Presenting Author: Debby Walser-Kuntz
, Professor of Biology at Carleton Col.
Abstract:
The widespread use of bisphenol-A (BPA) in the mass production of polycarbonate plastics and its presence in surface water and wastewater runoff poses a threat to both humans and wildlife. BPA is widely known to disrupt estrogen activity by binding to ER α and β and affecting reproduction, yet it also modulates the immune response. Previously, our lab found that BPA-exposed zebrafish had decreased tail fin regeneration after injury and decreased neutrophil recruitment to the site. We hypothesized that neutrophils directly or indirectly affect regeneration by promoting the resolution of inflammation. Reactive oxygen species (ROS) generation is tightly regulated and essential for neutrophil recruitment, wound healing, and regeneration in zebrafish. To investigate BPA’s impact on reactive oxygen species production in response to injury in zebrafish, we induced a tail fin injury at 3 days post fertilization. We measured neutrophil migration and ROS generation immediately and at 2, 6, 24, and 48 hours post-injury in live, agarose-mounted larvae using CELLROX Deep Red and confocal microscopy to quantify fluorescence. To explore the link between BPA, neutrophil migration, and ROS, mpo::GFP zebrafish with labeled neutrophils were used to colocalize ROS generation and neutrophils. We found that exposure of zebrafish embryos to 100ng/ml BPA modulates ROS generation. Our study provides a mechanism to explain BPA’s reduction of neutrophil migration and tail fin regeneration in zebrafish.
Bisphenol-A (BPA) modulates reactive oxygen species generation in larval zebrafish.
Category
Poster
Description
Custom CSS
double-click to edit, do not edit in source
Date: May 4 Presentation Time: 03:15 PM to 04:30 PM Room: Exhibit Hall F1