs exceeded those of their relatively hydrophobic counterparts, while ether-based PFASs showed lower BAFs than similar PFAAs in above-ground tissues of citrus trees. In the risk assessment of residents consuming contaminated citruses, precursor degradation contributed approximately 36.07% to total PFASs exposure, and therefore should not be ignored.

2,3,4',5-Tetrahydroxystilbene-2-O-ß-D-Glucoside (THSG) Activates the Nrf2 Antioxidant Pathway and Attenuates Oxidative Stress-Induced Cell Death in Mouse Cochlear UB/OC-2 Cells.

Oxidative stress plays a critical role in the pathogenesis of hearing loss, and 2,3,4',5-tetrahydroxystilbene-2-O-ß-D-glucoside (THSG) exerts antioxidant effects by inhibiting reactive oxygen species (ROS) generation. With the aim of developing new therapeutic strategies for oxidative stress, this study investigated the protective mechanism of THSG in vitro using a normal mouse cochlear cell line (UB/OC-2). The THSG and ascorbic acid have similar free radical scavenger capacities. H2O2, but not THSG, reduced the UB/OC-2 cell viability. Moreover, H2O2 might induce apoptosis and autophagy by inducing morphological changes, as visualized by microscopy. As evidenced by Western blot analysis and monodansylcadaverine (MDC) staining, THSG might decrease H2O2-induced autophagy. According to a Western blotting analysis and Annexin V/PI and JC-1 staining, THSG might protect cells from H2O2-induced apoptosis and stabilize the mitochondrial membrane potential. Furthermore, THSG enhanced the translocation of nucleus factor erythroid 2-related factor 2 (Nrf2) into the nucleus and increased the mRNA and protein expression of antioxidant/detoxifying enzymes under H2O2-induced oxidative stress conditions. Collectively, our findings demonstrate that THSG, as a scavenging agent, can directly attenuate free radicals and upregulate antioxidant/detoxifying enzymes to protect against oxidative damage and show that THSG protects UB/OC-2 cells from H2O2-induced autophagy and apoptosis in vitro.