Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant widely detected in aquatic ecosystems, but its subcellular targets and the mechanisms by which it disrupts light resource utilization in photosynthetic protozoa remain poorly understood at environmentally relevant concentrations. Here, Euglena gracilis was exposed to environmentally relevant PFOS concentrations. Subcellular distribution, phototaxis, photosynthetic light reactions, and energy metabolism were investigated using isolated chloroplast assays, transcriptomics, and proteomics. PFOS accumulated prominently in the eyespot and chloroplasts. Eyespot accumulation impaired phototactic motility and increased the light perception threshold. PFOS did not acutely inhibit overall photosynthesis; instead, a transient upregulation of photosynthesis-related genes and a slight stimulation of oxygen evolution were observed, which weakened with prolonged exposure. PFOS significantly reduced ATP levels and the photosynthetic electron transport rate (ETR), while Fv/Fm remained unchanged and non photochemical quenching (NPQ) was elevated. Isolated chloroplast assays confirmed direct inhibition of Mg²⁺ ATP synthase and thylakoid electron transport. Transcriptomic and proteomic analyses revealed compensatory upregulation of photosynthesis pathways but suppression of ATP synthesis and redox homeostasis. Mechanistically, PFOS directly targets chloroplast ATP synthase, leading to proton gradient accumulation, feedback inhibition of electron transport, and increased NPQ. Together with eyespot mediated phototaxis impairment, PFOS dually disrupts light acquisition (behavioral) and light conversion (physiological). This dual impairment may compromise the ecological fitness of Euglena in PFOS contaminated environments, especially under prolonged exposure.

Per- and polyfluoroalkyl substances (PFASs) are persistent synthetic chemicals of global concern. While most research has focused on their occurrence and toxicity, far less attention has been paid to their impacts on the global carbon cycle. This review synthesizes current evidence on how PFASs influence carbon cycling across soils, aquatic systems, and the atmosphere. In soils, PFASs alter organic carbon inputs by affecting plant biomass and root exudates and shift microbial community composition and enzyme activities, thereby modulating organic matter decomposition. In aquatic ecosystems, PFASs biologically impair carbon sequestration by inhibiting plankton, and abiotically interact with extracellular polymeric substances to prolong the cycling of dissolved organic carbon. The atmosphere acts as a key mediator as follows: thermal treatment of PFASs generates perfluorocarbons, potent greenhouse gases that exacerbate global warming and further disturb carbon cycling. Despite clear disruptive effects, major knowledge gaps remain. Future research should use quantitative structure–property relationship modeling to assess PFAS alternatives (e.g., PFHxS), and employ advanced molecular tracking (e.g., isotopic labeling, NanoSIMS) and machine learning to unravel nonlinear PFAS–carbon dynamics. Improved detection technologies are needed to identify greenhouse gas byproducts from PFAS thermal treatment. Ultimately, deploying high-resolution flux observation networks and integrating PFAS dynamics into Earth system models and carbon-accounting frameworks are critical for predicting carbon–climate feedback and supporting global carbon neutrality goals.

Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant widely detected in aquatic ecosystems, but its subcellular targets and the mechanisms by which it disrupts light resource utilization in photosynthetic protozoa remain poorly understood at concentrations spanning environmentally typical to supra-environmental levels. Here, Euglena gracilis G.A. Klebs was exposed to PFOS at concentrations spanning environmentally typical (0.5 µg/L), hotspot-relevant (5 µg/L), and supra-environmental (50 µg/L) levels. Subcellular distribution, phototaxis, photosynthetic light reactions, and energy metabolism were investigated using isolated chloroplast assays, transcriptomics, and proteomics. TEM-EDS mapping revealed pronounced fluorine signal enrichment, attributable to PFOS, in the eyespot and chloroplasts. Eyespot fluorine enrichment was associated with impaired phototactic motility and an altered light perception threshold. PFOS did not acutely inhibit the maximum photochemical efficiency of photosystem II (Fv/Fm); instead, a transient upregulation of photosynthesis-related genes was observed, which weakened with prolonged exposure, whereas the photosynthetic electron transport rate (ETR) was significantly reduced. PFOS significantly reduced ATP levels and ETR, while Fv/Fm remained unchanged and non-photochemical quenching (NPQ) was elevated. Isolated chloroplast assays revealed that PFOS inhibits Mg²⁺-dependent ATP hydrolytic activity in the chloroplast-enriched fraction and impairs thylakoid electron transport, consistent with impaired chloroplast ATP synthase function, though the specific molecular target and mechanism remain to be conclusively demonstrated. Transcriptomic and proteomic analyses revealed compensatory upregulation of photosynthesis pathways but suppression of ATP synthesis and redox homeostasis. Collectively, our results suggest that PFOS impairs chloroplast ATP synthase function, accompanied by reduced ETR and elevated NPQ. Together with the eyespot-associated phototaxis impairment, these effects suggest that PFOS may dually disrupt light acquisition (behavioral) and light conversion (physiological) in E. gracilis. This dual impairment may compromise the ecological fitness of Euglena in PFOS-contaminated environments, especially under prolonged exposure. It should be noted that the subcellular fluorine mapping is qualitative, the phototaxis assay reflects population-level responses, and the ATP synthase impairment interpretation is indirect; the proposed mechanistic model remains a hypothesis requiring further direct experimental validation.