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Biomedical subjects

D I Roshchupkin

Publications and source records attributed to D I Roshchupkin.

At least 19 recordsLinked to original sources
PubMed2004

Structure and oxidation capacity of amino acid chloramine derivatives and their effects on platelet aggregation.

Comparison of antiaggregation capacity of N-chloramine acids with different position of the chloramine group in the molecule showed that in the most efficient compounds the distance between the chloramine and carboxyl groups was 3-5 carbon atoms. This feature of antiaggregation activity was not related to the difference in oxidation capacity of N-chloramine acids. It was hypothesized that the revealed structural dependence of antiaggregation activity of N-chloramine acids is determined by the structure of platelet membrane, in particular, the presence of a negatively charged group near the site of interaction between N-chloramine acids and platelet membrane.

Amino Acids↗
PubMed2002

Antithrombotic activity of N,N-dichlorotaurine on mouse model of thrombosis in vivo.

Intravenous injection of chloramine derivatives of amino acids and taurine reduced the mortality rate in mice with thrombosis induced by intravenous injection of ADP or collagen-epinephrine mixture. Intravenous injection of N,N-dichlorotaurine caused 50% inhibition of platelet aggregation induced by ADP and measured in the platelet-enriched plasma in vitro. The antithrombotic effect of chloramine derivatives of amino acids and taurine is related to their ability to suppress functional activity of platelets.

Adenosine Diphosphate↗
PubMed1998

Free-radical and cyclooxygenase-catalyzed lipid peroxidation in membranes of blood cells under UV irradiation.

The data on the role of lipid peroxidation in the effects of UV irradiation of blood are reviewed. Lipid photoperoxidation in blood cells is the result of photochemical transformation of lipid hydroperoxides, both existing and newly formed ones, into free radicals and direct photolysis of photooxidants. Dark lipid autoperoxidation is also induced by UV radiation. Both peroxidation and photooxidation of lipids are inhibited by low concentrations of antiradical antioxidants. The cyclooxygenase-catalyzed peroxidation of arachidonic acid in blood cells is stimulated by UV radiation. This process is suppressed by acetylsalicylic acid and indomethacin. The therapeutic activity of the blood that was UV-irradiated and then infused into rats with peritonitis was due to the cyclooxygenase activation.

Animals↗
PubMed1995

[Molecular mechanisms of the effects of sodium hypochlorite on thrombocytes and lipoproteins].

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.

Animals↗
PubMed1986

[Anti-aggregation action of hypochlorite on the thrombocytes].

Sodium hypochlorite at concentrations higher than 1 mM suppresses ADP-dependent aggregation of blood platelets. The effect was associated with the process of cell modification. Blood platelet aggregation may be depressed partially by ADP destruction. Products of ADP-sodium hypochlorite interaction may lead to the induction of blood platelet aggregation, which is not so intensive than the ADP-induced one.

Adenosine Diphosphate↗
PubMed1984

PUVA-induced erythema and changes in mechanoelectrical properties of skin. Inhibition by tocopherols.

Influence of antioxidants on two phototoxic effects of 8-methoxypsoralen (8-MOP) was studied: erythema and changes in mechanoelectrical properties of skin. alpha-Tocopherol and its analogs with shortened lateral hydrocarbon chains at C2-atoms of chromane groups (chromanols) were used as antioxidants. alpha-Tocopherol and its analogs inhibited both phototoxic effects of 8-MOP. Inhibition was observed only if antioxidants were present in skin during irradiation. When applied after irradiation these antioxidants produce no inhibitory effect. The antioxidant antierythemal action depends greatly on their concentration. The protective effects is maximal at antioxidant concentrations 2.5 . 10(-10) - 5 . 10(-9) mol . cm-2 of skin, at concentrations higher than 5 . 10(-9) mol . cm-2 the protective action is decreased. The protective effect of antioxidants depends on the irradiation dose.

Animals↗
PubMedDate not supplied

[Chemiluminescence in oxidation of luminol by chloramine derivatives of biogenic compounds].

Chloramine derivatives of amino acids induce chemiluminescence of a luminol solution. The chemiluminescence is more prolonged than the emission of luminol produced by hypochlorite. Persistent chemiluminescence also appears under the action of hypochlorite on a mixture of luminol and amino acids. It is assumed that the chemiluminescence of luminol in suspensions of stimulated phagocytes may be associated with its oxidation by chloramines.

Chloramines↗
PubMedDate not supplied

[Kinetic characteristics of luminol chemiluminescence caused by chloramine compounds].

The decaying part of the kinetic curves of luminol chemiluminescence (0.02 mM) induced by N-chlorphenylalanine is approximated by an exponential dependence, which varies insignificantly as chloramine concentration is changed from 0.2 to 0.7 mM. On the whole, the chemiluminescence of luminol is a result of its oxidation, which occurs in three stages with the formation of two intermediate products. N-Chlorphenylalanine is involved in the process at the initial stage. The reciprocal of the time the luminescence reaches a maximum increases linearly with the growth of N-chlorphenylalanine concentration. According to the calculations using the equations that reflect three stages of luminol conversion in the presence of excess chloramine, the rate constant for the initial stage is about 10(3) l/(mol.min). The rate constant for one stage of the conversion of luminol oxidation product is approximately 0.2 min-1, and the rate constant of the other is severalfold greater. Luminol chemiluminescence induced by low concentrations of N,N-dichlortaurine is more durable. Probably, it is composed of two types of emission one of which slowly decays.

Alanine↗