Iron and Copper Toxicity in Rat Liver: A Kinetic and Holistic Overview

Authors

  • Rosario Musacco-Sebio
  • Christian Saporito-Magriñá
  • Juan M. Acosta
  • Alberto Boveris
  • Marisa G. Repetto

Keywords:

GSH: Reduced glutathione, SOD1, Cu, Zn-superoxide dismutase, GPx: Glutathione peroxidase, Nrf2: Nuclear factor erythroid 2-related factor 2

Abstract

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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Published

2017-01-10

How to Cite

Rosario Musacco-Sebio, Christian Saporito-Magriñá, Juan M. Acosta, Alberto Boveris, & Marisa G. Repetto. (2017). Iron and Copper Toxicity in Rat Liver: A Kinetic and Holistic Overview. Liver Research, 2(1), 9–13. Retrieved from https://openventio.us/index.php/LROJ/article/view/1019

Issue

Vol. 2 No. 1 (2017): Volume 2 Issue 1 2017

Section

Articles

License

All content published in Liver Research – Open Journal (LROJ) is licensed under the Creative Commons Attribution 4.0 International License (CC BY 4.0). This license allows anyone to copy, distribute, transmit, and adapt the work — including for commercial purposes — provided appropriate credit is given to the original author(s) and source.

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