Presenter: Firdaus Muhammad
Faculty Sponsor: Alicia Timme-Laragy
School: UMass Amherst
Research Area: Public Health and Epidemiology
Session: Poster Session 5, 3:15 PM - 4:00 PM, Auditorium, A23
ABSTRACT
Environmental exposures to perfluorooctanesulfonic acid (PFOS) and other per- and polyfluoroalkyl substances (PFAS) during early development can permanently alter organ structure and function, shaping disease risk across the lifespan. These persistent chemicals are widely detected and linked to adverse developmental and metabolic outcomes. Developmental PFOS exposure disrupts pancreatic organogenesis in zebrafish (Danio rerio), resulting in shortened exocrine pancreas length, reduced digestive enzyme expression, and impaired nutrient processing. Emerging evidence indicates that oxidative stress plays a central role in PFOS toxicity. This process implicates the nuclear factor erythroid 2–related factor 2 (Nrf2) signaling pathway, which is a key regulator of cellular antioxidant defenses involved in tissue protection and recovery. However, whether targeted activation of Nrf2 can promote post-exposure recovery from PFOS-induced pancreatic defects has remained unclear. This project investigated whether pharmacological activation of Nrf2 enhanced recovery of pancreatic morphology following developmental PFOS exposure in zebrafish. Tg(ptf1a:GFP) embryos were exposed to 8 μM PFOS during specific developmental windows from 3-48 hpf and assessed for exocrine pancreas shortening. At 5 days post-fertilization, larvae were treated with a canonical Nrf2 activator, and pancreatic size was quantified through fluorescence imaging. Quantitative morphometric analysis of pancreas and body length was used to assess whether Nrf2 activation promoted structural recovery relative to PFOS-exposed controls. By linking oxidative stress signaling to pancreatic recovery, this study provides mechanistic insight into pathways that mitigate toxicant-induced developmental damage and clarifies how early life PFOS exposure contributes to long term metabolic dysfunction.
