Iron and Copper Toxicity in Rat Liver: A Kinetic and Holistic Overview
Keywords:
GSH: Reduced glutathione, SOD1: Cu, Zn-superoxide dismutase, GPx: Glutathione peroxidase, Nrf2: Nuclear factor erythroid 2-related factor 2Abstract
Iron (Fe) and copper (Cu) overloads in rats showed a dose and time dependent metal accumulation
in liver with its associated toxicity. The increased contents of the transition metals markedly
enhanced the endogenous free-radical mediated processes of phospholipid peroxidation. In
vivo liver chemiluminescence showed an increased production of 1
O2
, and a consumption of
reduced glutathione (GSH), the main intracellular antioxidant. Results fit with a Haber-Weiss
type molecular mechanism in which Fe or Cu and endogenously produced O2
-
and H2
O2
, yield
HO•
that initiates free-radical mediated phospholipid peroxidation and protein oxidation.

