ISSUE FOCUS 26 FEED & ADDITIVE MAGAZINE July 2022 to chaperone proteins and/or metallothionein (MT) to avoid cellular toxicity and to further transport copper outside the enterocyte. Cu is exported via the portal venous system to the liver, which is the central regulatory organ of copper homeostasis; but it can be then taken up by other tissues (brain, kidney, heart…). On its entry to the hepatocyte, Cu is again rapidly taken up by cytosolic ligands such as MT and glutathione. The main role of MT is the storage of Cu in a “safe compartment” and the sequestration of an intracellular excess of Cu in response to supra-physiological Cu exposure, which can generate hydroxyl radicals and be potentially toxic. Because the liver is the main storage site for Cu, the bioavailability of Cu sources has been traditionally evaluated by using liver Cu accumulation as the key criterion. This kind of studies have been performed at nutritional dosages, to allow homeostatic regulation. More recently, however, feeding trials with high Cu levels for pigs have also used hepatic Cu as an indicator of bioavailability. These levels, which by far exceed the requirements of pigs, demonstrate with the Cu accumulation in the liver, a way that the organ finds to avoid Cu toxicity. Into hepatocytes, Cu is associated to different enzymes and the excess is removed from the liver through biliary excretion. The Figure 4. Effect of dietary copper from CuSO4 on its concentration in the liver (A) and final body weight (B) of fattening pigs after 133 days of trial. Figure 3. Concentrations of Cu in liver, in the bile and Cu excreted in feces. Results are in percentage of Cu intake. Data are from a trial with piglets from 35 to 63 days of age fed 250 ppm of Cu from CuSO4.
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