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At least 1,153 records · Page 64Linked to original sources
PubMed1991

Increased lung copper-zinc-superoxide dismutase activity and absence of magnetic resonance imaging-detectable lung damage in copper-deficient rats exposed to hyperoxia.

The effects of hyperoxia on physiological responses, pathological lung lesions detected noninvasively by proton magnetic resonance imaging (MRI), and the oxygen free radical defense enzymes were measured in Cu-deficient rats. Exposure to 85% oxygen seemed to impose a stress on the whole animal as indicated by two physiological responses, decreased food intake and decreased body weight of ad libitum-fed rats. However, all rats exposed to 85% oxygen, including the Cu-deficient group, were able to survive 1 wk of hyperoxia exposure. The target organ specificity for hyperoxia exposure was in the lung as indicated by the increased lung:body weight ratio in all hyperoxia-exposed rats regardless of dietary treatment. All dietary treatment groups exposed to hyperoxia had a similar increase in lung:body weight ratio, but none of the hyperoxia-exposed rats had MRI-detectable lung damage. After 7 d of hyperoxia exposure, all dietary treatment groups, including the Cu-deficient rats, had increased activity of lung CuZn-superoxide dismutase (CuZnSOD), but changes in CuZnSOD activity were not related to lung Cu or Zn concentrations. We propose that the ability to increase CuZnSOD activity is the most important factor of the enzymatic oxygen free radical defense system for protection against hyperoxia-induced lung damage detected by MRI. Even though lung Cu concentration was decreased in Cu deficiency, it seems that Cu-deficient rats are still able to increase lung CuZnSOD activity in response to 85% oxygen exposure.

Animals↗
PubMed1994

Copper-amino acid complexes are partially protected against inhibitory effects of L-cysteine and L-ascorbic acid on copper absorption in chicks.

Chick experiments were conducted to investigate whether two new Cu-amino acid complexes, Cu-methionine (Cu-Met) and Cu-lysine (Cu-Lys), would differ from a standard Cu source (analytical-grade CuSO4) in their reaction to the inhibitory dietary effects of physiologic doses of L-cysteine (4000 mg/kg diet) or L-ascorbate (1000 mg/kg diet) on Cu absorption. Whether absorbed actively (as evaluated by a bile Cu assay at low Cu doses) or passively (as evaluated by a liver Cu assay at high Cu doses), cysteine inhibited Cu absorption more than did ascorbate. In addition, the inhibitory effects of cysteine and ascorbate were not additive, but they enhanced the inhibitory effect of Zn when evaluated at low Cu doses. Ascorbate inhibited Cu utilization from CuSO4 to 58.0% of the unsupplemented reference group at low Cu doses, which was greater (P < 0.05) than the inhibitory effect of ascorbate of Cu-Lys (78.7%) or Cu-Met (89.1%). Cysteine inhibited Cu utilization from CuSO4, Cu-Lys and Cu-Met at low Cu dose levels to 49.1, 44.1 and 50.2%, respectively, of unsupplemented reference groups of each source. These values were not different from each other. On the other hand, cysteine inhibited Cu utilization from CuSO4 to 8.5% of the unsupplemented reference group at high Cu doses, which was greater (P < 0.05) than the inhibitory effect on Cu-Lys (29.5%) or Cu-Met (39.9%). Ascorbate reduced Cu utilization from CuSO4, Cu-Lys and Cu-Met at high Cu doses to 72.8, 63.7 and 68.3%, respectively, of unsupplemented control groups of each source.

Animals↗
PubMed1995

Chronic intake of a marginally low copper diet impairs in vitro activities of lymphocytes and neutrophils from male rats despite minimal impact on conventional indicators of copper status.

We investigated the impact of chronic intake of a diet marginally low in Cu on traditional indicators of Cu status and in vitro activities of splenic mononuclear cells and neutrophils. Pregnant Sprague-Dawley rats were fed diets containing either 2.8 (LCu) or 6.7 [adequate (ACu)]mg Cu/kg from midgestation through lactation. Weaned male and female offspring were fed the same diets as their dams until 6 months of age. Dietary Cu level did not alter growth, heart weight, the concentrations of Cu or the activities of cuproenzymes in serum and most tissues. In contrast, splenic mononuclear cells (MNC) from males, but not females, fed the LCu diet were less responsive to in vitro mitogenic activation and generated less interleukin-2 bioactivity than cultures prepared from males fed the ACu diet. Repletion with the ACu diet for 2 wk restored in vitro activities of splenic MNC to control levels. The phorbol myristate acetate-induced generation of superoxide anion by elicited neutrophils from male rodents fed the LCu diet was only 60% that of cells from the ACu diet group. Brain Cu in adult rats fed LCu diet was irreversibly decreased compared with those fed ACu diet. These data show that the in vitro activities of T lymphocytes and neutrophils isolated from adult male rats chronically fed a diet marginally low in Cu were significantly suppressed without marked alterations in the traditional indicators of Cu status.

Animals↗
PubMed2004

Increase in the conformational flexibility of beta 2-microglobulin upon copper binding: a possible role for copper in dialysis-related amyloidosis.

A key pathological event in dialysis-related amyloidosis is the fibril formation of beta(2)-microglobulin (beta 2-m). Because beta 2-m does not form fibrils in vitro, except under acidic conditions, predisposing factors that may drive fibril formation at physiological pH have been the focus of much attention. One factor that may be implicated is Cu(2+) binding, which destabilizes the native state of beta 2-m and thus stabilizes the amyloid precursor. To address the Cu(2+)-induced destabilization of beta 2-m at the atomic level, we studied changes in the conformational dynamics of beta 2-m upon Cu(2+) binding. Titration of beta 2-m with Cu(2+) monitored by heteronuclear NMR showed that three out of four histidines (His13, His31, and His51) are involved in the binding at pH 7.0. (1)H-(15)N heteronuclear NOE suggested increased backbone dynamics for the residues Val49 to Ser55, implying that the Cu(2+) binding at His51 increased the local dynamics of beta-strand D. Hydrogen/deuterium exchange of amide protons showed increased flexibility of the core residues upon Cu(2+) binding. Taken together, it is likely that Cu(2+) binding increases the pico- to nanosecond fluctuation of the beta-strand D on which His51 exists, which is propagated to the core of the molecule, thus promoting the global and slow fluctuations. This may contribute to the overall destabilization of the molecule, increasing the equilibrium population of the amyloidogenic intermediate.

Algorithms↗