BACKGROUND: Previous studies have suggested abnormal copper metabolism in patients with primary sclerosing cholangitis (PSC). In the present work the trace element metabolism was studied in a group of 32 patients with PSC. METHODS: Hepatic copper and selenium concentrations were determined with a sensitive electrothermal atomic absorption technique. Serum concentrations of copper and zinc were determined by conventional atomic absorption. RESULTS: For the patient group serum copper values (20.3 +/- 4.5 mumol/l) were higher than those for the control group (14 +/- 3 mumol/l), and average hepatic copper concentrations were greater by a factor of four. Serum selenium values were slightly lower, although the average hepatic selenium was significantly higher than in the healthy control group. Previous studies have discussed possible toxic effects of hepatocellular copper accumulation, which may be accompanied by formation of activated oxygen species and depletion of glutathione. In the present study, however, it could not be demonstrated that the concentration of the lipoperoxidation product, malonic dialdehyde, was higher than normal in blood. Furthermore, blood concentrations of glutathione and glutathione peroxidase were not abnormal. CONCLUSION: Although a protective effect of the raised selenium concentrations in the liver might be discussed, it is apparent that the copper accumulation in the liver cells described here did not induce detectable changes in the indices studied.
BACKGROUND: Previous studies have suggested abnormal copper metabolism in patients with primary sclerosing cholangitis (PSC). In the present work the trace element metabolism was studied in a group of 32 patients with PSC. METHODS: Hepatic copper and selenium concentrations were determined with a sensitive electrothermal atomic absorption technique. Serum concentrations of copper and zinc were determined by conventional atomic absorption. RESULTS: For the patient group serum copper values (20.3 +/- 4.5 mumol/l) were higher than those for the control group (14 +/- 3 mumol/l), and average hepatic copper concentrations were greater by a factor of four. Serum selenium values were slightly lower, although the average hepatic selenium was significantly higher than in the healthy control group. Previous studies have discussed possible toxic effects of hepatocellular copper accumulation, which may be accompanied by formation of activated oxygen species and depletion of glutathione. In the present study, however, it could not be demonstrated that the concentration of the lipoperoxidation product, malonic dialdehyde, was higher than normal in blood. Furthermore, blood concentrations of glutathione and glutathione peroxidase were not abnormal. CONCLUSION: Although a protective effect of the raised selenium concentrations in the liver might be discussed, it is apparent that the copper accumulation in the liver cells described here did not induce detectable changes in the indices studied.
Authors: Anke Van Summeren; Johan Renes; Daneida Lizarraga; Freek G Bouwman; Jean-Paul Noben; Joost H M van Delft; Jos C S Kleinjans; Edwin C M Mariman Journal: OMICS Date: 2013-01-11