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At least 145 records · Page 8Linked to original sources
PubMed1983

Effects of vincristine on cell survival, cell cycle progression, and mitotic accumulation in asynchronously growing Sarcoma 180 cells.

The effects of vincristine (VCR) on cell survival, cell cycle progression, DNA synthesis, and metaphase accumulation were studied in relation to drug concentration and drug exposure duration in Sarcoma 180 cells in vitro. VCR was found to affect cells in interphase, producing a transient G2 block at all drug concentrations and drug exposure durations studied. VCR did not affect DNA synthesis directly. Increases in the metaphase index were delayed and always peaked at approximately 8 hr after drug removal, regardless of the duration of drug exposure. Increases in the metaphase index of sufficient magnitude to be commensurate with VCR lethality were observed only with prolonged drug exposure. VCR produced both nuclear fragmentation and polyploidy. The proportion of cells undergoing polyploidy increased progressively with increasing drug exposure duration. Interference with cytokinesis during prolonged VCR exposure may represent a lethal effect of VCR that is separate from its short-term effects. This could serve as the basis for the clinical study of the antitumor effects of prolonged VCR infusions.

Animals↗
PubMed1981

Kinetic effects of sangivamycin in sarcoma 180 in vitro.

The lethal and sublethal effects of sangivamycin (SGM) were studied in sarcoma 180 in vitro in relation to drug concentration and duration of drug exposure. SGM lethality was found to be dependent on both drug concentration and duration of drug exposure. Pronounced effects on cell survival were observed only when SGM exposure was prolonged; with prolonged drug exposure, small increments in SGM concentration resulted in large increases in cell killing. Log-phase cells were more susceptible to the lethal effects of SGM than were early-plateau-phase cells. Measurements of incorporation of [3H]thymidine and [3H]uridine into the acid-insoluble cell fraction demonstrated inhibition of both DNA and RNA synthesis by SGM which was also dependent on drug concentration and duration of drug exposure, reflecting the lethality characteristics of SGM. As SGM concentration was increased, DNA synthesis was inhibited more rapidly than was RNA synthesis. Flow cytometry demonstrated a concentration- and time-dependent accumulation of cells in the late S and G2-M region of the DNA histogram. Our findings indicate that maximum lethality is obtained by prolongation of SGM exposure, and they suggest that pharmacokinetic studies may be important for determining regimens which provide such exposure in humans.

Animals↗
PubMed1982

Enhancing effects of mini-cells prepared from Salmonella typhimurium on anti-tumor immunity in sarcoma 180-bearing mice.

The enhancing effect of mini-cells of Salmonella typhimurium which do not contain chromosomal DNA on anti-tumor immunity in mice was studied. The growth of sarcoma 180 cells which were subcutaneously transplanted into ICR mice was significantly retarded in mice treated with Salmonella mini-cells at the same time or 7 days after S180 transplantation, while no or only a little growth inhibition was observed in mice treated 7 days prior to S180 transplantation. Treatment with mini-cells inoculation alone did not increase the survival time of mice that had received intraperitoneal transplants of S180 cells. However, a statistically significant increase of survival time was observed in mice treated with a combination of mini-cells and surgical resection of subcutaneous tumors when S180 cells were injected 7 days after the surgical resection. The injection of mini-cells restored macrophage chemotaxis in S180-bearing mice in which macrophage chemotaxis was greatly retarded but lymphocyte activity was not.

Animals↗
PubMed1985

Reversal of natural resistance to bouvardin (NSC 259968) in sarcoma 180 cells in vitro and in vivo by verapamil.

Reversal of natural resistance to bouvardin (NSC 259968) has been attained in vitro and in vivo, by the calcium influx blocker verapamil in sarcoma 180 cells insensitive to bouvardin. Verapamil increased the in vitro lethality of the tumor cells following exposure with cells for 1 and 3 h as a result of the cytotoxic effect of bouvardin. Similar results were observed in vivo when the tumor cells were exposed to verapamil and then treated with bouvardin, showing a significant percent increase in the lifespan to 30% and 45%. This suggested that this calcium channel blocker had interacted with tumor cell membrane to modulate the response of the cells, and make them more amenable to the drug action.

Animals↗
PubMed1987

Modulation of in vitro response to adriamycin by verapamil in murine P388 leukaemia, Ehrlich ascites carcinoma and sarcoma 180.

Experiments were carried out in vitro on adriamycin (ADR) accumulation and cytotoxicity alone and in combination with calcium channel antagonist, verapamil (VRP), in ascites murine tumour models of Ehrlich carcinoma (EAC), sarcoma 180 (S180) and P388 lymphocytic leukaemia (P388). The cytotoxicity was assayed as the inhibition of [3H]-thymidine incorporation into the cellular DNA. ADR, a broad-spectrum anticancer drug, at a concentration of 10 micrograms/ml showed a cytotoxic effect in the order S180 greater than P388 greater than EAC. VRP alone exhibited the DNA synthesis inhibiting activity. The enhanced DNA biosynthesis inhibition of ADR along with VRP was maximal in S180 and marginal in P388 and EAC. The ADR retention after 3 hr of incubation in these tumour models correlated with the cytotoxicity. VRP enhanced the accumulation of ADR in all these cell lines. The property of potentiation in the activity and accumulation of ADR in these tumours exposed to a non-toxic concentration of VRP can best be utilized in cancer chemotherapy where the massive cytotoxic therapy, with a single large dose of ADR, can be substituted with a low dose, along with this drug-response modulator, for better therapeutic results.

Animals↗
PubMed1986

Enhancement of the in vitro cytotoxicity of bouvardin by verapamil alone and combined with hyperthermia in Sarcoma 180 and Ehrlich ascites carcinoma cells.

The cytotoxic effect of bouvardin (BVD) a protein synthesis inhibitor was studied separately and in combination with verapamil (VRP), a vasodilator and hyperthermia (43 degrees C) against Sarcoma 180 (S 180) and Ehrlich ascites carcinoma (EAC) tumour cells in vitro. S 180 cells exhibited natural resistance to hyperthermia and BVD, whereas EAC tumour cells were found to be sensitive. VRP alone did not show cytotoxicity to either tumour cells. A combination of BVD and VRP at an elevated temperature resulted in a greater cell kill in the EAC tumour cell line whereas the natural resistance of S 180 tumour cells to the drug BVD and hyperthermia was circumvented by combination with VRP. Combination of BVD, hyperthermia and VRP resulted in greater cell kill, compared to separate treatment with the single agents. The cytotoxicity was evaluated by comparing the inhibition of incorporation of 3H-thymidine in treated cells to that in untreated cells.

Animals↗
PubMed2003

Antitumour potential of a polysaccharide-rich substance from the fruit juice of Morinda citrifolia (Noni) on sarcoma 180 ascites tumour in mice.

An immunomodulatory polysaccharide-rich substance (Noni-ppt) from the fruit juice of Morinda citrifolia has been found to possess both prophylactic and therapeutic potentials against the immunomodulator sensitive Sarcoma 180 tumour system. The antitumour activity of Noni-ppt produced a cure rate of 25%-45% in allogeneic mice and its activity was completely abolished by the concomitant administration of specific inhibitors of macrophages (2-chloroadenosine), T cells (cyclosporine) or natural killer (NK) cells (anti-asialo GM1 antibody). Noni-ppt showed synergistic or additive beneficial effects when combined with a broad spectrum of chemotherapeutic drugs, including cisplatin, adriamycin, mitomycin-C, bleomycin, etoposide, 5- fl uorouracil, vincristine or camptothecin. It was not beneficial when combined with paclitaxel, cytosine arabinoside, or immunosuppressive anticancer drugs such as cyclophosphamide, methotrexate or 6-thioguanine. Noni-ppt also demonstrated beneficial effects when combined with the Th1 cytokine, interferon gamma, but its activity was abolished when combined with Th2 cytokines, interleukin-4 or interleukin-10, thereby suggesting that Noni-ppt induces a Th1 dominant immune status in vivo. The combination of Noni-ppt with imexon, a synthetic immunomodulator, also demonstrated beneficial effects, but not when combined with the MVE-2 copolymer, a high molecular weight immunomodulator. It was also not effective when combined with interleukin-2 or interleukin-12.

Animals↗
PubMedDate not supplied

Ultrastructure of sarcoma 180 cells after ultrasound irradiation in the presence of sparfloxacin.

BACKGROUND: Sonodynamic synergistic antitumor effects have been well described to date, but detailed ultrastructural studies in this field are still lacking. MATERIALS AND METHODS: A suspension of sarcoma 180 cells was exposed to ultrasound (US) in the presence of sparfloxacin (SPFX), one of the new quinolone antibiotics, at 2 W (0.64 W/cm2) for 30 seconds. The antitumor effect was evaluated by the survival rate of cells and cell morphology by scanning and transmission electron microscopy. RESULTS: After US irradiation, the survival rate of tumor cells in the SPFX-added group was 30.9%, significantly lower than 78.7% in the control group (p = 0.0002). Most cells in the control group were spherical, but in the SPFX-added group the cells were aspherical. Cell membranes were often ruptured and numerous pores of various sizes were observed. Some cells were totally disintegrated. CONCLUSION: The most characteristic changes of the synergistic antitumor activities of US and SPFX were on the cell membrane.

Animals↗
PubMed1990

Detection of DNA strand breaks in HeLa cells in vitro and in mouse sarcoma 180 cells in vivo induced by an alkylating agent, carboquone, using in situ nick translation.

We determined the correlation between DNA strand breaks and the toxicity of carboquone (CQ) in HeLa cells in vitro and in mouse sarcoma 180 (S-180) cells in vivo, using in situ nick translation. The break sites in the DNA were translated artificially in the presence of Escherichia coli DNA polymerase I and [3-H]-labelled dTTP, and sites in the DNA were visualized by autoradiographic observation of grains in the nuclei. These breaks appeared as early as 5 min in the CQ-treated HeLa cells and increased in a dose- and time-dependent manner compared to findings in the control cells, i.e., 10.2-fold at 3 x 10(-6) M in 60 min. Strand breaks in the S-180 cells appeared in a dose- and time-dependent manner, i.e., 6.1-fold after the mice had been exposed to CQ (3.6 mg/kg) for 2 h. This level correlated with the increase in host life span. Our findings show that the survival response of cells decreases, while the level of DNA strand breaks increases following exposure to CQ. The nick translation method is a rapid in situ assay for determining drug-induced DNA damage of tumor cells, under in vitro and in vivo conditions and in a semiquantitative manner.

Animals↗
PubMed2002

Delayed lethal response to Aspergillus fumigatus infection in sarcoma 180 tumor-bearing mice.

A longer survival and a decrease in the number of fungal cells in kidneys and brain were observed in groups of mice inoculated with Aspergillus fumigatus conidia 2-3 weeks (especially 3 weeks) after sarcoma 180 tumor transplantation compared to groups of non-tumor-bearing (control) mice inoculated with fungal cells only. The 3-4-week tumor-bearing mice had significantly decreased levels of serum iron and increased levels of unbound iron binding capacity in the serum compared to those of the non-tumor-bearing mice.

Animals↗
PubMed1989

The effect of marijuana smoke exposure on murine sarcoma 180 survival in Fisher rats.

Fisher rats were treated for 28 or 60 days to multiple exposures to the smoke of marijuana or marijuana placebo cigarettes. Primary, secondary and in some instances tertiary tumor implants were performed. Murine sarcoma 180 tumor cells (7.5 x 10(7)) were implanted subcutaneously on day 1, 14 and 28 following initiation of smoke exposure (28 day studies) or on day 1, 14 after cessation of smoke exposure (60 day studies). Tumor areas were measured on alternate days beginning on the second or third day after implantation for 13 or 14 days. Exposure to both marijuana and placebo smoke for 28 days (6, 9 and 18 cigarettes per day) resulted in suppressed growth of secondary and tertiary implants. Administration of delta 9 tetrahydrocannabinol (50 mg/kg, i.p., 20 days) failed to suppress the growth of primary and secondary tumors. This suggests that noncannabinoid constituents of the smoke may contribute to the suppression of tumor growth. Exposure of rats to 9, but not 4 or 6, marijuana or placebo cigarettes per day for 60 days suppressed the growth of primary but not secondary tumors. Thus, the effects of smoke exposure appear to be lost by two weeks after cessation of treatment. The possible existence of a non-cannabinoid immunostimulant in the smoke is discussed.

Animals↗
PubMedDate not supplied

Induced multidrug-resistance in murine sarcoma 180 cells grown in vitro and in vivo and associated changes in expression of multidrug-resistance DNA-sequences and membrane glycoproteins.

The aim of this investigation was to analyze the resistance to doxorubicin and daunorubicin of murine sarcoma 180 cells grown in vitro (monolayer) and in vivo (ascites form). The colchicine-resistant CHO cells were used as controls. A multidrug-resistant phenotype was found in all investigated cell lines. Multidrug resistant cells grown in tissue culture or as ascites tumor cells needed more time to accumulate rhodamine 123 than their sensitive parental cells. In order to evaluate whether the resistant cells show alterations in the plasma membranes, different methods were applied (immunocytochemistry, immunofluorescence, immunoblotting) using the monoclonal antibodies 265/F4 and C 219. These methods all revealed an increased expression of the glycoprotein Mr 170 kd in the multidrug-resistant cell lines. To determine whether multidrug DNA sequences were expressed in the resistant cell lines, slot blots and Northern blots with RNA of sensitive and resistant cells were performed using the clones pDR 7.8 and pcDR 1.5. Elevated RNA levels were detected in all resistant cell lines.

Animals↗
PubMed1990

Cysteine proteinase inhibitor in the ascitic fluid of sarcoma 180 tumor-bearing mice is a low molecular weight kininogen. Partial NH2- and COOH-terminal sequences and susceptibility to various glandular kallikreins.

It has been proposed that a cysteine proteinase inhibitor (CPI) found in the ascitic fluid of Sarcoma 180 tumor-bearing mice is a kind of kininogen (Itoh, N., Yokota, S., Takagishi, U., Hatta, A., and Okamaoto, H. (1987) Cancer Res. 47, 5560-5565). The first 40 NH2-terminal residues and 54 residues of the COOH-terminal sequence, including the bradykinin moiety of highly purified ascites CPI, were determined and compared with those of mammalian low molecular weight kininogens (LMWK). The significant identity between these amino acid sequences with those of other mammalian LMWKs suggests that ascites CPI corresponds precisely to mouse LMWK. This kininogen has a light chain composed of 43 amino acid residues, which contains a unique Met-Ala-Arg-bradykinin sequence. Hydroxyproline, which was recently identified in the bradykinin sequence of kininogen from the ascitic fluid of a cancer patient, was not found in the kinin moiety of this mouse kininogen. Among purified glandular kallikreins from human, hog, rat, and mouse, only mouse submaxillary gland kallikrein was able to release bradykinin from this kininogen. Kinetic studies using a newly synthesized fluorogenic substrate, N-t-butoxycarbonyl-Met-Ala-Arg-MCA, revealed that mouse kallikrein hydrolyzes this substrate approximately 80-fold faster than does hog kallikrein, suggesting that the unique Met-Ala-Arg-bradykinin sequence is responsible for the varied susceptibility of mouse kininogen to different kallikreins.

Amino Acid Sequence↗
PubMed2001

Effects of carp and tuna oils on 5-fluorouracil-induced antitumor activity and side effects in sarcoma 180-bearing mice.

In this study, we examined the effects of fish oils on 5-fluorouracil (5-FU)-induced antitumor activity in mice. First, we examined the antitumor activity of the oral administration of two fish oils (carp oil and tuna oil) in sarcoma 180-bearing mice. Carp oil (0.2 and 0.4 mL/mouse) and tuna oil (0.2 and 0.4 mL/mouse) had no effects on tumor growth. Next, we examined the combined effects of 5-FU plus two fish oils (carp oil and tuna oil) on the antitumor activity and side effects compared to the effects of 5-FU alone (12.5 mg/kg/d). We found that carp oil (0.4 mL/mouse) or tuna oil (0.2 or 0.4 mL/mouse) enhanced the ability of 5-FU (12.5 mg/kg/d) to prevent tumor growth, without increasing side effects such as myelotoxicity and immunocompetent organ toxicity. Tuna oil (0.2 mL/mouse) slightly reduced body weight as compared to the effects of 5-FU alone and water alone (control). The area under the curve (AUC) (0-120 min) of blood 5-FU levels was reduced by the oral co-administration of 5-FU with carp oil or tuna oil. Apparent Tmax was shortened by the oral co-administration of 5-FU with carp oil or tuna oil. On the other hand, AUC (0-4 h) of 5-FU incorporation into tumor RNA fraction was not affected by the oral co-administration of 5-FU with carp oil or tuna oil.

Animals↗
PubMed1989

Initial and early effects of adriamycin in murine sarcoma 180 cannot be restored in a resistant subline by increasing the uptake and external concentration of the drug.

We demonstrate the early effects (1 day) of Adriamycin (ADM) on proliferation-stimulated and quiescent sensitive, and ADM-resistant cells of the murine tumor sarcoma 180 (S 180). By investigating cell-cycle distribution and thymidine labeling, it can be shown that sensitive cells are strongly affected by the drug, even in a proliferationarrested state. A remarkable but slow DNA synthesis is the prominent effect of this drug treatment on sensitive cells, even under nonstimulating conditions. In resistant cells, neither an increase in concentration nor a variation in drug uptake can induce effects that could be compared with those observed in the sensitive line. From these results we conclude that the early effects of ADM are not modulated by drug uptake.

Animals↗
PubMed1985

The effect of methotrexate pretreatment on 5-fluorouracil kinetics in sarcoma 180 in vivo.

Synergy of sequential MTX and 5-FU has been shown in several in vitro and in vivo systems. In the present study the influence of time interval between MTX and 5-FU and MTX dose on 5-FU accumulation in tumor cells has been examined in Sarcoma 180 in vivo. There was a clear relationship between MTX dose applied and amount of 5-FU detected in the acid-soluble fraction, the RNA fraction and the thymidylate synthase complex fraction. Also, the MTX-5-FU time interval affected clearly the amount of 5-FU detected in all three fractions, the optimum time interval being 8-12 hr. The results indicate that for sequential application of MTX and 5-FU selection of an adequate MTX dose and a sufficient time interval is crucial to achieve synergistic action.

Animals↗