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Biomedical subjects

F V Donenko

Publications and source records attributed to F V Donenko.

At least 37 records · Page 2Linked to original sources
PubMed1992

[The effect of ascitic fluid globulins on the growth of leukemia P388/DOX and Ehrlich's carcinoma in mice].

The study was performed to investigate the effect of ascitic fluid globulins of tumor on tumor growth and life span of mice. The globulins are shown to shorten the life span of Ehrlich tumor mice from 86.8 to 61.8 days, to increase 3-5-fold the growth rate of Ehrlich carcinoma and P388/DOX tumor. It was found that globulins of ascitic fluids and serum globulins of tumor have equal effects of tumor growth. It is proposed to use globulins of ascitic fluid to study the globulin role in tumor growth.

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↗
PubMed1992

[Mouse serum inhibition of cytotoxicity of goat antibodies against mouse thymocytes].

It is shown that the serum of Balb/c, C57Bl/6 and F1(C57Bl/6 x CBA) mice inhibits cytotoxicity of goat antithymocyte antibodies. The addition of the serum into the incubation medium increases the proportion of alive cells from -5% up to 95%. Cytotoxicity was also inhibited by the globulin fraction of the mice serum. It is suggested that normal mice serum contains factors which block cytotoxicity of antibodies against antigen host determinants.

Animals↗
PubMed1992

[The effect of ascitic fluid on the growth of Ehrlich tumor and Lewis carcinoma].

In the study of the effect of ascitic fluid and dialysate of Ehrlich ascites tumor cells (m.m. less than 15 kDa) on the growth of Ehrlich and Lewis carcinoma it was found that the ascitic fluid significantly decreased the size of Ehrlich tumor (by more than 50% on day 9-25 after the tumor cell inoculation). It also reduced Lewis carcinoma tumor volume by more than 30% during 3 weeks after the tumor cells inoculation. Dialysate of Ehrlich tumor cells significantly inhibited the growth of Ehrlich tumor too. It is suggested that this test-system simulates inhibition of a small tumor by a big tumor in vivo.

Animals↗
PubMed1992

[The modelling of the growth of Ehrlich carcinoma and teratoma T-36 with ascitic fluid and tumor-cell dialysate].

The study of the effect of ascitic fluid and dialysate of Ehrlich ascites tumor cells (M.m. less than 15 kDa) on the growth of Ehrlich carcinoma and teratoma T-36 has shown that both the ascitic fluid and dialysate can protect tumor cells in vivo. The number of animals with tumors increased from 0% in control animals to 60 and 20%, respectively, in experimental ones after transplantation i.m. of 20 x 10(3) Ehrlich tumor cells into mice. Compared to control, ascitic fluid and dialysate of Ehrlich ascites tumor cells increased the rate of tumor growth to 195 and 153%, respectively. It is suggested that this test-system simulates the effect of tumor humoral factors in vivo.

Animals↗
PubMed1991

[The expression of P-glycoprotein in leukemia P388 cells with induced doxorubicin resistance].

beta-D-galactose-containing glycoproteins were prepared from cells P-388 leukemia and from P-388 leukemia cells with induced resistance to doxorubicin. It was shown by HPLC method that plasma membranes from resistant cells contain 4-4.5% P-glycoproteins and plasma membranes from sensitive cells contain P-glycoproteins about 10 times lower.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1991

[Changes in glutathione-S-transferase activity during induction of resistance of leukemia P 388 and Ehrlich ascitic tumor cells to doxorubicin].

We have studied by uridine short term test the level of resistance of murine leukemia cell lines P 388/Dx and ELD/Dx carcinoma cells with induced resistance to doxorubicin, P 388/Fp + Dx cells with induced resistance to combination of finoptOFF++ and doxorubicin in vivo. It was shown that the level of resistance was 6 fold for P 388/Dx cells, 4.5 fold for ELD/Dx cells and 2 fold for P 388/Fp + Dx cells. It was shown that the P 388/Dx cells and P 388/Fr + Dx cells had a 3.5 and 4.4 fold increase level of glutathione-S-transferase activity than P 388 cells. No increase in the activity of glutathione-S-transferase was detected in ELD/Dx cells. We conclude that increase of cellular glutathione-S-transferase activity is not associated with the development of resistance to doxorubicin.

Animals↗
PubMed1991

[Effect of Triton X-100 on accumulation and therapeutic effect of doxorubicin in mice with leukemia P-388 with induced resistance to cytostatic agents].

Using P 388 and P 388/Dx tumour-bearing mice BDF1 it has been studied effect Tritton X-100 on accumulation and therapeutic action of doxorubicin (Dx). It has been shown that LD50 of Tritton X-100 is 153.6 mg/kg and MTD is 80 mg/kg body weight of animals. It has been shown that Tritton X-100 in dose 40 mg/kg body weight increases initial level of Dx in P 388/Dx cells to 215% and doesn't change accumulation of Dx in P 388 cells. It has been shown that Tritton X-100 doesn't influence the therapeutic effect of Dx in P 388 and P 388/Dx tumour-bearing mice.

Animals↗
PubMed1991

[The effect of finoptin on the metabolism and pharmacological action of cyclophosphane in vivo and in vitro].

Phynoptin (Ph) and cyclophosphamide (CP) gave rise to a type I spectral changes with liver microsomal fraction. KS were 15 microM and 2150 microM, respectively. Ph increases the concentration of NBP product(s) of CP and acrolein in the blood plasma of animals. Ph increases a toxicity of CP. LD50 was 388.0 +/- 13.9 mg/kg for CP and LD50 was 342.8 +/- 16.9 mg/kg for CP in combination with Ph. Ph changes a therapeutic action of CP in mice with hemocytoblastosis La. Pharmacokinetic interactions have been demonstrated between calcium antagonists Ph and CP.

Animals↗
PubMed1990

[Comparative accumulation of the Hoechst 33258 fluorescent probe in leukemia P388 cells sensitive and resistant to doxorubicin].

The authors studied accumulation of the fluorescent probe Hoechst 33258 in leukemia P 388 sensitive (P 388/0) and resistant to doxorubicin (P 388/DOX) cells. It was shown that intensity of fluorescence of the dye increased after binding with nuclear DNA during 25 min for both lines of the cells. Intensity of fluorescence was 40% greater in sensitive than resistant cells. If Triton X-100 was added no difference between two lines of the cell was observed. When doxorubicin was added to the cells with dye, the intensity of fluorescence decreased. It was suggested to use Hoechst 33258 for assessment extent doxorubicin accumulation in nuclei of the cells.

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↗
PubMed1990

[Modification of doxorubicin action with artificial hyperglycemia].

Approximately a 1.6-fold increase in the antitumor action of doxorubicin used in combination with artificial hyperglycemia was shown on mice C57B1/6 with hemocytoblastosis La. Artificial hyperglycemia was found to change the doxorubicin pharmacokinetics in the experimental animals evident from increased in antibiotic half-life to 42.3 min against 26.5 min in the controls, the apparent initial concentration of doxorubicin being increased 1.6 times. Accumulation of doxorubicin in the bone marrow cells of the mice did not change with artificial hyperglycemia. It was suggested that the increase in the therapeutic effect of doxorubicin used in combination with artificial hyperglycemia was associated with changes in drug pharmacokinetics.

Animals↗
PubMed1989

[Changes in amino acid metabolism at the onset of colchicine resistance in Dzungarian hamster fibroblast cell culture].

We have studied amino acid up-take from incubation media by colchicine-resistant and colchicine-sensitive Djungarian hamster fibroblast cells. It has been shown that arginine and asparagine amino acid contents in the medium are different for colchicine-sensitive and colchicine-resistant cells. Amino acids concentration is not reduced in the medium after incubation of resistant cells, while it is decreased after incubation of sensitive cells. We can suggest that penetration of low-weight sources of nitrogen into sensitive cells is hampered. It can also be suggested that protein macromolecules are the main source of nitrogen for these cells. The protein up-take levels from the incubation medium, as assessed by the ammonia and amino acid contents of cell counts don't exceed 5% of their initial concentrations in the medium.

Amino Acids↗
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↗