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A B Syrkin

Publications and source records attributed to A B Syrkin.

At least 19 recordsLinked to original sources

[The drop in toxicity and the rise in the effectiveness of antineoplastic chemotherapy by correcting the activity of liver monooxygenases: from the experiment to the clinical practice].

The paper reviews both the data available in the literature and the authors' own results of long-term experimental and clinical investigations of the involvement of hepatic monooxygenases (HMO) in the biological activity of antitumor drugs. It reports data of evaluation of HMO activity in pediatric and adult cancer patients, which has shown a decrease in HMO activity in one third of patients without clinical signs of hepatopathy and two thirds of those with toxic hepatic damages after prior chemotherapy. Decreased HMO activity has been found to be stimulated with the enzyme inductor zyxorin. Altered biochemical parameters, such as total bilirubin, ALT and AST, can be corrected with HNO, even if they show a 10-fold deviation from the normal physiological level. The efficacy of zyxorin was tested in patients with advanced cancer and concomitant toxic or viral hepatic disorders (grades II-IV by the WHO classification). Stimulation of inhibited HMO activity allows both decrease and prevention of the manifestations of hepatic toxicity due to anticancer chemotherapy providing a beneficial effect, the dose of cytostatics being not reduced. The authors concluded that the findings provide strong evidence for their assumption that the efficiency of antitumor chemotherapy can be enhanced in patients with concurrent hepatic abnormality by stimulating monooxygenases whose activity is diminished in the majority of these patients.

Adolescent↗

CD95 (FAS/APO-1) antigen is a new prognostic marker of blast cells of acute lymphoblastic leukaemia patients.

We analyzed CD95(Fas/APO-1) antigen expression on bone marrow blasts in 38 children with acute lymphoblastic leukemia (ALL) receiving a treatment in the Department of Leukaemias at the Cancer Research Center in 1987-1989 years (n = 22) and in 1994-1997 years (n = 16). CD95 antigen expression was studied by monoclonal antibodies (MoAbs) IPO-4 in indirect immunofluorescence analysis. CD95 antigen was expressed on 35.8 +/- 7.5% bone marrow blasts, most frequently (63.6%) in the clinically favourable Pre-B ALL. Only in this group CD95 antigen expression was correlated with CD10 antigen expression that has a positive influence to the time of complete remission in ALL patients. Our data showed that CD95 expression on blast cells is a favourable prognostic sign, associated with increased relapse-free and total survival. On the contrary, the absence of CD95 antigen on blasts is an unfavourable sign for disease evolution.

Adolescent↗

[Effect of calcium gluconate on the toxicity and antitumor of doxorubicin in mice].

The effect of calcium gluconate on the toxicity and specific activity of the anthracycline antibiotic doxorubicin was studied on mice with transplanted hemoblastosis La or plasmocytoma MOPS-406. In both cases after the animal exposure to nontoxic therapeutic doses of doxorubicin no influence of calcium gluconate on the antibiotic antitumor activity was observed. When doxorubicin was used in toxic (and even lethal) doses the antitoxic effect of calcium gluconate and an increase of the antibiotic therapeutic activity were stated. The combination of calcium gluconate and doxorubicin made it possible to significantly increase the maximum therapeutic effect of doxorubicin (higher levels of the animal survival and some cures) and to widen the ranges of the drug therapeutic doses at the account of decreasing the toxicity of the antibiotic and increasing its dose. The results suggested that the antitoxic modifier calcium gluconate could be used for increasing anticancer efficacy of doxorubicin which is given now at the total dose limit of 550 mg/m2 even in cases with preserved tumor sensitivity to the drug.

Animals↗

[The effect of calcium gluconate on the acute and chronic toxicity of doxorubicin in mice].

The effect of calcium gluconate on the toxicity of the anthracycline antibiotic doxorubicin (DOX) in mice was studied. Calcium gluconate showed a significant protective action with respect to the DOX acute toxicity. When DOX was used in the lethal doses, up to the LD50s calcium gluconate protected all the mice from death. At the DOX LD100 or higher the antitoxic effect of calcium gluconate manifested itself in a lower death rate and/or in a higher lifespan of the animals (at least 2-fold). When DOX was used for the treatment course its chronic toxicity in the presence of calcium gluconate was 2 or more times lower by all the quantitative indices: the lifespan of the animals that died, the maximum and minimum total lethal doses of DOX, the latent period before the first mouse death, the overall duration of the DOX treatment course. The antitoxic effect of calcium gluconate also manifested itself in a lower DOX acute and chronic toxicity with respect to the gastrointestinal tract. Thus, calcium gluconate proved to be an effective DOX antitoxic modificator which provided the use of about 2 times higher single and courses doses of DOX in mice.

Animals↗

[ICO-166 monoclonal antibodies against the CD45RA antigen].

Monoclonal antibodies (MCA) ICO-166 against CD45RA antigen were generated and characterized. In the indirect IFA, MCA ICO-166 reacted with 54.1 +/- 1.9% lymphocytes of human peripheral blood and 15.2 +/- 2.3% monocytes but not with granulocytes or thrombocytes. The method of double labelling of cells demonstrated that MCA ICO-166 detected all B-lymphocytes, all NK-cells and 31% of mature T-lymphocytes but only 55% of CD8 suppressor cells and only 21% of CDA helper cells carried this antigen on the surface. Experiments were carried out to block binding of FITC-labeled MCA ALB11 against CD45RA antigen with human lymphocytes by pretreatment of cells with different concentrations of MCA ICO-166. Treatment of cells with MCA ALB11 blocked binding of MCA ALB11-FITC by 85% on the average. MCA ICO-166 blocked binding of MCA ALB11-FITC by 66% on the average. When different dilutions of MCA ICO-166 were used, the dose-dependent effect of blocking of MCA ALB11-FITC binding was observed. MCA ICO-166 immunoprecipitated a protein band of molecular weight 220 kDa from lysates of mononuclear cells of the human peripheral blood.

Animals↗

[Dextran-ferrite distribution in the body of animals in a nonuniform permanent magnetic field].

Dextran-ferrite (DF) was injected via the femoral artery to the dogs and followed by local magnetization (induction 0.3 T, grade 0.024 T/cm). It has been shown that the local retention of the iron in some tissues of the leg was 3-5 times as high as the control. The magnetization did not increase the local retention of the iron after intravenous injection of DF to mice and rabbits.

Animals↗

[Antidotal and antineoplastic properties of copper sulfate].

Copper sulfate in peroral administration to small experimental animals has an inhibitory effect on the growth of transplanted solid tumors and possesses antidote properties in respect to cisplatin. An antitumor effect of the compound was registered at doses ranging from 10 to 120 mg/kg. Antidote properties are manifested clearly when copper sulfate is applied at a single dose 10 mg/kg, 24 hours before cisplatin administration. It has been determined that copper sulfate decreases acute toxicity, nephro- and hemotoxicity of cisplatin, but fails to change its antitumor effect. The experimental data obtained give the ground for the clinical studies of copper sulfate.

Animals↗

[Antitumor and toxic effects of amotin].

An indole alkaloid isolated from Catharanthus roseus in the Soviet Union and named amotin differs in terpenoid moiety structure of the indole part of the molecule from the foreign preparation vinblastine and its Soviet analog rosevine. In experimental study amotin has exhibited a high antileukemic activity which was more expressed than that of vinblastine. Tolerant doses of amotin cause moderate reversible morphological alterations in hematopoietic organs, gastrointestinal mucosa, liver, kidney, adrenals, testes, ovaries.

Animals↗

[Effect of the induction and inhibition of liver monooxygenases on the toxic and therapeutic action of vincristine].

The influence of phenobarbital and ziksorin, liver monooxygenase inductors and the influence of inhibitor SKF 525-A on the toxic and therapeutic effects of vincristine were studied on CBA and C57Bl mice (with hemoblastosis La or intact). It was shown that acute toxicity and therapeutic activity of vincristine lowered on induction of the liver monooxygenases, whereas inhibition of this enzymatic system resulted in increased toxicity and lowered therapeutic activity of vincristine. The possible use of these results in treatment of cancer patients is discussed.

Animals↗

[Mitigation of cisplatin toxicity by the complexon tetacin-calcium].

A possibility to decrease toxic properties of intraperitoneally injected platidiam (cis-platin, CSSR) administered by means of edtacal, a complexon (tetracinium-calcium, CSSR), administered per os is studied. It is established in intact mice that administration of edtacal simultaneously with platidiam or 1 h before decreases the mortality rate, diarrhea incidence and animal body mass loss. Edtacal is shown to have also an antiemetic action. Edtacal administered simultaneously with platidiam as well as 1 and 3 h before its injection does not decrease the antitumour activity of the preparation in (C57B1 X CBA)F1 mice with the Ehrlich ascite carcinoma.

Animals↗

[Effect of phenobarbital and SKF 525-A on the toxic and therapeutic action of adriamycin in mice with Ehrlich ascites cancer].

The toxic action of adriamycin (AD) in mice with the ascitic Ehrlich carcinoma was reduced by preliminary administration of phenobarbital (PB), an inductor of liver monooxygenases, and was increased after administration of SKF 525-A, an inhibitor of this enzymatic system. PB and SKF decrease the therapeutic action of AD. Incidentally, induction or inhibition of the liver enzymes was equivalent to the decrease in the AD dose in mice with the intact liver. It was also shown that the essence of PB and SKF influence on the AD therapeutic effect is its action on liver monooxygenases activity and not the interaction between PB or SKF and AD or the change of AD sensitivity of tumour cells. The possible role of cytochrome P-450 in manifestation of the AD toxic and therapeutic activity is discussed. The authors believe that for prevention of AD toxicity in patients with liver disorders the treatment following stimulation of the liver metabolic activity up to the normal liver level may be effective.

Animals↗