Abstract by Nicholas Brown
Chemistry and Biochemistry
Effects of Ceruloplasmin on Liver Ferroportin
Nicholas Brown 2018 SRC Abstract
Iron is essential to sustain life but free iron catalyzes the formation of Reactive
Oxygen Species (ROS) and oxidative stress. Normally, cells store iron in ferritin but
inflammation disrupts ferritin iron loading leaving free iron in the cell to produce
ROS. A secondary method to protect against oxidative stress is to pump iron out of
the cell through an iron export protein called ferroportin (FPN). FPN requires a co-
export copper enzyme, ceruloplasmin (CP) to function. Our hypothesis is that
copper-deficiency may inhibit iron release from stressed cells and increase
oxidative stress. HepG2 cells were cultured on normal media and low Cu media.
Iron export was measured using iron chelators added to the media. Additionally,
cells were treated with cuprizone a copper chelator to inactivate CP. Results show
that inactivation of CP disrupts iron export through FPN causing elevated free iron
in cells and increasing oxidative stress.