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The influence of short and prolonged diet containing silver ions (Ag-diet) on copper metabolism was studied. Two groups of animals were used: one group of adult rats received a Ag-diet for one month (Ag-A1) and another group received a Ag-diet for 6 months from birth (Ag-N6). In Ag-A1 rats, the Ag-diet caused a dramatic decrease of copper status indexes that was manifested as ceruloplasmin-associated copper deficiency. In Ag-N6 rats, copper status indexes decreased only 2-fold as compared to control rats. In rats of both groups, silver entered the bloodstream and accumulated in the liver. Silver was incorporated into ceruloplasmin (Cp), but not SOD1. In the liver, a prolonged Ag-diet caused a decrease of the expression level of genes, associated with copper metabolism. Comparative spectrophotometric analysis of partially purified Cp fractions has shown that Cp from Ag-N6 rats was closer to holo-Cp by specific enzymatic activities and tertiary structure than Cp from Ag-A1 rats. However, Cp of Ag-N6 differs from control holo-Cp and Cp of Ag-A1 in its affinity to DEAE-Sepharose and in its binding properties to lectins. In the bloodstream of Ag-N6, two Cp forms are present as shown in pulse-experiments on rats with the liver isolated from circulation. One of the Cp isoforms is of hepatic origin, and the other is of extrahepatic origin; the latter is characterized by a faster rate of secretion than hepatic Cp. These data allowed us to suggest that the disturbance of holo-Cp formation in the liver was compensated by induction of extrahepatic Cp synthesis. The possible biological importance of these effects is discussed.

The studies reported here addressed the endothelium-protecting action of local and remote ischemic preconditioning of the brain in rats. Cerebral ischemia lasting 30 min was reproduced by thermocoagulation of the vertebral arteries with simultaneous clamping of the carotid arteries, the procedure being followed by reperfusion via the carotid arteries for 120 min (controls). The early and late phases of ischemic preconditioning and remote preconditioning were reproduced. Brain blood flow was recorded using high-frequency Doppler ultrasonography. The early and late phases of local ischemic preconditioning and the late phase of remote ischemic preconditioning were found to have endothelium-protecting actions apparent as improvements in the recovery of brain blood flow in the post-ischemic period in preconditioned rats, with lower levels of endothelial desquamation and cerebral edema. Blockade of nitric oxide synthesis eliminated the protective effects of both phases of preconditioning.