The study of the sporocyst broodsacs coloring in Leucochloridium paradoxum (Trematoda: Brachylaemidae).

The secretory cells were found in the subtegument of the sporocysts Leucochloridium paradoxum by histological assay. Pigment granules are formed by these cells. The movement of granules from secretory cells to the tegument external layer was observed. These pigment granules provide the yellow color of sporocysts broodsacs and the brown color of protuberant spots in the terminal part of broodsacs. It was shown that the pigment granules did not contain proteins, nucleotides, lipids and carbohydrates. The positive result was received while staining on bile pigments. The question on the nature of the green pigment remains open. The paletot on the surface of sporocyst formed by spreading hemocytes was observed. This structure was not described before in brachylaemid parthenites.

Development of laboratory rats receiving silver-enriched ration for a long time.

We studied the effect of silver ions on the status and metabolism of copper in rats receiving Ag-diet from the first day of life and for 6 months. The effect of silver ions on copper metabolism was assessed by body weight, relative weight of organs (body weight/organ weight), oxidase activity, content of immunoreactive ceruloplasmin and copper concentration in blood serum, by the expression of copper-transporting protein genes in the liver, and copper and silver distribution in liver and brain cells. Brain functions were evaluated by open-field behavior and passive avoidance conditioning. No acute deficiency of ceruloplasmin-associated copper was observed in rats receiving silver-enriched diet starting from the early postnatal period; copper metabolism in the liver did not change, psychoemotional state and memory corresponded to the control. However, Ag-diet almost 2-fold decelerated the growth of experimental rats. We hypothesize the existence of an unknown mechanism of copper delivery to organs in rats that is activated during the early ontogeny under conditions of ceruloplasmin-associated copper deficiency.

Effect of a deficiency of ceruloplasmin copper in blood plasma on copper metabolism in the brain.

Copper deficiency in adult rats was induced by addition of silver chloride to the feed. The concentrations of silver, copper, iron, and zinc and relative activity of genes for copper transporting proteins and copper enzymes were measured in the cortex, cerebellum, hippocampus, amygdala, pituitary gland, and hypothalamus. Silver was accumulated only in the hypothalamic-pituitary system. These changes were accompanied by a decrease in the concentration of copper and increase in the contents of iron and zinc. Activity of genes for copper transport enzymes (high-affinity copper transporter; and two copper transport ATPases, ATP7A and ATP7B) and copper enzymes that were formed in the intracellular secretory pathway did not decrease in the brain of rats with copper deficiency. Relative activity of genes for intracellular copper enzymes (Cu(2+)/Zn(2+) superoxide dismutase and subunit IV of cytochrome c oxidase), concentration of immunoreactive polypeptides of superoxide dismutase, and enzymatic activity of superoxide dismutase remained unchanged under these conditions.

Changes in copper metabolism in different compartments of the brain in rats with induced fibrillogenesis.

Fibrillogenesis was induced in rats by injection of a fragment of neurotoxic protein, beta-amyloid protein precursor, into the cerebral ventricle. Copper, iron, and zinc concentrations and relative activities of genes of copper-transporting protein and extracellular and intracellular cuproenzymes were evaluated in different brain compartments of these animals. Copper and zinc concentrations decreased significantly in different compartments of the brain of rats with experimental fibrillogenesis, while iron content did not change. According to the data of RT-PCR analysis, activities of genes of copper-transporting protein and extracellular coenzyme decreased. The expression of intracellular cuproenzyme genes and the content of SOD1 protein did not change, SOD1 activity in the cytosol decreased, and active SOD1 was detected in the mitochondrial intermembrane space. The relationship between fibrillogenesis and copper metabolism is discussed.

The effects of silver ions on copper metabolism in rats.

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.