N-ethyl perfluorooctane sulfonamidoethanol (N-EtFOSE), a known volatile perfluorooctane sulfonate (PFOS) precursor (PreFOS), has been widely detected in the environment. However, the mechanisms underlying the behaviors and phytotoxicity of N-EtFOSE in plants are unknown. Integrative physio-biochemical and transcriptomic analyses were used to reveal the accumulation, biotransformation, and toxicity of N-EtFOSE in pakchoi ( Brassica chinensis L . ) through root and foliar exposure experiments. Root uptake from exposure medium and efficient translocation to shoot, and foliar uptake from air and inefficient root transfer of N-EtFOSE were observed. N-EtFOSE was biotransformed into various PreFOSs and ultimately into PFOS, with N-ethyl perfluorooctane sulfonamide (N-EtFOSA) identified as the major intermediate. Enzyme assays and gene expression analyses indicated that this biotransformation was mediated by alcohol dehydrogenase, aldehyde dehydrogenase, cytochrome P450, glutathione S-transferase, and ATP-binding cassette transporters. N-EtFOSE led to inhibition of plant growth, photosynthetic rate, and respiration rate, as well as to lipid peroxidation, oxidative damage and subcellular damage. Transcriptomic analysis revealed that differentially expressed genes (DEGs) mainly relative to plant endogenous phytohormones homeostasis, regulation of photosynthesis and respiration, oxidative stress, and xenobiotic metabolism and detoxification. This study highlighted the degradation and stress response mechanisms of N-EtFOSE in plants, providing important information to evaluate the environmental risks of volatile per/polyfluoroalkyl substances (PFASs).
Shuyan Zhao,Tianqi Liu,Bohui Wang,Jia Fu,Tiankun Liang,Zhe Zhong,Jingjing Zhan,Lifen Liu
While N-ethyl perfluorooctane sulfonamidoethanol (EtFOSE) is a precursor of perfluorooctane sulfonate (PFOS), its bioaccumulation, transformation and toxicological effects in earthworms ( Eisenia fetida ) exposed to quartz sands are poorly understood. The present study showed that except for parent EtFOSE, N-ethylperfluorooctane sulfonamide acetate (EtFOSAA), N-ethyl perfluorooctane sulfonamide (EtFOSA), perfluorooctane sulfonamide acetate (FOSAA), perfluorooctane sulfonamide (FOSA) and PFOS were detected in earthworms, with EtFOSAA as the primary biotransformation product. The biota-to-sand accumulation factor (BSAF) and uptake rate coefficient ( k u ) of EtFOSE were 5.7 and 0.542/d, respectively. The elimination rate constants ( k e ) decreased in the order EtFOSA (0.167/d) ∼ FOSAA (0.147/d) > FOSA (0.119/d) ∼ EtFOSAA (0.117/d) > EtFOSE (0.095/d) > PFOS (0.069/d). No significant effects were observed in malondialdehyde (MDA) contents and acetylcholinesterase (AChE) activities between EtFOSE treatments and controls. EtFOSE could cause significant accumulation of reactive oxygen species (ROS) in earthworms. Peroxidase (POD), superoxide dismutase (SOD) and catalase (CAT) were significantly activated by 41.4–74.3%, 37.2–44.4% and 32.4–52.3% from day 4–10, respectively, while 8-Hydroxy-2-deoxyguanosine (8-OHdG) levels were elevated by 47.7–70.3% from day 8–10, demonstrating that EtFOSE induced oxidative stress and oxidative DNA damage in earthworms. Significant increase of glutathione-S-transferase (GST) with 41.6–62.8% activation (8–10 d) gave indirect evidence on the conjugation of EtFOSE or its corresponding metabolites during phase II of detoxication. This study provides important information on the fate and potential risks of EtFOSE to terrestrial invertebrates.
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