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PubMed1979

Effects of systemic acidification of mice with Sarcoma 180.

The effects of dietary-induced acidosis on the growth and rates of complete regression of Sarcoma 180 in mice have been studied. The experiments here reported have demonstrated that mineral acidification of laboratory food produces a late decrease in tumor growth and significantly increases the rates of complete tumor regression. Blood acid-base studies also demonstrate the effects of these diets in altering the acid-base balance, and seemingly, this is independent of starvation and/or ketosis. The relationships of such in vivo acid-base metabolic changes to the control of tumor metabolism are briefly discussed. A therapeutic potential for this preliminary approach is considered.

Acid-Base Equilibrium↗
PubMed1993

A 5' exoribonuclease from cytoplasmic extracts of mouse sarcoma 180 ascites cells.

An exonuclease that appears to represent the predominant nuclease activity in cytoplasmic extracts of sarcoma 180 ascites cells has been partially purified and characterized. The enzyme attacks RNA chains in a 5' to 3' direction, and releases 5'-mononucleotides. The initial cleavage, however, can occur at either the first, second and probably third phosphodiester linkage in some RNAs. The enzyme attacks transcripts terminated with a 5'-triphosphate more slowly than those with a 5' monophosphate, and releases a compound larger than GTP from transcripts that begin with a pppG. Capped transcripts are cleaved at least as readily as those with a 5'-P, yielding a compound larger than 7mGpppGm. The occurrence of an such an exonuclease capable of attacking capped RNAs would make it possible for mammalian cells to initiate mRNA degradation by a 5' exonucleolytic mechanism.

Animals↗
PubMed1981

Isolation of alpha-actinin from sarcoma 180 ascites cells plasma membranes and comparison with smooth muscle alpha-actinin.

alpha-Actinin from Sarcoma 180 ascites cell plasma membranes was purified after extraction in 10 mM Tris, 1 mM EDTA, 1 mM mercaptoethanol, pH 8.5, by chromatography on DEAE and hydroxyapatite for comparisons with smooth muscles alpha-actinin purified from turkey gizzard by the same procedure. The two proteins were found to be very similar by sedimentation analysis, gel filtration and dodecyl sulfate gel electrophoresis. Direct comparisons of smooth muscle, skeletal muscle and ascites alpha-actinin by amino acid analysis indicated a closer relationship between the smooth muscle and ascites proteins than between the smooth and skeletal muscle proteins. Both smooth muscle and ascites alpha-actinins cross-link F-actin filaments. The results suggest that the smooth muscle protein is a better system for understanding properties of non-muscle alpha-actinins than is the skeletal muscle protein.

Actinin↗
PubMed1982

Growth of sarcoma 180 in normal and splenectomized BALB/c mice immunized with BCG.

An evaluation was made on the growth of Sarcoma 180 (S 180) in normal and splenectomized BALB/c mice which had been immunized 40 days before the tumor challenge with BCG, either intradermally or in diffusion chambers placed in the peritoneal cavity. Immunization with intradermal BCG did not modify the growth of subcutaneous S 180, whereas it provided significant protection when the tumor was inoculated with BCG. Previous treatment with BCG in diffusion chambers had no effect on the development of S 180, but significantly decreased the percentage of survival of mice inoculated with S 180 mixed with BCG, as compared to the homologous group immunized with intradermal BCG. Splenectomy performed before the challenge with S 180, enabled 56% of mice lacking previous immunization to survive and increased this percentage to 100% when the tumor was inoculated mixed with BCG. As for splenectomized mice immunized with BCG within diffusion chambers and challenged with S 180, there was 90% of survival and 69% in those challenged with S 180 mixed with BCG. These results would suggest that the action of BCG on the growth of S 180 differs according to whether the mycobacteria are in direct contact with the host or exert their effect by means of soluble antigens capable of passing through the millipore filter of the diffusion chambers. These effects would be conditioned by the immunological state of the host.

Animals↗
PubMed1999

Sonodynamically induced effect of rose bengal on isolated sarcoma 180 cells.

PURPOSE: The ultrasonically induced effect of rose bengal (RB) on isolated tumor cells was investigated. METHODS: Sarcoma 180 cells were suspended in air-saturated phosphate-buffered saline and exposed to ultrasound in standing wave mode for up to 60 s in the presence and absence of RB. Cell viability was determined by the ability to exclude trypan blue. RESULTS: The rate of inducing cell damage by ultrasound was enhanced two to three times with 160 microM RB. while no cell damage was observed with RB alone. This enhancement was significantly inhibited by histidine. CONCLUSIONS: Ultrasonically induced in vitro cell damage was significantly enhanced by RB. A sonochemical mechanism may be suggested since the enhancement was significantly inhibited by an active oxygen scavenger.

Animals↗
PubMed1976

[Animal experiment studies on the use of ozone in irradiated and non-irradiated tumors. I. Intravenous ozone therapy of Crocker's sarcoma 180 and Ehrlich carcinoma in the white mouse].

The fractionated tangential local X-ray therapy, in cases of sarcoma 180 in white mice with a total dose of 1500 R, effects a shrinking of the tumours as well as a certain number of cures. Intravenous administration of ozone in a total dose of 0.15 times 10(-7)g, 1.5 times 10(-7)g, and 15 times 10(-7)g - by itself or together with irradiation - has as consequence neither an inhibitory effect on the tumour growth, nor an increase in radiation effect that are surpassing the diffusion width of the model and are reproducible in an exact manner. It has been possible to prove an inhibition of the tumour growth in the solid Ehrlich's carcinoma of white mice after a fractionated 2000 R irradiation, but also in these cases, no effect of the ozone application was stated.

Animals↗
PubMed1981

Purification and characterization of a lipolytic factor (toxohormone-L) from cell-free fluid of ascites sarcoma 180.

A lipolytic substance in the ascites fluid of mice with Sarcoma 180, called toxohormone-L, was purified and characterized. The lipolytic activity of toxohormone-L was measured in vitro using rat adipose tissue slices. Toxohormone-L, purified approximately 90-fold from the ammonium sulfate fraction, gave a single band on polyacrylamide gel electrophoresis. Its molecular weight was about 75,000, and its isoelectric point was 4.7. Toxohormone-L is heat labile and nondialyzable, but, on its digestion with trypsin, an active fragment that was heat stable and dialyzable was produced. Toxohormone-L is a protein and is also present in the ascites fluid of patients with hepatoma and Grawitz's tumor.

Animals↗
PubMed1976

Interaction of Vibrio cholerae toxin with sarcoma 180 cell membranes.

Three discrete phases are discernible in the activation, by Vibrio cholerae toxin, of adenylate cyclase in fragments of sarcoma 180 cell membranes. In the first, or preparatory, phase the toxin must be exposed to dithiothreitol or nicotinamide adenine dinucleotide (NAD) in the absence of the membranes. In the second phase, the prepared toxin is dissociated to yield a macromolecular cyclase-activating factor (MCAF) in the presence of the membranes. In the third phase, membrane basal adenylate cyclase is activated by MCAF in the presence of NAD. The integrity of the catecholamine or beta-receptor associated with sarcoma adenylate cyclase is irrelevant in the activation of cyclase by MCAF. This activation proceeds undiminished even if the beta-receptor is desensitized or blocked by propranolol.

Adenosine Triphosphate↗
PubMed1975

Zinc suppression of initiation of sarcoma 180 growth.

Subcutaneous administration of 80 mug zinc daily to mice that had received an intraperitoneal inoculation of 1 times 10-6 sarcoma 180 cells within the preceding 2 days resulted in protection of up to 60% of the hosts. In animals in which tumors grew, daily injections of zinc did not alter the rate of tumor cell growth. We hypothesized that the metal suppressed initiation of tumor cell reproduction, possibly by stimulation of host defense cell mechanisms.

Animals↗
PubMed1991

Decrease in dopamine and norepinephrine concentration in different brain regions of mice during progression of Sarcoma 180 tumour.

The distribution and concentration of dopamine (DA) and norepinephrine (NE), the catecholamine neurotransmitters, were studied in discrete brain areas of Sarcoma 180 tumour bearing mice. With the progression of tumour, marked depletion of DA and NE concentration was observed in some brain areas richly innervated with dopaminergic and noradrenergic neurons suggesting an inverse relationship between brain CA and tumour growth. Since brain CA influence different important physiological activities like hormonal and immunological functions, it's alteration in brain areas during malignant growth suggests the possibility that the hormonal and immunological alterations during tumour growth is at the level of brain CA.

Animals↗
PubMed2007

Comparison between sonodynamic effect with protoporphyrin IX and hematoporphyrin on sarcoma 180.

PURPOSE: The comparison between sonodynamic antitumor effect with protoporphyrin IX (PPIX) and hematoporphyrin (Hp) at a concentration of 5 mg/kg on Sarcoma 180 (S180) cells was studied in vivo, and the potential cell damage mechanism was also investigated. METHODS: The sonodynamically induced anti-tumor effect of PPIX was studied in mice bearing S180 solid tumors. In order to determine the optimum timing of ultrasound exposure after administration of PPIX, the PPIX concentrations in plasma, skin, muscle and tumor were determined by the fluorescence intensity of tissue extractions with a fluorescence spectrophotometer based on the standard curve. Anti-tumor effects were estimated by measuring the tumor size and the tumor weight. Additionally, the morphological changes of S180 cells were evaluated by transmission electron microscope (TEM) observation immediately after sonodynamic therapy (SDT) treatment. RESULTS: A time of 24 h after the intravenous administration of PPIX was chosen as the best time for ultrasound exposure. The antitumor effect induced by PPIX mediated sonodynamic therapy (PPIX-SDT) was in a dose dependent manner when ultrasound intensity was at or above the inertial cavitation threshold (5 W/cm(2)). A significant tumor growth delay was observed both in PPIX mediated sonodynamic therapy and in Hp mediated sonodynamic therapy treatments (Hp-SDT), and the tumor weight inhibition ratios after the synergistic treatments were 42.82 +/- 0.03 and 35.22 +/- 0.03%, respectively, this difference was significant at P < 0.05. While ultrasound alone (5 W/cm(2)) showed a slight tumor growth inhibitory effect compared with the control group, and PPIX or Hp alone showed almost no significant effect. Furthermore, TEM observation indicated cell damage was more serious in PPIX-SDT treatment group than in Hp-SDT treatment group. After sonication, the cell ultra-structure such as cell membrane destruction, mitochondria swelling, chromatin condensation might be important factors that inhibited the tumor growth and even induced cell death. CONCLUSIONS: The comparative results suggested that PPIX as a sonosensitizer might have more potential cytotoxicity than Hp when irradiated with ultrasound, and the ultra-structural changes may account for cell destruction induced by sonodynamic therapy in our experiment mode.

Animals↗
PubMed1975

Incorporation of L-2,5-dihydrophenylalanine into cell proteins of Escherichia coli and sarcoma 180.

l-2,5-Dihydrophenylalanine is extensively incorporated as a phenylalanine analogue into cell proteins. Phenylalanine-requiring Escherichia coli ATCC 9723f and sarcoma 180 grow at normal rates initially with the analogue and maximally replace 65 and 33%, respectively, of phenylalanine in the peptide residues of their cell protein without death. With the analogue alone growth of E. coli becomes non-steady-state and asymptotically inhibited. In mixtures of the analogue and phenylalanine, growth eventually becomes steady state or logarithmic. The logarithmic rate is inversely proportional to the extent of incorporation of this analogue or of p-fluorophenylalanine, and the projected maximal replacement is the same as that obtained asymptotically with the analogue alone. Thus, the toxicities in steady-state and non-steady-state growth are closely related. Moreover, it is proposed that single salient protein defects may determine the extent of growth rate reduction.

Animals↗
PubMed1986

Metabolism of phosphatidyl-dCMP in sarcoma 180 cells. Effect of chlorpromazine, phosphatidic acid and inositol.

The synthesis and degradation of phosphatidyl-dCMP was studied in intact and permeabilized Sarcoma 180 cells as well as in isolated nuclei. It was verified that chlorpromazine greatly enhanced phosphatidyl-dCMP synthesis and completely abolished its hydrolysis in intact cells. The former effect was reversible and was partially lost upon permeabilization or isolation of nuclei. Phosphatidic acid also increased liponucleotide synthesis and the combination of phosphatidic acid with chlorpromazine was not additive. When inositol was added to cells which had accumulated phosphatidyl-[3H]dCMP, the recovery of radioactivity in the organic phase decreased; this effect was dose-dependent and specific for inositol, and was accompanied by an increased release of [3H]dCMP to the cell medium. In isolated microsomes, addition of Ptd-dCMP determined incorporation of [3H]inositol into phosphatidyl-inositol. These results strongly suggest that phosphatidyl-dCMP is utilized for the synthesis of phosphatidyl-inositol.

Animals↗
PubMed1978

Further studies on liver glyoxalase I and glyoxalase II. Activity in mice bearing sarcoma 180 and L1210 leukemia.

Determinations were made of glyoxalase I and glyoxalase II acitivity in the liver of mice (BDF1 and DBA2 strains) bearing sarcoma 180 and L1210 leukemia in ascites form. A progressive decrease in the both glyoxalase I and glyoxalase II activities to about 40--60% of that of the control groups was observed within the developing period 8--9 days. Test results are interpreted in the light of the postulated role of this enzyme system in cell division and in the tumor development process.

Animals↗
PubMed1986

Antitumoral activity of polysaccharide isolated from Cyttaria johowii on the growth of sarcoma 180 in normal and splenectomized mice.

The antitumoral activity of the polysaccharide (PCj3) isolated from the Cyttaria johowii fungus on the growth of solid Sarcoma 180 (S180) in normal and splenectomized BALB/c mice was studied, observing that this treatment inhibited tumor growth in normal and splenectomized mice. At the same time, the effect of PCj3 on peripheral blood leukocyte populations on the 8th, 15th and 25th day of the experiment was evaluated. Results obtained on day 8 showed that all groups inoculated with S180 suffered an increase in the number of lymphocytes and neutrophils, corresponding the greatest values to splenectomized tumor bearing mice treated with PCj3. Neutrophils increase continued in all animals even without PCj3 treatment until the end of the experiment, while lymphocytosis was only maintained in the splenectomized groups. There was an increase in the number of monocytes on day 8 caused by PCj3 treatment with respect to normal values. It was concluded that PCj3 treatment more effectively delayed S180 growth in splenectomized mice, increasing the survival days as well as the lymphocytes, neutrophils and monocytes values on the 8th day of tumor growth with respect to the other groups.

Animals↗
PubMed1983

Schedule dependence of vincristine lethality in Sarcoma 180 cells following partial synchronization with hydroxyurea.

The effects of exposure to 0.1, 0.5, or 2 microM vincristine for 4 hr were studied in Sarcoma 180 cells at various times after synchronization with 5 mM hydroxyurea for 1 hr. Maximum sensitivity to the lethal effects of vincristine was observed at 10 to 14 hr after hydroxyurea exposure at the higher vincristine concentrations, compared to a period of a maximum sensitivity to a second dose of hydroxyurea at 8 to 12 hr. Serial flow cytometry studies indicated that the apparent decrease in sensitivity to vincristine at 14 to 18 hr was due to the division of cells in the leading segment of the synchronized wave and their entry into the relatively resistant G1 phase prior to vincristine exposure. Synchronized cells that had not divided at the time of vincristine exposure were blocked transiently in G2. Serial metaphase index studies suggested that the G2 cells closest to the end of the cell cycle at the time of vincristine exposure were likely to exhibit the greatest degree of mitotic disorganization when they overcame the G2 block and entered metaphase. The present studies suggest that sensitivity to vincristine increases progressively as cells approach mitosis. The molecular mechanisms underlying this phenomenon are considered in relation to the increase in cell tubulin content during the course of cell cycle progression.

Animals↗
PubMed1994

Ascites sarcoma 180, a tumor associated with hypercalcemia, secretes potent bone-resorbing factors including transforming growth factor alpha, interleukin-1 alpha and interleukin-6.

Ascites sarcoma 180 (S180A) is a transplantable tumor which causes hypercalcemia in tumor-bearing mice, and stimulates bone resorption without parathyroid hormone-like activity. In the present study, parathyroid hormone-related protein (PTHrP) mRNA could not be detected in total RNA from S180A cells. Bone-resorbing activity (BRA) derived from serum-free conditioned medium of S180A cells (S180A-CM) was coeluted with either transforming growth factor alpha (TGF alpha) activity (peak A, approximate M(r), 29 kDa) or lymphocyte-activating factor (LAF) activity (peak B, M(r), 20.1-24 kDa) in Bio-Gel P-100 column chromatography. Fractions in peak A and B contained IL-6 but not tumor necrosis factor alpha (TNF alpha). Subsequent separation of peak A by reverse-phase high performance liquid chromatography produced a single fraction which contained both BRA and TGF alpha activity. Recombinant human TGF alpha-induced bone resorption was completely inhibited by indomethacin. The BRA in peak A was partially inhibited by indomethacin and almost completely inhibited by simultaneous treatment of indomethacin and anti-IL-6 antibody. The BRA in peak B was partially inhibited by neutralization with anti-IL-1 alpha antibody and was completely inhibited by simultaneous treatment with anti-IL-1 alpha and anti-IL-6 antibody in the absence of indomethacin. Bone resorption induced by S180A-CM was associated with an increased production of prostaglandin E2 (PGE2) by calvaria. The BRA in S180A-CM, however, was not completely abolished by the simultaneous addition of indomethacin and anti-IL-1 alpha, anti-IL-1 beta and anti-IL-6 antibodies. Our findings indicate that (1) BRA derived from S180A cells includes TGF alpha, IL-1 alpha, IL-6 and some other unknown factor(s), distinct from PTHrP, IL-1 beta and TNF alpha, and (2) these unknown factors resorb bone in part via a PGE2-independent pathway.

Animals↗