A Kinetic and Holistic Review of Iron and Copper Toxicity in Rat Liver
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 1O2, 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 H2O2, yield HO• that initiates free-radical mediated phospholipid peroxidation and protein oxidation.
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