Abstract
One of the features at the molecular level of inflammatory disorders is the enhanced peroxidative conversion of polyunsaturated fatty acids, both enzymatically, to prostaglandins, thromboxane and (poly)hydroxy-fatty acids, and also nonenzymatically. Lipid peroxidation may be induced by altered levels of copper and iron in and around cells. Both metals have more than one valence state, which render them to redox-active ions. Paradoxically, hydrated copper ions and copper chelated by amino acids or bound to superoxide dismutase and ceruloplasmin, have the ability to catalyze the dismutation of superoxide radicals. Another trace element, zinc, has a univalent cationic form and is an inhibitor of lipid peroxidation. Interactions of copper and zinc will speculatively be discussed in relation to inflammation and inherent hepatic changes.
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Bonta, I.L., Bragt, P.C., Muus, P. (1982). Hepatic Adaptation Process during Inflammatory Conditions: Role of Trace Elements, Lipid Peroxidation and Ceruloplasmin. In: Sorenson, J.R.J. (eds) Inflammatory Diseases and Copper. Experimental Biology and Medicine, vol 2. Humana Press. https://doi.org/10.1007/978-1-4612-5829-2_24
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DOI: https://doi.org/10.1007/978-1-4612-5829-2_24
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