Abstract
Copper (Cu) toxicosis, associated with increased hepatic Cu content, occurs as a familial disorder (Wilson’s disease) in humans (1) and some breeds of dogs (2,3). The Cu-loaded rat has proved to be a useful model in which to investigate Cu-associated diseases (4,5). The mechanisms by which Cu exerts its toxic effect on the cell are still unclear, cell death may occur due to lipid peroxidation of lysosomal membranes (6) or as a consequence of nuclear disorganization (7). It is also possible that copper enters the nucleus as a consequence of lipid peroxidation of nuclear membranes (8). Selenium (Se), an essential trace element, is part of the glutathione peroxidase (GSHPx) and other selenoenzymes involved in removal of hydrogen peroxide and lipid peroxides produced during oxidative processes in cells (9).
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© 1996 Springer Science+Business Media New York
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Fuentealba, I.C., Horney, B., Daley, J., Tasony-Ferraro, A. (1996). The Role of Selenium in Copper-Induced Damage in Copper Loaded Rats’ Livers. In: Nève, J., Chappuis, P., Lamand, M. (eds) Therapeutic Uses of Trace Elements. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0167-5_45
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DOI: https://doi.org/10.1007/978-1-4899-0167-5_45
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