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Biomedical subjects

S M Sitdikova

Publications and source records attributed to S M Sitdikova.

At least 19 recordsLinked to original sources
PubMed2006

Peculiarities of hemoglobin interaction with serum proteins of mice with Ehrlich carcinoma.

In male C57Bl/6 mice with transplanted Ehrlich carcinoma, hemoglobin forms a complex with serum proteins characterized by a molecular weight of about 300 kDa. The complex incorporates proteins weighing 100, 68, 65, and 15 kDa identified by MALDI-TOF mass spectrometry as haptoglobin, serum albumin, gi/26341396 nameless protein Mus musculus, and alpha-hemoglobin, respectively. This complex can possess biological activity and contribute to the control of tumor growth.

Animals↗
PubMed2005

Lectin binding to mouse blood lymphocytes during tumor growth.

Binding of FITC-labeled lectins to lymphocytes from intact mice and mice with transplanted Ehrlich carcinoma and CaO-1 ovarian carcinoma was studied by flow cytofluorometry. Specific binding of lectins by mannose and N-acetylgalactosamine was demonstrated. Lectin binding to lymphocytes from animals with tumors decreased by more than 50% in comparison with intact animals. Changed protein glycosylation during tumor growth is specific and differs for tumors of different origin.

Acetylgalactosamine↗
PubMed2003

Partial elimination of lymphocytes in mice with Ehrlich carcinoma.

Elimination of about 30% lymphocyte population was observed in female Balb/c mice on day 11 after transplantation of Ehrlich carcinoma in comparison with animals without tumor. It was hypothesized that the eliminated population can block the tumor growth. Studies of the temporal and quantitative parameters of lymphocyte elimination with consideration for tumor size are considered to be perspective. The described model can be used for studies of immunodeficiency in animals with tumors.

Animals↗
PubMed2003

Tumor-specific changes in mouse serum during Ehrlich carcinoma growth.

Using the method of flow cytofluorometry we found that proteinase activity eliminating antigenic determinants from the surface of tumor cells disappeared from the serum of mice with Ehrlich carcinoma. This activity towards Ehrlich carcinoma cells is present in the sera of mice without tumors and in mice with other transplanted tumors. The serum from mice of one strain with Ehrlich carcinoma showed no protease activity against Ehrlich carcinoma cells in mice of other strain. Hence, Ehrlich carcinoma growth is associated with tumor-specific changes in the serum resulting in disappearance of specific protease activity of the serum against tumor cells.

Animals↗
PubMed2000

Antitumor activity of specific immunotherapy with mucin containing CA 125 antigen in mice with CaO 1 ovarian carcinoma.

Experiments in CBA mice with transplanted CaO 1 ovarian carcinoma possessing common antigenic determinants with human ovarian carcinoma showed that specific immunotherapy with mucin containing CA 125 antigen inhibited tumor growth by 60% and prolonged animal lifespan by 40-60% in comparison with the control. The correlation coefficient between the tumor size and antibody titer after injection of mucin was -0.4 for IgM and -0.6 for IgG. Titration of IgG may be used for monitoring of the efficiency of specific immunotherapy.

Animals↗
PubMed2000

Immunotoxicological characteristics of preparations based on carcinoembryonic antigen and mucin containing CA 125 antigen.

Experiments on male hybrid mice demonstrated that specific immunotherapy with preparations based on carcinoembryonal antigen and mucin containing CA 125 antigen was not associated with general toxicity, local irritating effect, and hepatorenal dysfunction. The absence of toxicity is apparently due to the fact that antigens injected intramuscularly or subcutaneously virtually do not enter the blood. Injections of preparations based on carcinoembryonal antigen and mucin containing CA 125 antigen to mice induced a standard immune response with predominance of class M immunoglobulins during the early terms and class G immunoglobulins at later terms.

Animals↗
PubMed1993

[The cross resistance to cytostatics of leukemia P388 cells with induced resistance to doxorubicin].

Using BDF1 mice it has been shown that P388 leukemia tumor cells with induced resistance to doxorubicin (P388/DX) were cross-resistant to daunomycin, carminomycin, actinomycin D, vincristine and mitomycin C. It has been shown that P388/DX leukemia tumor cells were sensitive to bleocina, bleomycitina, cyclophosphamide, 5 fluorouracil. It has been discussed the ways of cross-resistance of P388/DX leukemia tumor cells to cytostatic drugs.

Animals↗
PubMed1992

[The characteristics of Ehrlich carcinoma recurrence and metastasis].

It was shown that surgical removal of Ehrlich carcinoma growing i. m. in male mice F1 (CBA C57Bl/6) does not entail longer survival in comparison with intact tumor-bearing mice (59.4 and 62.2 days, respectively). Postoperative relapses appear in 40-60% of the animals, metastases in 100% of animals. Metastases were not observed in intact tumor bearing mice. The second-challenge tumor was not observed in operated mice despite metastatic growth and recurrences of the same tumor. We suggest that metastatic growth depends on the tumor cell features and that this process is controlled by host organism.

Animals↗
PubMed1990

Verapamil effect on the accumulation of doxorubicin in the leukemia P388 cells with induced antibiotic resistance.

Using mice BDF1 it has been shown that the period of retention of Doxorubicin (Dx) is shorter in the leukemia P388 cells with induced antibiotic resistance (P388/Dx) as compared to P388 cells sensitive to Dx. Administration of Verapamil (Vp) to animals leads to an increase of Dx concentration in the leukemia P388/Dx cells during a 240 min observation period. Vp promotes the therapeutic effect of Dx on P388/Dx bearing mice. It can be suggested that the mechanism of Vp action consists in the damaged Dx elimination from cells with induced resistance, since Vp doesn't change the period of circulation of the antibiotic in the blood plasma of mice.

Animals↗
PubMed1990

[The effect of finoptin on doxorubicin accumulation in leukemia P-388 cells with induced resistance to the combination of finoptin and doxorubicin].

Using hybrid mice BDF1 doxorubicin (Dx) accumulation has been determined in leukemia P388 cells (P388/0), P388 cells with induced resistance to Dx (P388/Dx) and P388 cells with induced resistance to the finoptin (Fp) + Dx combination (P388/Fp + Dx). It has been shown that Fp doesn't affect Dx accumulation in or elimination from leukemia cells P388/0 or P388/Fp + Dx. The resistance of P388/Fp + Dx cells to the Fp + Dx combination develops during 6 passages. It can be concluded that Fp application doesn't abolish the problem of tumor cells' resistance to cytostatics.

Animals↗
PubMed1989

[The effect of finoptin on the accumulation of doxorubicin in leukemia P388 cells with induced resistance to the antibiotic].

Using male mice BDF1, it has been shown that the retention period of doxorubicin (DOX) is shorter in the leukemia P 388 cells with induced antibiotic resistance (P 388/DOX) as compared to the P 388 cells, sensitive to DOX. Administration of finoptin (FP) to animals leads to the increase of DOX concentration in the leukemia P 388/DOX cells during 240 min observation. FP promotes the therapeutic effect of DOX on mice bearing leukemia P 388/DOX. It can be suggested that the mechanism of FP action is the damaged DOX elimination from cells with induced resistance, since FP doesn't change the period of antibiotic circulation in the murine blood plasma.

Animals↗
PubMed1989

[Lowering of adriamycin toxicity by its combined administration with a copper Cu-2 complex].

Cu-2, a new Soviet copper-complexed cytostatic, decreased acute and hematologic toxicity after lethal doses of adriamycin (AD) were given to male CBA mice. Cu-2 (3.5 mg/kg) was first injected 10 minutes after AD was given, and a second injection followed 50 minutes after the first. Relative to controls given AD alone, the mortality of Cu-2 treated mice was decreased and their lifespan increased. Leukopenia also was less pronounced and of shorter duration. The observed effect of Cu-2 may be related to its superoxide dismutase activity, which may inactivate free radical by-products of AD metabolism known to contribute significantly to the toxicity of this anti-cancer antibiotic.

Animals↗