Phytodegradation and phytotoxicity of N-ethyl perfluorooctane sulfonamidoethanol (N-EtFOSE) in pakchoi (Brassica chinensis L.) via root and foliar uptake from physio-biochemical and transcriptomic perspectives

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).