Association of CD2 with fibrinogen in human plasma: depletion of the soluble E-receptor in blood clotting.

The soluble E-receptor (SER) of lymphocytes that is related to CD2 was detected in human plasma and serum using immunoelectrophoresis with sheep antiserum. All plasma samples (n=18) demonstrated reactivity with antiserum, whereas the reactivity of the corresponding sera remained low or undetectable. The depletion of SER in clotting is associated with fibrinogen, as shown by crossed-affinity immunoelectrophoresis with antisera to plasma proteins. The SER-associated fibrinogen was purified and analysed by the SDS-polyacrylamide gel electrophoresis and immunoblotting. A band close to 66 kDa was detected with monoclonal antibodies to CD2. The association of CD2 and other soluble receptors with fibrinogen via domains is suggested. It is recommended that the fresh plasma, not serum, should be used to study circulating receptors because coagulation may appreciably diminish their physiological level in blood samples.

The isolation and characterization of human natural alphaGal-specific IgG antibodies applicable to the detection of alphaGal-glycosphingolipids.

The Galalpha1-3Galbeta (alphaGal) hapten is xenogeneic for humans; natural anti-alphaGal antibodies are present in human serum. To study the possible abnormal expression of the alphaGal in humans and the pathophysiological role of antibodies, the method of affinity purification of human anti-alphaGal IgG was developed. The specificity of antibodies was evaluated using polyacrylamide (PAA)-based glycoconjugates in direct and competitive enzyme-linked immunosorbent assays (ELISA). The purified antibodies exhibited alphaGal-restricted specificity. The IC50 value for alphaGal-PAA was equal to 4 x 10(-8) M. In a competitive assay, the Galalpha1-3(Fucalpha1-2)Galbeta-PAA (trisaccharide of blood group B) was found to be one hundred times less active inhibitor than alphaGal-PAA. The multivalent alphaGal-PAA was 1100 times more potent an inhibitor than the monovalent spacered alphaGal-saccharide. The antibodies did not show any reactivity to the negatively charged antigens (DNA, human tumor-derived mucins). At a concentration of 2 microg/mL, the antibodies agglutinated rabbit erythrocytes but not hare erythrocytes. The high reactivity of antibodies to the alphaGal-glycosphingolipids of rabbit erythrocytes and the pig kidney was shown by a modified sensitive method of thin-layer chromatography with immunodetection.

[Photolysis of aflatoxin B1 in the presence of pyridine N-oxide]. / Fotoliz aflatoksina B1 v prisutstvii N-okisi piridina.

Aflatoxin B1 (AFB1) photolysis in presence of pyridine N-oxide was studied. It was established that AFB1 ethanol solution irradiated with UV-light lambda = 362 nm demonstrated an increase of the fluorescence as a result of appearance of AFB1 product which was formed by pyridine N-oxide oxygen binding to AFB1 molecules in position 2,3.

[Microsomal and photochemical oxidation of aflatoxin B1]. / Mikrosomal'noe i fotokhimicheskoe okislenie aflatoksina B1.

The UV irradiation (lambda = 362 nm) of aflatoxin B1 (AfB1) dissolved in water resulted in the formation of an oxidized product. The process was not inhibited by ionol, a routine inhibitor of the radical processes. The oxidized product was not found in the system where AfB1 was metabolized by the 3-methylcholanthrene-activated rat liver microsomes. It is suggested that the product is identical with 2,3-dihydrodiol of AfB1.

[Kinetics of benzo[a]pyrene penetration into the mouse skin after treatment with various phenols]. / [Kinetika proniknoveniia benz[a]pirena v kozhu myshei pod vliianiem razlichnykh fenolov.

A mathematical method for the study of benzo(a)pyrene (BP) penetration into the skin of nude mice was elaborated and supported by the experimental data. BP, whose concentration was measured by its fluorescence intensity, was applied to the skin using a "dry" technique. The effect of certain phenols and products of oxybenzene oxidation was studied. It was found that only butylated hydroxytoluene inhibits essentially the rate of BP metabolism.