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The comparative evaluation of the reactogenic and immunogenic properties of vaccine "Euvax B" in adolescents aged 16-18 years was carried out in factory housing estate Lvovsky, the Podolsk district, the Moscow region, and in the Yamalo-Nenets Autonomous District (AD): in towns Salekhard, Noyabrsk, Muravlenko, in housing estate Tarko-Sale. The evaluation demonstrated that the use of this vaccine in a dose of 20 mg/ml produced no postvaccinal complications and the frequency of postvaccinal reactions was insignificant. Postvaccinal anti-HBs were detected, on the average, in protective concentrations in 98.4 +/- 1.8% of the vaccines (99.0 +/- 1.9% in the Moscow region, 97.7 +/- 3.2% in the Yamalo-Nenets AD). In most of the vaccinated adolescents high concentrations of postvacinal anti-HBs were detected: in 51.4 +/- 9.7% of the vaccinees in the Moscow region and in 89.7 +/- 6.4% in the Yamalo-Nenets AD they exceeded 1,000 I.U./lit. The conclusion was made that in the territories located in subarctic latitudes vaccinal prophylaxis against hepatitis B was safe and highly effective and have no limitations connected with the conditions of the Far North.

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Using the immunoblotting method, the synthesis of two copper-transporting P1-type ATPases, ATP7A (a candidate for the product of the Menkes disease gene) and ATP7B (presumed product of the Wilson disease gene), in the yolk sac cells of rat embryos at days 11 and 20 of embryogenesis was demonstrated. Concomitantly, yolk sac cells produce ceruloplasmin, a soluble copper-transporting glycoprotein, a proportion of which in secreted proteins progressively diminishes, attaining 5.2% at day 11 and 3.1% at day 20 of development. At different stages of embryogenesis, yolk sac cells synthesize two molecular forms of [14]C-ceruloplasmin, one of which is secreted towards the embryo, whereas the other, towards the decidual membrane. Two forms of ceruloplasmin secreted in polar directions differ in the rate of secretion. The role of the yolk sac as a key organ controlling the delivery and secretion of copper in the embryo during the postimplantation period is discussed.

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The interaction was studied of ceruloplasmin (Cp, EC 1.16.3.1), a copper-containing plasma protein, with two synthetic peptides P15 and P16 whose structures correlate with those of the noncytosolic regions of the copper transfer P1 type ATPase (ATP7A), apparently encoded by the Menkes disease gene (Atp7a). Pentadecapeptide P15 and hexadecapeptide P16 were synthesized using the solid phase method. They correspond to fragments of two extracellular loops ATP7A, of which one loop is apparently involved in the copper ion transfer (P16) whereas the other is not (P15). The protein footprinting showed that P16 binds to a fragment of the ceruloplasmin domain 6. Kinetics of the ceruloplasmin-P16 binding was studied by affinity chromatography on P16 immobilized on a macroporous disk, and the Kd value (1.5 x 10(-6) M) of this interaction was determined. The ATP7A involvement in the copper ion transfer to nonhepatocyte cells is discussed.

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In chase experiments, we followed the distribution of [125I]-ceruloplasmin prepared from human breast milk orally administered to young rats. Experiments were conducted using six-day-old rat pups (the embryonic type of copper metabolism) or 35-day-old ones (the adult type of copper metabolism). Using the technique of rocket immunoelectrophoresis, we have demonstrated that in six-day-old rats [125I]-ceruloplasmin was transferred from the gastrointestinal tract to the bloodstream and could be detected there over a period of 4 h. In 35-day-old rats, milk ceruloplasmin was digested in the upper part of the intestinal tract. The dynamic aspects of the distribution of labeled milk ceruloplasmin in the body of six-day old rats over a period of 4 h point out that, under the conditions of embryonic copper metabolism, it can serve as a transporter of copper ions to extrahepatic organs. We discuss the role of milk ceruloplasmin in copper metabolism in mammals during the neonatal period.

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Based on an analysis of correlations between variation in the amount of alveolar macrophages of rat lungs and activity of enzymes localized in these cells (acid phosphatase, beta-galactosidase, beta-glucosidase, lactate dehydrogenase), the cytobiochemical changes in the function of pulmonary alveolar macrophages have been defined with the use of a model of permanent inhalation exposure to sulfur dioxide. The use of the model enables the dilimitation of the stages of defence-compensatory reactions and their transition to an unfavourable biological effect. The results obtained may serve as a theoretical basis for recommending a wider experimental application of the tests in question during regulation of environmental factors.

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Early energy changes in lungs, liver, and kidneys during the introduction of a benz a pyrene and phenol (as the possible carcinogen activator) were studied. It was observed that 10 days after a single instance introduction of 5 mg benz a pyrene per 0.9% NaCl (60 rats), oxidative phosphorylation in the lungs and livers is disturbed in the test rats, accompanied by a reduction of adenine nucleotides in these tissues. It is assumed that at this stage, the detoxication of benz a pyrene is intensified by free oxidation systems and by the respiratory chain of mitochondria. A chronic 3-month exposure to benz a pyrene and phenol (150 rats, each 5 mg of benz a pyrene per month intratracheally and 0.4 mg/m3 of phenol round-the-clock) results in greater disturbances of the energy exchange in the lungs, liver and kidneys. Benz a pyrene and phenol, individually and in combination, inhibit oxidative phosphorylation in the lungs. This significantly decreases the content of adenine nucleotides in this tissue. Activation of anaerobic glycolysis (twofold) and of aerobic glycolysis (eightfold) does not make up for the energy insufficiency in the tissue. The effect of benz a pyrene and phenol in the liver also results in suppressing oxidative phosphorylation and in the activation of glycolysis (anaerobic 2.5 times, the aerobic 3.7 times). Changes in the bioenergy of the kidneys are not as great. Phenol in its combined effect with benz[a]pyrene intensifies the effect of the latter, as shown primarily to the greater activation of anaerobic and aerobic glycolysis in the lungs and livers of test rats. The observed disturbances as concern the weight dynamics of the animals (weight loss in test rats), vitamin metabolism (their decrease in the organs in in urine) and hemopoiesis of red blood cells (erythropenia) attest to the toxic effect of benz a pyrene phenol on the organism, which is greater in the case of the combined action of the studied agents. No changes were discerned in the morphology of white blood cells.

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