Orally-administered beta-cyclodextrin as a novel countermeasure for perfluorooctane sulfonic acid toxicity in mice.

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.