Toxicology communications · 2026
Orally-administered beta-cyclodextrin as a novel countermeasure for perfluorooctane sulfonic acid toxicity in mice.
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Kalinin Sergey, Saji Andrea, Alemani Rebecca, McDonald Zachary, Ahmad Intakhar, Sargis Robert, Rubinstein Israel, Feinstein Douglas L
Аннотация
INTRODUCTION: Perfluoroalkyl substances (PFAS) are associated with an increased risk of several cancers, immune disorders, and neuropathology. These actions are compounded by their long half-lives.
METHODS: We tested if exposure to perfluorooctane sulfonic acid (PFOS) worsens disease progression or reduces survival in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, and if treatment with beta-cyclodextrin (βCD, which encapsulates PFOS) mitigated PFOS effects. Adult female C57BL/6 mice were provided drinking water containing 0 (control) or 20 μg/mL PFOS for 2 weeks, immunized to develop EAE, then provided standard chow or chow containing 2% w/w βCD.
RESULTS: Control EAE mice exhibited typical disease progression, irrespective of being on standard or βCD chow. By 10 days post immunization, PFOS-exposed EAE kept on standard chow began to die, reaching nearly 60% mortality (5/8) at day 17. In contrast, in PFOS-exposed EAE mice provided βCD chow, mortality was reduced to 12% (1/8). The quantification of plasma PFOS concentrations showed an approximately 60% reduction in βCD-treated mice compared to mice kept on standard chow.
DISCUSSION: These findings suggest that PFOS led to systemic immune dysregulation upon immunization or that EAE induction lowered the threshold for PFOS-induced mortality.
CONCLUSION: Providing dietary βCD can accelerate PFOS clearance.
METHODS: We tested if exposure to perfluorooctane sulfonic acid (PFOS) worsens disease progression or reduces survival in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, and if treatment with beta-cyclodextrin (βCD, which encapsulates PFOS) mitigated PFOS effects. Adult female C57BL/6 mice were provided drinking water containing 0 (control) or 20 μg/mL PFOS for 2 weeks, immunized to develop EAE, then provided standard chow or chow containing 2% w/w βCD.
RESULTS: Control EAE mice exhibited typical disease progression, irrespective of being on standard or βCD chow. By 10 days post immunization, PFOS-exposed EAE kept on standard chow began to die, reaching nearly 60% mortality (5/8) at day 17. In contrast, in PFOS-exposed EAE mice provided βCD chow, mortality was reduced to 12% (1/8). The quantification of plasma PFOS concentrations showed an approximately 60% reduction in βCD-treated mice compared to mice kept on standard chow.
DISCUSSION: These findings suggest that PFOS led to systemic immune dysregulation upon immunization or that EAE induction lowered the threshold for PFOS-induced mortality.
CONCLUSION: Providing dietary βCD can accelerate PFOS clearance.