[Effect of mutations affecting coat color on the blood lymphocyte structure in the American mink (Mustela vison Schreber, 1777)].

American minks with different genotypes containing the Aleutian coat color allele in the homozygous state, including the single recessive Aleutian (a/a); double recessive sapphire (a/a p/p) and lavender (m/m a/a); triple recessive violet (m/m a/a p/p); and dominant-recessive cross sapphire (S/+ a/a p/p), sapphire leopard (S(K)/+ a/a p/p), and shadow sapphire (S(H)/+ a/a p/p) minks, as well as American minks without the Aleutian allele, including the standard (+/+); single recessive silver-blue (p/p) and hedlund-white (h/h); double recessive pearl (k/k p/p), Finnish topaz (t(S)/t(S) b/b); incompletely dominant royal silver (S(R)/+), standard leopard (S(K)/+), and black crystal (C(R)/+); and dominant-recessive snowy topaz (C(R)/+ t(S)/t(S) b/b) and Kujtezhy-spotted (S(K)/+ b/b) minks have been studied. Homozygosity for the a allele has been found to disturb the subcellular structure of leukocyte, namely the formation of abnormally large granules.

[Morphology and cytochemistry of abnormal cytoplasmic granules in blood leukocytes in sapphire minks (cytological and cytochemical study)].

Detailed morphological and cytochemical investigation of blood leukocytes was performed in minks of three genotypes: dark-brown minks (n=10), which had the color resembling that of the wild type, mutant silver-blue (p/p) minks (n=10), and sapphire minks (a/a p/p) (n=10). The sapphire minks were demonstrate to have a hereditary defect of leukocyte granules containing peroxidase, nonspecific esterases and non-enzymatic cationic protein. These granules have abnormally large size, the neutrophil cytoplasm contains one to several abnormal granules, they are numerous in eosinophil and basophil cytoplasm and rare in lymphocytes and monocytes. Morphological and cytochemical features indicate the similarity of hereditary leukocytes pathology of sapphire mink with that one found in human Chediak-Higashi syndrome.

[Influence of light regimens, melatonin, and epitalon on amylase activity in the pancreas and small intestine in rats of different age].

The study shows that keeping rats in different light modes has a different impact on pancreatic and intestine amylase activity and has its peculiarities in regard of age as well as geroprotectors' influence on it. Melatonin use entails pancreatic amylase activity increase in mature animals in natural light of the North-West of Russia (NL) and 24-hour constant light (LD) and on the contrary amylase activity drops in case of using epitalon. Simultaneously, the enzyme activity in young and old rats under LD, melatonin and epitalon decreases. Intestine amylase activity influenced by both preparations rises in NL and drops in LD mode with respect to the control group.

[Effect of age, different light conditions, melatonin, and epitalon on lysosomal proteinase activity in the liver and kidneys of rats].

Ageing, melatonin, epithalon (tetrapeptide Ala-Glu-Asp-Gly) and different light conditions effects on protein content and cathepsins B and D activities in rat liver and kidneys lysosomal fractions were studied. Ageing leads to decrease of cathepsins activity in rat liver lysosomal fractions. Constant light and darkness conditions result in earlier age decline of cathepsins activity. Absence of day and night succession in comparison with alternating light conditions causes decline of both general and specific cathepsin D activity. Melatonin and epithalon administration resulted in decrease of cathepsin D activity in liver only under control interchangeable light conditions. Cathepsin B activity in liver and kidneys lysosomal fractions declined in all experimental light conditions. Cathepsins activity decrease under the influence of epiphysial factors is evidently connected with their inhibitory effect on protein and general metabolism.

[Species specificity of the isoenzyme profile of lactate dehydrogenase in organs of rodents of various ecogenesis]. / Vidovaia spetsifichnost' izofermentnykh profilei laktatdegidrogenazy organov gryzunov razlichnogo ékogeneza.

Separation of isoenzymes of lactate dehydrogenase (LDH, EC. 1.1.1.27) in extracts of heart, kidney, liver, spleen, lungs of nutrias, chinchillas by agar gel electrophoresis reveals a species specificity in ratio of electrophoretic fractions of the enzyme. The isoenzymes of LDH were seem to play an important role in adaptation of fur animals to environmental conditions. It has been shown that in semiaquatic mammals--nutrias, the relative content of the A-subunits in the isoenzymatic spectrum of LDH in organs was increased as compared with terrestrial animals--chinchillas, whereas relative content of B-subunits in these organs of chinchillas was very high. This is an example of subtle biochemical specialisation of function at molecular level to environmental conditions.

[Isozyme patterns of lactate dehydrogenase from tissues of mink and arctic fox during postnatal development]. / Izofermentnye spektry laktatdegidrogenazy organov norok i pestsov v postnatal'nom razvitii.

Isozymes of lactate dehydrogenase extracted from heart, kidney, and liver of mink (Mustela vison Briss.) and Arctic fox (Alopex lagopus L.) during postnatal development were separated by agarose gel electrophoresis. Tissue-specific isozyme pattern of lactate dehydrogenase can be revealed at the age of one month, while the definitive pattern is formed at the age of four months. The isozyme patterns of lactate dehydrogenase in the studied tissues of mink and Arctic fox share the properties specific for animal species of various ecogenesis.

[Effect of mutilus hydrolysate in Aleutian disease of minks]. / Effekt gidrolizata iz midii pre aleutskoi bolezni norok.

Addition of mutilus hydrolysate MIGI-K to rations of minks with virus plasmacytosis involving grave immunological disorders led to changes in the ratio of serum protein fractions and in the differential blood count. Normalization of the protein spectrum of minks with Aleutian disease apparently inhibits the development of disorders caused by hypergammaglobullnemia.