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At least 163 records · Page 9Linked to original sources
PubMed1993

Reversal of doxorubicin-resistance in sarcoma 180 tumor cells by inhibition of different resistance mechanisms.

Resistance of tumor cells to doxorubicin is a multifactorial phenomenon. In the present investigation, the ability of resistance modifiers against different resistance mechanisms was analysed. Substances which block P-glycoprotein (P-170) function circumvented resistance of doxorubicin-resistant sarcoma 180 (S180) cells completely (verapamil, thioridazine) or partially (hycanthone), whereas inhibitors of glutathione S-transferase (ethacrynic acid, N-ethylmaleimide, buthionine sulfoximine), and protein kinase C (staurosporine, acridine orange) caused only a partial reversion of resistance. In contrast, an inhibitor of alkaline phosphatase (levamisole) did not overcome doxorubicin-resistance. These results indicate that P-glycoprotein blockers might be more effective to modulate doxorubicin-resistance of S180 cells as compared to other modifiers. Further investigations using other MDR cell lines are required to clarify the generality of these findings.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

The synthetic peptide related to the central part of human interleukin-2 molecule accelerates growth and vascularization of sarcoma 180 in mice.

The synthetic peptide C-1-6 related to the central part of human interleukin 2 molecule (sequence 59-72; N- and C-modified) had been shown previously to inhibit cytotoxic activity of macrophages converting them to synthesis of growth factors. In this paper the effect of C-1-6 on growth of sarcoma 180 in mice was studied. C-1-6 significantly accelerated tumor growth having been injected into mice in dose 5 or 50 microg per animal since the 4th day after tumor cells transplantation. Supernatants of Mphi in vitro activated by C-1-6 (10 microg/ml) and injected into mice also accelerated significantly sarcoma mass diurnal increasing as compared to mice treated with supernatants of non-activated Mphi or activated with bacterial lipopolysaccharide. A single injection of C-1-6 into mice either at the day or at the next day of tumor cells inoculation increased significantly the number of vessels growing up to transplant, thus the forming of the vascular bed had preceded tumor volume enlargement.

Animals↗
PubMed2006

Anticancer effect of jinlongshe granules on in situ-transplanted human MKN-45 gastric cancer in nude mice and xenografted sarcoma 180 in Kunming mice and its mechanism.

AIM: To study the antitumor effect of Chinese compound jinlongshe (JLS) granules on sarcoma 180 and MKN-45 human gastric cancer cell lines in vivo and its mechanism. METHODS: After establishment of S180 sarcoma (S180) and MKN-45 gastric cancer model of nude mice, the tumor-bearing mice were divided into 5 groups at random. Three experimental groups were respectively given the aqueous extract of JLS granules at doses of 120 g, 60 g and 20 g/(kg per 6/wk, i.g.) for 3 wk in S180 and 6 wk in nude mice model. Positive control was given cyclophosphamide (Cy) at a dose of 50 mg/(kg per 3/wk, i.g.) for 3 wk in S180 models and 5-Fluorouracil (5-FU) 20 mg/(kg per 3/wk, i.g.) for 3 wk in nude mice model. Negative control was given normal saline (NS) at a dose of 0.18 g/(kg per 6/wk, i.g.) respectively. After 3 wk in mice bearing S180 tumor and 6 wk in nude mice model, the experimental animals were sacrificed and the masses of tumor were weighed, and the rates of tumor inhibition of each treated group were calculated respectively. To determine the antitumor mechanisms, the morphological changes, cell cycle and apoptosis were observed in MKN-45 nude mice model. Annexin V-FITC/PI double staining FCM assay was used to further determine the live cells, apoptotic cells, necrotic cells and debris. RESULTS: The inhibitory rates of JLS granules at the doses of 20 g/kg, 60 g/kg and 120 g/kg were 50.31%, 55.94% and 68.13% (P < 0.01) in nude mice models and 40.90%, 50.32% and 58.46% (P < 0.01) in S180 model. The inhibitory rate of Cy was 85.22% in S180 models and the inhibitory rate of 5-FU was 53.43% in nude mice model (P < 0.01). Nuclear chromatin and margination were observed under a transmission electron microscope (TEM). The G0/G1 phase was arrested, typical apoptotic peak appeared, the apoptotic rate was 22.81%-38.54% in three JLS granule-treated groups. Annexin V-FITC/PI double staining FCM assay showed that the apoptotic cells were 4.36%, 3.08% and 7.08% in three dosages, most cells were localized in the low right quadrant. CONCLUSION: Jinlongshe granules possess anti-tumor effects on experimental tumor models in vivo, and apoptosis induction is one of its anti-tumor mechanisms.

Animals↗
PubMed1979

[Effect of a DNA-rubomycin complex on the molecular mass, radiosensitivity and reparation of gamma-induced single-stranded breaks in the DNA of sarcoma 180 cells].

The use of the DNA-rubomycin complex resulted in appearance of one-thread breaks (OB) in DNA and markedly increased the number of the DNA OB determined immediately after irradiation. The DNA-rubomycin complex decreased the volume of the repaired OB and induced postreparation degradation of the one-bond DNA (oDNA) in the sarcoma 180 cells. The effect of the decrease in the molecular mass of the oDNA 6 hours after the irradiation to the level of the initial damage is probably in favour of the fact that degradation takes place in the areas of the repaired breaks. The data indicated that the viscosimetric method for the analysis of the OB in DNA may be promising in estimation of the efficacy of radiation and chemotherapy of solid tumors.

Animals↗
PubMed1983

Augmentation of host's immunity by combined cryodestruction of sarcoma 180 and administration of protein-bound polysaccharide, EA6, isolated from Flammulina velutipes (Curt. ex Fr.) Sing. in ICR mice.

Augmentation of the host's immunity by combined in situ freeze-destruction of the tumor (cryosurgery) and administration of the antitumor active protein-bound polysaccharide, EA6, isolated from a hot water extract of an edible mushroom, Flammulina velutipes (Curt. ex Fr.) Sing., was investigated in sarcoma 180 bearing ICR mice. Oral administration (p.o.) of the EA6 stimulated anti-sheep red blood cells (SRBC) IgM antibody-producing activity of the spleen cells, and also delayed hypersensitivity (DTH) against SRBC in swelling of the foot pads of the tumor-bearing hosts. When EA6 p.o. was combined with cryosurgery, further augmentation of IgM-producing activity and DTH reaction to SRBC was recognized as compared with the EA6 single use. But the reticuloendothelial system of the mice, estimated by carbon clearance test, was not activated by EA6 p.o. or combined with cryosurgery.

Agaricales↗
PubMed1988

Prolonged survival time of sarcoma 180-bearing mice treated with lipid microspheres-entrapped antitumor marine coral prostanoids.

Antitumor marine coral prostanoids (clavulone II and chlorovulone I) were entrapped into lipid microspheres of 0.2 micron diameter to make lipo-drugs. Daily treatment with lipo-chlorovulone I (1.6 mg/kg/day, i.p.) and lipo-clavulone II (12.5 mg/kg/day, i.p.) on days 1 through 5 markedly prolonged the survival time (135% ILS and 73% ILS, respectively) of mice inoculated with sarcoma 180 as compared with that of a corresponding dose of respective free chlorovulone I and clavulone II. These results suggest that lipid microspheres may be used as drug delivery carriers for antitumor coral prostanoids in vivo.

Animals↗
PubMed1980

Growth-inhibitory activity of the D-mannan of Saccharomyces cerevisiae X2180-1A-5 mutant strain against mouse-implanted sarcoma 180 and Ehrlich-carcinoma solid tumor.

The D-mannan of Saccharomyces cerevisiae X2180-1A-5 mutant strain, which possesses a main chain composed of alpha-(1 yields 6) linked D-mannopyranosyl residues and a small proportion of branches composed of alpha-(1 yields 2)- and alpha-(1 yields 3)-linked D-mannopyranosyl residues, showed strong growth-inhibitory activity against mouse-implanted Sarcoma 180 and Ehrlich-carcinoma solid tumor. The observation that the level of this activity was nearly identical with that of the D-mannan of a wild-type strain of bakers' yeast, which possesses a high proportion of branches composed of alpha-(1 yields 2)-and alpha-(1 yields 3)-linked D-mannopyranosyl residues, suggests that the branches are not essential for antitumor activity. The partial acid-degradation products of both D-mannans, the molecular weight of which was one-third of that of each parent D-mannan, had only one half of the antitumor activity of the parent D-mannans. This suggests that molecular size is the most important factor for the differences in acitvity of the polysaccharides of wild and mutant strains.

Animals↗
PubMed1997

Cytotoxicity of platinum (II) dinuclear complexes with 1-alkylthymine ligands against mouse sarcoma 180 cells.

We synthesized five platinum (II) dinuclear complexes containing 1-alkylated thymines. Two of the 1-alkylated thymine, 1-MeThy and 1-EtThy, complexes afforded good crystals. The X-ray structures of these complexes were determined. The 1-MeThy complexes has a head-to-head (H-H) arrangement, while the 1-EtThy complex has a head-to-tail (H-T) arrangement. The 1-MeThy complex (H-H) shows high electrophilicity against chloride anion (CI-) and high cytotoxicity against mouse sarcoma 180 (S-180) cells in vitro. The 1-EtThy complex (H-T) is inactive. The other 1-MeThy complex does not produce CDDP in the reaction with chloride ion and is inactive against the S-180 cell line. This complex is assumed to have an H-T arrangement. Similarly, two different 1-Pr(n)Thy complexes, one with high electrophilicity and cytotoxicity and the other without, must have an H-H and H-T arrangement, respectively. For comparison, we investigated six complexes, 1-methyluracil (1-MeUra) (H-H) dimer, alpha-pyridone (H-T) dimer, alpha-pyridone blue tetramer (PPB), 1-methylcytosine (1-MeCyt) (H-T) dimer, acetate dimer, and 1-MeUra monomer complexes. The alpha-pyridone (H-T), PPB, 1-MeCyt (H-T) dimer, and 1-MeUra monomer complexes are inert to chloride ion and inactive against mouse sarcoma S-180. The 1-MeUra (H-H) dimer and acetate dimer complexes show high electrophilicity and high cytotoxicity. Cellular accumulation of the platinum complexes phenomenally shows that all are incorporated to cancer cells to a lesser extent than CDDP. The relationships between the accumulation, the electrophilicity, and the interaction of these complexes with proteins are discussed.

Alkylation↗
PubMed1975

The mechanisms of glutaraldehyde-fixed sarcoma 180 ascites cell aggregation.

Sediment height analysis was employed to investigate the mechanisms of cell aggregation by glutaraldehyde-fixed sarcoma 180 ascites cells. The aggregation of these cells proceeds by a polymer bridging mechanism in which the surface molecules of one cell associate directly with the surface molecules of adjacent cells by nonbonding interactions. The ability of adhesive surface macromolecules to serve as polymer bridges is regulated by hydrophobic and coulombic interactions. Hydrophobic interactions are not significantly involved in polymer bridging per se, but instead appear to operate either intramolecularly or between adjacent molecules of the same cell surface, and regulate the conformation and ability of such molecules to form stable intermolecular associations with the surface adhesive molecules of a nearby cell. A disruption of these intrasurface hydrophobic interactions generally promotes cell aggregation. Coulombic forces generated by the fixed charges of surface molecules inhibit aggregation; their diminution by charge neutralization promotes aggregation. It is likely that coulombic repulsive forces regulate intramolecular associations, interactions between adjacent molecules arising from the same cell surface, and interactions between macromolecules arising from different cell surfaces. The actual forces which serve to aggregate two fixed cells are not hydrophobic, but have characteristics commonly attributed to hydrogen bonding. Ion-pairing does not seem to play a role in the aggregation of fixed cells under physiological electrolyte conditions, nor does disulfide bridging.

1-Propanol↗
PubMed1986

Intracavitary chemotherapy with activated cyclophosphamides and simultaneous systemic detoxification with protector thiols in Sarcoma 180 ascites tumor.

Activated cyclophosphamides such as 4-sulfoethylthiocyclophosphamide (mafosfamide) are suitable for a local intracavitary chemotherapy, whereas cyclophosphamide requires a metabolic activation. Mafosfamide administered i.p. in mice was less toxic (50% lethal dose, 640 mg/kg) than its i.v. application (50% lethal dose, 480 mg/kg). A further remarkable reduction of toxicity with an increase of the 50% lethal dose of mafosfamide to 1500 mg/kg was obtained by the simultaneous i.v. application of the protector thiol cysteine (mafosfamide:cysteine ratio, 1:5 on molar weight basis). In comparison with the i.v. injection of mafosfamide, the local i.p. application resulted in a 20 times higher concentration versus time product of peritoneal drug levels. The molar ratio of sulfhydryl groups to activated cyclophosphamide (resorbed from the peritoneal cavity) remained high in blood. Therapy studies on Sarcoma 180 ascites tumor of mice revealed that the coadministration of cysteine i.v. in mafosfamide i.p. treatment is superior to mafosfamide i.p. application alone. On the contrary, the simultaneous i.p. application of cysteine is accompanied by a loss of antitumor efficacy. The regimen of local i.p. chemotherapy with activated cyclophosphamide and simultaneous systemic detoxification by an appropriate thiol allows the reduction of the systemic toxicity of treatment without influence on the cancerotoxic activity at the site of local injection and the exposing of the intraabdominal tumor to a much higher concentration of the cytostatic agent.

Animals↗
PubMed1995

Properties of water-insoluble mitomycin C-albumin conjugate as a sustained release drug delivery system in mice inoculated with Sarcoma 180.

In order to improve the deposition of mitomycin C (MMC) in the administered site, water-insoluble mitomycin C-albumin conjugate (MMC-G-BSA) was prepared. MMC was covalently attached to the glutarylated bovine serum albumin (G-BSA) in the presence of 1-ethyl-3-(3-dimethyl-aminopropyl) carbodiimide hydrochloride (EDC) to give MMC-G-BSA. The MMC content of the conjugate (16.3% (w/w)) was higher than that of water-soluble mitomycin C-albumin conjugates. MMC was liberated from MMC-G-BSA suspended in a phosphate buffer (pH 7.4, 37 degrees C) with a half-life of 155.3 h. In the same buffer system containing alpha-chymotrypsin, MMC-G-BSA was dissolved perfectly within 24 h due to enzymatic degradation, and the liberation of MMC from the conjugate was significantly accelerated (t1/2 = 24.5 h). After intraperitoneal injection in mice, most of the MMC-G-BSA was retained in the abdominal cavity. Furthermore, the survival time of mice inoculated with Sarcoma 180 was significantly increased by the intraperitoneal injection of MMC-G-BSA. These findings suggest that MMC-G-BSA is a biodegradable macromolecular hybrid which acts as a sustained release delivery system of MMC.

Albumins↗