[The practical application of marker -2proPSA and health index of prostate phi in diagnostics of prostate cancer].

The article demonstrates that prostate-specific antigen (PSA) has some limitations in detection of cancer of prostate. It was demonstrated that isoform of free PSA - 2proPSA has higher specificity in comparison with total PSA (tPSA) and percentage tPSA and free PSA (%free PSA) in detection of cancer of prostate. The application of Prostate Health Index including such indicators as -2PSA, free PSA and tPSA makes it possible to increase degree of detection of cancer of prostate, to increase specificity and to decrease number of optional biopsies. Besides, correlation was established between value of Prostate Health Index and degree of aggressiveness of forms of cancer of prostate.

Hypochlorite induces lipid peroxidation in blood lipoproteins and phospholipid liposomes.

The accumulation of lipid peroxidation products reacting with 2-thiobarbituric acid (TBARS) has been observed both in very low density blood lipoprotein (VLDL) and suspensions of liposomes prepared from VLDL phospholipids incubated with hypochlorite. Butylated hydroxytoluene (BHT) completely inhibited TBARS formation at a concentration of 100 microM, at which it decreased the concentration of hypochlorite in the absence of liposomes only by 7%. The formation of lipid peroxidation products in course of the incubation of egg yolk phospholipid liposomes with hypochlorite has been revealed using three methods: (1) measurement of TBARS, (2) measurement of additional amounts of TBARS resulting from the introduction of excess Fe2+ to peroxidized liposomes (delta TBARS), and (3) measurement of the chemiluminescence flash amplitude appeared upon the addition of Fe2+ to the suspension. The results obtained by all these methods were similar: Lipid peroxidation products were accumulated during the first 2 to 3 h of liposome incubation with 100 microM hypochlorite, and the amount of lipid peroxidation products accumulated after incubation was directly proportional to the initial hypochlorite concentration. These data suggest that hypochlorite can initiate lipid peroxidation both in lipoproteins and phospholipid liposomes.

[The effect of hypochlorite on electrical surface properties of human blood lipoproteins]. / Vliianie gipokhlorita na élektricheskie svoistva poverkhnosti lipoproteinov krovi cheloveka.

Surface potential of human blood lipoproteins was studied by the use of Mn(2+)-ions as a positively charged spin probe. The calculated values of surface potential of low density lipoproteins (LDL) appeared to be -17.7 +/- 1.2 mV. It was shown that hypochlorite (OCl-) induced an increase of negative surface potential of LDL. Agarose gel electrophoresis was used for the comparative analysis of electrophoretic mobility of human blood lipoproteins of different classes. It was shown that the interaction of hypochlorite with lipoproteins caused the partial degradation of lipoproteins and the increase in surface charge. High density lipoproteins appeared to be more resistant to the action of OCl- than LDL and especially very low density lipoproteins.

[Molecular mechanisms of the effects of sodium hypochlorite on thrombocytes and lipoproteins]. / Molekuliarnye mekhanizmy deistviia gipokhlorita natriia na trombotsity i lipoproteiny.

Hypochlorite seems to inhibit platelet aggregation in the platelet-rich plasma (PRP) by modifying fibrinogen receptors. The hypochlorite-inactivated isolated platelets are completely repaired by native plasma. Platelet aggregation in PRP is suppressed by hypochlorite by its direct interaction with cells and indirectly due to plasma modification. The indirect action of hypochlorite is a reversible reaction between the platelet active groups and the products of plasma modification. The reaction may involve sulphur-containing groups. The spin-probe method shows that hypochlorite penetrates into the lipid phase of human blood lipoproteins. It initiates lipid peroxidation and causes the disturbance of the lipid structure and the protein please.

Peroxidation of human blood lipoproteins induced by exogenous hypochlorite or hypochlorite generated in the system of "myeloperoxidase + H2O2 + Cl-".

Oxidation of human plasma lipoprotein (LP) was studied in the presence of exogenous hypochlorite anion (OCl-) or OCl- generated in the "myeloperoxidase + H2O2 + Cl-" system. OCl- effectively initiates peroxidation of lipids extracted from LP and those within LP particles, as can be judged from accumulation of secondary (thiobarbituric acid [TBA] reactive) and final (Schiff bases) products of lipid peroxidation (LPO) in LP after incubation with myeloperoxidase or exogenous OCl-. Very low density and low density lipoproteins classified as atherogenic LP are more sensitive to OCl(-)-induced LPO than high density lipoproteins. These data allow us to propose that OCl- secreted by activated neutrophils and monocyte-macrophages can produce oxidative modification of LP in vivo. The latter is known as a risk factor in the development of atherosclerosis.

[A spin-probe study of the structural change in human blood lipoproteins under the action of sodium hypochlorite]. / Issledovanie metodom spinovykh zondov izmeneniia struktury lipoproteinov krovi cheloveka pod deistviem gipokhlorita natriia.

The spin-probe technique was used to study structural changes in the surface proteolipid layer of human blood low-density lipoproteins (LDL) peroxidized to different degree by sodium hypochlorite (NaOCl). The paramagnetic analogs of stearic acid were employed as spin labels that contained nitroxide groups localized at different distances from the LDL surface. In addition, a positively charged spin label was used which was distributed at the lipid-water interface, in the area of polar phospholipid groups. NaOCl was shown to induce the lipid peroxidation of LDL. It diminished the mobility of polar "heads" as well as of acyl phospholipid chains up to 1.7 nm from the LDL particle surface and increased the polarity of lipid phase in this region. In the deeper layers (2.0-2.2 nm) the structural alterations in LDL were registered only at NaOCl concentration more than 1 mM.

[Capacity of hypochlorite to penetrate into the lipid phase of human blood lipoproteins]. / Izuchenie sposobnosti gipokhlorita pronikat' v lipidnuiu fazy lipoproteinov krovi cheloveka.

In order to elucidate the possibility of hypochlorite (NaOCl) presenting in aqueous media to penetrate into the surface proteolipid layer of low density lipoproteins (LDL), the kinetics of NaOCl-induced oxidation of spin probes localized within the lipid phase was studied. The paramagnetic analogs of stearic acid were employed as spin probes that contained doxyl groups localized at different positions on the carbon chain (at positions 5, 13 and 16). It was shown that all the three probes are oxidated by hypochlorite with the same rate both in aqueous media and in LDL. The results obtained indicate that hypochlorite in water may interact with groups in the lipid phase of LDL, including unsaturated--HC = CH--bonds.