[A new strain of ascites sarcoma (Hirosaki-strain) similar to the Yoshida sarcoma].
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Inactivation of membrane-bound (Na+ +K+)-ATPase of Yoshida sarcoma cells and cobra venom cytotoxin complex with the glycolipid components of the enzyme system.
The molecular mechanisms involved in the inactivation of (Na+ + K+)-stimulated ATPase of Yoshida sarcoma cells by a cytotoxic protein (P6) from cobra venom have been examined. The overall data obtained using purified (Na+ + K+)-stimulated ATPase of Yoshida sarcoma cells suggest that cytotoxin P6 combines with phosphatidyl serine and a glycolipid which are closely associated with (Na+ + K+)-stimulated ATPase which in turn may lead to the inactivation of the enzyme in this cell system.
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The interaction of dianhydrogalactitol with DNA in cultured Yoshida sarcoma cells.
Using alkaline sucrose gradient sedimentation centrifugation it was found that treatment of Yoshida sarcoma cells in culture for 1 h with increasing concentrations of dianhydrogalactitol (DAG) enhanced the sedimentation rate of DNA in a dose-dependent manner. There was no difference between the amount of protein which co-sedimented with DNA released from treated and untreated cells. When DNA was extracted from the cells using a p-amino-salicylate-phenol mixture, the protein content of DNA seemed not to be affected by DAG. The possibility that DAG could form interstrand cross-linking in cellular DNA was suggested from renaturation studies. The appearance of a fast sedimenting DNA in the alkaline sucrose gradient and the evidence for a cross-linked DNA detected by renaturation technique, only appeared later than 6 h after treatment. A similar delayed effect on the depression in the rate of DNA synthesis was also observed. These data suggest that the inhibition of DNA synthesis may be related to the delayed formation of DNA interstrand cross-linked.
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Anticancer potential of N,N-diethylaminoethyl ethers of flavanone oximes: a comparison with mitoxantrone action on rat Yoshida sarcoma cells in vivo.
This study was performed to evaluate the anticancer abilities of four biologically active N,N-diethylaminoethyl ethers of flavanone oximes against rat Yoshida Sarcoma cells in vivo, and to investigate the mechanism(s) involved. The effects were compared with those of anthraquinone drug (mitoxantrone) action. The presented results provide the first evidence that all the investigated substances induce programmed cell death (apoptosis) of Yoshida Sarcoma cells in vivo. On interpretative grounds, the administration of investigated flavanone derivatives in the promotion phase of the disease led to both growth inhibition (cell cycle perturbation) and apoptosis. A correlation was found between structure of the substituent(s) at B-ring of substances and the revealed anticancer activity. The data suggest that flavanone derivatives (oxime ethers) besides their antiradical, antioxidant and radioprotector properties observed before, may act as promising anticancer agents acting in the promotion phase of disease. This finding prompted us to consider the development of a new strategy: modulation of effects using combination therapy involving mitoxantrone and flavanone oximes.
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Analysis of incipient growth of Yoshida sarcoma in vivo after transplantation of a small number of tumor cells.
Incipient growth of Yoshida sarcoma in ascitic and solid forms was analyzed after transplantation of a small number of tumor cells varying from 1 to 10(6). Growth curves of the ascites tumors revealed that the duration of the incipient growth was much longer than the length of subsequent advanced stage and that the ascites tumor during its incipient stage appeared to grow exponentially and most rapidly in the entire course of the tumor development. Growth rate analyses of the ascites and solid tumors showed that, during their incipient stage, the population doubling time prolonged gradually as the inoculum size increased. This phenomenon was thought to suggest probable cell death on account of the transplantation procedure.
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The influence of daunomycin on development of Yoshida sarcoma after nonspecific stimulation of the immunologic system.
Injection of BCG in rats inoculated with Yoshida sarcoma had no influence on the development of the tumor or survival time of the rats in comparison with the control group. On the other hand, survival time was increased more than threefold in a group of rats injected with daunomycin in a single dose of 1 mg/kg i.p. Longest survival and lowest mortality were observed in a group of rats treated with daunomycin and BCG, in which survival time was six times longer than in the controls, and mortality after 50 days was 30% lower, and after 100 days even 50% lower than in the group of rats that were treated only with daunomycin.
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Alterations in whole body, muscle, liver, and tumor tissue protein synthesis and degradation in Novikoff hepatoma and Yoshida sarcoma tumor growth studied in vivo.
The rate of protein synthesis in vivo was assessed in tumor tissue, skeletal muscle, liver, and the whole body of rats bearing either the Yoshida sarcoma or Novikoff hepatoma after 18 days of tumor growth and compared to tumor-free controls. Changes in size of the whole animal and tumor (i.e., growth) were measured, and fractional rates of growth, synthesis, and degradation were estimated. Muscle protein synthesis and whole-body growth were significantly reduced in both groups of tumor-bearing rats after 18 days of tumor growth. In addition to reductions in muscle protein synthesis, whole-body protein synthesis was significantly reduced in the Yoshida tumor-bearing group (587 +/- 36 versus 401 +/- 40 mg/h; mean +/- SEM; control versus Yoshida group, respectively, P less than 0.01). Tumor protein synthesis was not statistically different between the Yoshida tumor (76 +/- 21 mg/h) and the Novikoff tumor (50 +/- 8) after 18 days of growth despite the fact that the Yoshida tumors were significantly larger (33.9 +/- 4.2 g versus 11.9 +/- 1.2 g; P less than 0.01). The fractional synthesis rate (Ks) was, in fact, significantly slower in the Yoshida versus the Novikoff tumor (36.8 +/- 7.6 versus 55.1 +/- 4.8%/day). Tumor growth (Kg) followed first order growth rates for both tumor types (r = 0.945, 0.869; Kg = 17.2 +/- 1.6, 15.5 +/- 1.9%/day; Yoshida and Novikoff, respectively). The fractional degradation rate of tumor protein (Kd) was determined as the difference between the two first order rate constants Ks and Kg. The tumor protein degradation rate was significantly reduced in the Yoshida tumors compared to the Novikoff tumors (19.6 +/- 8.2% versus 39.6 +/- 4.2%/day, respectively). The greater size in the Yoshida sarcoma can be attributed to reduction in fractional protein degradation rather than change in synthesis rates, which supports the theory that some tumors can regulate their growth by alteration in tumor protein degradation rates (J. A. Tayek et al., Cancer Res., 46:5649-5654, 1986).
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Effects of the plasma concentration of 5-fluorouracil and the duration of continuous venous infusion of 5-fluorouracil with an inhibitor of 5-fluorouracil degradation on Yoshida sarcomas in rats.
The correlations of the 5-fluorouracil (5-FU) level in the plasma and the duration of continuous 5-FU infusion with the antitumor activity of 5-FU on Yoshida sarcomas in rats were examined. The circadian variation in the plasma level of 5-FU during continuous infusion was prevented by treatment with 3-cyano-2,6-dihydroxypyridine (CNDP), which strongly inhibits 5-FU degradation. On continuous venous infusion of 2 to 30 mg/kg of 5-FU over 24 h with CNDP at a molar ratio of 1:10 into normal rats, the 5-FU level in the blood was linearly proportional to the dose of 5-FU. The optimum schedule for antitumor activity on Yoshida sarcomas in rats was found to be infusion of 5-FU at 5 mg/kg over 24 h for 6 consecutive days, which gave a plasma 5-FU level of 176 ng/ml. Continuous infusion of 5-FU to give a plasma level of 300 ng/ml for 6 consecutive days from day 5 after implantation of tumor cells, when the tumors weighed about 1.0 g, resulted in complete regression of the tumors in all rats.
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Antitumor activity of norditerpenoid dilactones in Podocarpus plants: structure-activity relationship on in vitro cytotoxicity against Yoshida sarcoma.
The in vitro cytotoxicity of norditerpenoid dilactones isolated from Podocarpus plants was determined against cultured Yoshida sarcoma cells. The dilactones involved 15 natural lactones as well as their derivatives, which include appropriate modifications necessary to the estimation of the structure-activity relationship. The unsaturated system on the B/C ring portion, the dienolide or the epoxyenolide moiety, is essential for the activity, but the gamma-lactone group on the A/B ring portion is not. Other oxygenated substituents on the skeletal carbons, such as hydroxyl, acyloxyl, or epoxide group, also show some significant effect.
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The effect of dibromodulcitol on the template activity of DNA chromatin and nuclei from Yoshida sarcoma cells.
It has been shown earlier that after in vivo administration, dibromodulcitol (DBD) reacts with DNA and to a greater extent with chromosomal proteins of Yoshida sarcoma cells. The present experiments were designed to show if the binding of DBD to the chromatin elements of Yoshida sarcoma cells causes any changes in RNA synthesis using either DNA or chromatin as template in bacterial RNA polymerase system. During 4 to 24 h following in vivo administration, DBD reduces the template activity of dna without detectable single-strand breaks in the template DNA in alkaline sucrose gradients. Using chromatin as template the same dose of DBD produces no or very slight inhibition of RNA synthesis. Measuring the DNA-dependent RNA synthesis in nuclei isolated from Yoshida cells of treated rats, the dose of DBD which markedly inhibited the template activity of DNA, resulted in a significant stimulation of the nuclear RNA synthesis. The increased RNA synthesis was not due to an inhibition of ribonuclease activity. The observed alterations of the transcriptive properties of chromatin and nuclei produced by DBD are interpreted as being due to a modification of the whole nucleoprotein structure caused by the interaction of DBD with both DNA and chromosomal proteins.
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Characterization of factors stimulating differentiation of mouse myeloid leukemia cells from a Yoshida sarcoma cell line cultured in serum-free medium.
A clone, YS-T22, of cells from Yoshida sarcoma cell line, YSSF-212T, grown in "serum-free" culture medium produced factors stimulating differentiation of mouse myeloid leukemia cells (M1) to macrophages and granulocytes. The formation of macrophages and granulocytes was accompanied by induction of phagocytosis, locomotive activity, and lysosomal enzyme activities. The rates of induction of these differentiated phenotypes were proportional to the concentration of the factor added and the period of treatment. The factor stimulating differentiation of M1 cells was a heat-labile, nondialyzable proteinaceous substance that was inactivated by trypsin but not by ribonuclease or glycosidases. On diethylaminoethyl cellulose chromatography, the factor stimulating differentiation of M1 cells from conditioned medium of YS-T22 cells was eluted in various fractions with or without activity of the colony-stimulating factor.
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Affinity of intraperitoneally injected activated carbon particles adsorbing mitomycin C to tumor surface of Yoshida sarcoma.
A new dosage form of mitomycin C (MMC-CH) comprising 0.75 mg/ml of activated carbon particles adsorbing mitomycin C at 124 micrograms/mg and 7 micrograms/ml of mitomycin C in a free state was injected intraperitoneally to male rats of Donryu strain transplanted intraperitoneally with 10(7) cells/rat of Yoshida sarcoma 4 days before injection. The rats were subjected to autopsy within 60 min after injection. MMC-CH adhered selectively to the tumor surface of Yoshida sarcoma growing intraperitoneally rather than to the surface of organs such as small intestines which the surface cancer did not affect. Within 120 min after injection, mitomycin C concentration in the tissue samples was bioassayed. Intraperitoneally injected MMC-CH distributed high levels of mitomycin C to the tumor rather than to the unaffected organ located intraperitoneally. Animals killed by cancer after the treatment of MMC-CH were autopsied. Histological effects of MMC-CH were studied microscopically. Mitomycin C adsorbed on activated carbon particles induced degenerative changes in the tissues of tumors to which the activated carbon particles had adhered.
Adsorption↗
Selective targeting of magnetic albumin microspheres to the Yoshida sarcoma: ultrastructural evaluation of microsphere disposition.
Magnetic albumin microspheres (1 micron average diameter) were selectively targeted to subcutaneous solid Yoshida sarcoma tumors (average size 450 mm2) in Holtzman rats. This was accomplished by placing an external magnet adjacent to the tumor while the microspheres were infused. Microspheres contained ultra-fine particles of Fe3O4 and no drug (placebo). Placebo microspheres were used due to the previously demonstrated rapid tumoricidal effect of targeted low-dose doxorubicin microspheres. Animals were killed 10 min, 60 min, 30 min, 24 hr and 72 hr after microsphere administration and tumors were examined by transmission electron microscopy to determine the in vivo disposition of the magnetically targeted microspheres. Using placebo microspheres, we have demonstrated microspheres endocytosed in endothelial cells as early as 10 min after infusion. By 30 min microspheres can be seen in the extravascular compartment, sitting adjacent to tumor cells and occasionally in tumor cells. By 24 hr the majority of microspheres have been endocytosed by tumor cells. Microspheres were still observed within tumor cells as late as 72 hr after administration. The rapid extravasation and cellular uptake of magnetically focused microspheres explains the extremely rapid tumoricidal effect previously observed when doxorubicin-containing microspheres were targeted to the tumor.
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Effects of hyperglycemia and hyperthermia on the pH, glycolysis, and respiration of the Yoshida sarcoma in vivo.
Tissue (extracellular) pH (pHe) and intracellular pH (pHi) were measured together in vivo in the solid Yoshida sarcoma and normal organs (liver, gastrocnemius muscle) of noninbred Wistar rats. pHe was monitored by insertion of a miniature capillary glass electrode, and pHi was measured indirectly by equilibrium partitioning of the weak organic acid 5,5-dimethyloxazolidine-2,4-dione across the cell membrane. Under normal conditions, tumor, liver, and gastrocnemius had a similar pHe of 7.05--7.30; tumor pHi was consistently higher (7.2) than that of the normal tissues (6.8--7.1). Curative hyperthermia (42 degrees C for 1 hr) did not significantly change tumor pHe or pHi. After ip glucose injection [6 g/kg body wt; blood glucose level greater than 400 mg/100 ml (22 mmoles/liter) for 4 hr], tumor pHe decreased markedly to 6.6 within 4 hours and did not return to normal for a further 12--14 hours, whereas tumor pHi was hardly affected. No marked change was noted in pHe or pHi of the normal organs following glucose loading of the host. In tumor slices removed from hyperglycemic hosts, marked reduction of both respiration and glycolysis was observed. Hyperglycemia (4 hr) plus hyperthermia at 40 degrees C (1 hr) had a synergistic inhibitory effect on metabolism that was equivalent to heat alone at 42 degrees C, and respiration and glycolysis almost ceased after 3--4 hours. However, tumor heating at 40 degrees C in hyperglycemic hosts was not equivalent to hyperthermia at 42 degrees C: With the former treatment, tumor regression did not occur, and animal survival did not differ from that of control untreated rats. The data do not support the postulate that the effects of heat on tumor cells are mediated via low pHi or that hyperglycemia leads to a lowered pHi which sensitizes the tumor to destruction at 40 degrees C instead of 42 degrees C.
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[Investigation on the detection of circulating antibodies in yoshida-sarcoma bearing rats by the serologic-nephelometric method of Hoigné (author's transl)].
Circulating antibodies against tumour antigens were detected by means of the serologic-nephelometric method of Hoigné et al. (1955). Under employment of homogenates of tumour tissue as antigen solutions in 95 per cent of the cases the sera of Yoshida-sarcoma bearing rats reacted positively, while only in 4 per cent of the normal animals a positive reaction was found. 11 per cent of tumour-bearing animals showed in addition positive reactions against the normal muscle tissue, normal rats reacted positively in 2 per cent of the cases. In 93 per cent the sera of tumour-bearing animals reacted with spleen homogenates of sarcoma-bearing rats positively, whereas serum of normal rats showed 20 per cent positive reactions with the same antigen. The results confirm the aptitude of the serologicnephelometric method of Hoigné et al. (1955) and of the employed animal model for investigations of tumour-immunological problems, and they underline the antigenicity of the Yoshida-sarcoma.
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Schedule dependent inhibition of thymidylate synthase and tumor growth by 5-fluorouracil in Yoshida sarcoma bearing rats.
Schedule dependent inhibition of thymidylate synthase (TS) and tumor growth by 5-fluorouracil (FUra) was examined in Yoshida sarcoma (YS) bearing Donryu rats. After implantation of YS cells (1 x 10(4), FUra (20 mg/kg/day) was continuously (group C) or daily bolus injection (group B) administered for 6 days. On day 7, tumor weight was 1.57 +/- 0.58 g in group C and 0.45 +/- 0.10 g in group B (P less than 0.01), free TS was 2.23 +/- 83 fmol/mg protein in group B and 96 +/- 55 fmol/mg protein in group C (P less than 0.05), and inhibition rate of TS was 88.3 +/- 5.3% in group C and 94.7 +/- 3.0% in group B (P less than 0.05). A significant correlationship was found between free TS and tumor weight (P less than 0.05). As the next step, continuous infusion (group C) or daily bolus injection (group B) for 6 days was started on day 5 after implantation of YS cells. The relative increase of tumor on day 9 was 256 +/- 111% in group C and 112 +/- 22.1% in group B (P less than 0.05). On day 11, total TS of the resected tumor was 650 +/- 153 fmol/mg protein in group C and 391 +/- 124 fmol/mg protein in group B (P less than 0.05), and inhibition rate of TS was 78.8 +/- 12.4% in group C and 84.4 +/- 8.6% in group B. Daily bolus injection of FUra causes a superior antitumor and antimetabolic effect. The schedule dependent cytotoxicity of FUra should be taken into account when a chemotherapeutic protocol is designed.
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[Reoxygenation in Yoshida sarcoma during different fractionated radiotherapy].
PURPOSE: Tumor reoxygenation is one of the most important factors determining the tumor control probability after radiotherapy. In experimental studies reoxygenation has been measured preferably after single dose irradiation. Only few data exist about changes in the hypoxic tumor fraction during fractionated radiotherapy. MATERIAL AND METHODS: The changes in the pO2 during fractionated radiotherapy were studied in Yoshida sarcoma transplanted to Wistar rats. Tissue oxygenation was assessed using a polarographic electrode system at the beginning, in the middle and at the end of radiation therapy. Different fractionation schedules were used: 10 x 3 Gy, 6 x 5 Gy and 3 x 10 Gy. RESULTS: In the statistical analysis significant changes emerged in the mean, median, 10%-percentile and 0 to 2.5 mm Hg and 0 to 5.0 mm Hg values dependent on time. The tumors were significantly more hypoxic at the end of therapy. This trend became more pronounced with decreasing dose per fraction. CONCLUSIONS: The Yoshida sarcoma has no effective reoxygenation during fractionated radiotherapy.
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The effect of Yoshida sarcoma cell transplantation to rats on the rate of acute-phase protein synthesis in the liver.
The effect of transplantation of Yoshida sarcoma cells into rats on the concentrations of both the acute-phase proteins (APPs) in the serum and their mRNAs in the liver has been investigated. In rats that responded to transplantation by forming solid tumors, the serum APP levels increased with tumor size. Some of the APP was found to be infiltrated in the area of the tumor cells. Concentrations of the APP mRNAs in the liver were enhanced to an extent comparable to that observed for the encoded proteins, indicating that hepatocytes were the major site of their synthesis. In rats in which no formation of solid tumors occurred, the serum APP concentrations expressed a tendency to decrease below the control values. An inverse relationship between the rates of APP synthesis and the capability of rats to prevent proliferation of transplanted ascites tumor cells in the solid tumor form was discussed.
Acute-Phase Proteins↗