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PubMed1979

Effect of uracil on metabolism of 5-fluorouracil in vitro.

The effect of uracil on the metabolism of 5-fluorouracil (5-FU) in vitro was studied. 5-FU was mainly phosphorylated in intact Yoshida sarcoma cells, whereas it was mainly degraded in liver slices. Uracil inhibited degradation of 5-FU much more than its phosphorylation; incubation of 2,500 microM of uracil with 2.5 microM of 5-FU (molar ratio, 1,000:1) inhibited the degradation of 5-FU by 70%, but did not affect its phosphorylation. With homogenates of Yoshida sarcoma or liver uracil inhibited degradation of 5-FU greatly, phosphorylation of 5-FU by alpha-D-ribose 1-phosphate (RiblP) and ATP to some extent, and phosphorylation by 5-phospho-alpha-D-ribosyl diphosphate (PPRibP) very little. The activities of the enzymes involved in the metabolism of 5-FU in various tissues were also determined. Degradation of 5-FU was much faster in liver than in other tissues and was very slow in tumor tissue. Phosphorylation of 5-FU with RiblP and ATP was rapid in Yoshida sarcoma and bone marrow. Phosphoribosyltransferase activity was high in Yoshida sarcoma and thymus, but low in bone marrow.

Animals↗
PubMed1983

[Experimental studies on the optimal therapeutic mode of intra-arterial infusion of 5-fluorouracil. (1) Preparation of an animal model for continuous intra-arterial infusion and comparison of the therapeutic and adverse effects of 5-fluorouracil delivered by various modes].

5-Fluorouracil (5-FU) is one of the most popular anticancer drugs, especially in treatment of for adenocarcinoma; however, an optimal therapeutic schedule of 5-FU is not determined even now. An animal model for continuous intraarterial infusion in rats was constructed using retrograde cannulation to aorta via right femoral artery in order to study the intraarterial and systemic effects of 5-FU on Yoshida sarcoma implanted in left fore limb and hind limb subcutaneously. By implanting Yoshida sarcoma in fore and hind limb and cannulating and infusing aorta, the regional and systemic antitumor effects could be compared in the same animal. Antitumor effect and toxicity after intraarterial 5-FU administration was studied at various infusion time and doses. The results revealed that intraarterial infusion of 5-FU was more effective than its systemic administration from view points of the antitumor effect. The antitumor effect after one shot intraarterial injection of 5-FU was ar superior to that after continuous infusion of 5-FU. However, toxicity after one shot injection was much more severe than continuous infusion. Consequently, the desirable administration schedule of 5-FU appears to be an intraarterial infusion as short time as possible within tolerable toxicity.

Animals↗
PubMed1983

IMP dehydrogenase. I. Studies on regulatory properties of crude tissue extracts based on an improved assay method.

Inhibition of conversion from IMP to uric acid, which interferes with both spectrophotometric and radioisotopic assays of IMP dehydrogenase, by addition of allopurinol (0.1 mM), an inhibitor of xanthine oxidase, to the incubation system made it possible to determine the enzyme activity in crude liver extracts. With this improved assay method, the regulatory properties of the enzyme in crude extracts of liver and Yoshida sarcoma ascites cells were examined. In both tissues IMP dehydrogenase was found in the postmicrosomal supernatant. However, further centrifugation resulted in precipitation of the enzyme, the enzyme from Yoshida sarcoma ascites cells being precipitated more easily than that from rat liver. It was also found that IMP dehydrogenase activity increased during liver regeneration and that this increase was associated with the precipitate from the postmicrosomal fraction. These findings suggest that such a large sedimentable complex including IMP dehydrogenase might be formed in relation to cell growth. Most of the enzyme activity in rat liver and Yoshida sarcoma ascites cells was extracted in the supernatant obtained by centrifugation at 105,000 X g for 4 h after treatment of tissue homogenates with 1 M KCl, 0.75 M (NH4)2SO4, 2 M dimethylsulfoxide, 2 M KSCN, 25% glycerol, or 0.8 M guanidine-HCl. Treatment with 2% deoxycholate, 2% Triton X-100 or 2 M urea gave limited extraction. The enzyme was retained on a phenyl-Sepharose CL-6B or octyl-Sepharose CL-6B column and eluted with 0.8 M guanidine-HCl. These results suggested that the enzyme molecule has not only ionic but also hydrophobic domains, through which it interacts with other molecules of the enzyme itself and/or postmicrosomal cellular components.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1975

Inactivation of (Na-++K-+)-stimulated ATPase by a cytotoxic protein from cobra venom in relation to its lytic effects on cells.

The mechanism of action of the cytotoxic protein P6 isolated from cobra venom (Naja naja) which shows preferential cytotoxicity particularly to Yoshida sarcoma cells has been studied by its effects on the membrane-bound enzyme (Na-++K-+)-ATPase (ATP phosphohydrolase, EC 3.6.1.3) of a variety of cell systems. Evidence obtained with Yoshida sarcoma cells, dog and human erythrocytes and three tissue culture cell lines KB (human oral carcinoma), Hela (human cervix carcinoma) and L-132 (human lung embryonic) shows that inhibition of (Na-++K-+)-ATPase by the P6 protein can be correlated with its lytic activity. (Na-++k-+)-ATPase of Yoshida sarcoma membrane fragments inactivated by P6 protein could be reconstituted by the addition of phosphatidylserine and phosphatidic acid. It is conceivable that lysis of cells by the P6 protein may be due to an imbalance of K-+ and Na-+ in the cell which leads to swelling and disintegration of the membrane structure. Observations indicate that the P6 protein combines with membrane constituents of susceptible cells. The overall evidence suggests that both the specificity of its protein structure and the highly basic nature of the P6 protein are factors which enable it to compete with the lipid moiety maintaining the (Na-++k-+)-ATPase of the susceptible cells in proper conformation for activity.

Adenosine Triphosphatases↗
PubMed1985

Cytolytic activity of cytotoxin isolated from Indian cobra venom against experimental tumor cells.

Cytolytic activity of cytotoxin isolated from the venom of the Indian cobra (Naja naja) on experimental tumor cells was far stronger than that on normal cells such as peritoneal exudate cells, spleen cells, and erythrocytes of the rat. The effect on Yoshida sarcoma cells was temperature-dependent, being stronger at 37 degrees C than at 0 degrees C. Intramolecular disulfide linkages and free amino groups in the cytotoxin molecule were shown to be essential for the lytic action on the cell membrane. Yoshida sarcoma cells treated with 0.1 mM N-ethylmaleimide reduced the cytolytic action of the toxin. Antitumor activity of the cytotoxin toward a Yoshida sarcoma inoculated intraperitoneally into a rat was not observed.

Animals↗
PubMed1979

Peripheral blood lymphocyte nucleoi of rats with Yoshida ascitic sarcoma and the effect of endotoxin.

Nucleoli of lymphocytes were studied in the peripheral blood of male Wistar rats bearing Yoshida ascitic tumor untreated and treated with Escherichia coli endotoxin. Both the neoplastic process and the endotoxin produced an increase of peripheral lymphocytes with "active" nucleoli in number. The treatment of experimental animals bearing the tumor with the endotoxin decreased their mortality and enhanced the increase of the lymphocytes with "active" nucleoli in their peripheral blood.

Animals↗
PubMed1975

DNA synthesis in tumor-bearing rats.

Thmidine (TdR) incorporation into DNA increased in the livers and spleens of rats bearing Yoshida sarcoma (solid type) or AH130 (solid type). TdR kinase and DNA polymerase activities increased in the serum, liver, and spleen of these rats, while thymidine monophosphate kinase activity increased appreciably only in the liver and spleen. On diethylaminoethyl cellulose column chromatography, 2 peaks of TdR dinase activity were separated from the serum and tumor tissues of rats bearing Yoshida sarcoma (solid type) while only 1 peak was obtained from the liver. TdR kinase activity in the serum decreased abruptly 7 hr after removal of the Yoshida sarcoma, while that in the liver decreased more slowly.

Animals↗
PubMed1980

Comparative study of three basic polypeptides from snake venoms in relation to their effects on the cell membrane of normal and tumor cells.

Basic polypeptides producing a variety of effects on animals and cells have been isolated from snake venoms. Many possess common structural features and also produce similar pharmacological effects. This has led to doubt as to the specificity of each polypeptide. Study of toxin gamma (cardiotoxin from Naja nigricollis), cytotoxin P6 (from naja naja, preferentially cytotoxic to certain cells) and neurotoxin alpha (Naja nigricollis) under identical conditions shows that they are separate entities though having some common structural properties. The amino acid composition shows certain resemblance between the nontoxic polypeptides, P6 and toxin gamma, as compared to the neurotoxin alpha. Their molecular weights are of the same order. Sulphydryl groups are absent in all but they possess a high proportion of disulphide linkages. The behavior of toxin gamma, cytotoxin P6 and neurotoxin alpha on Yoshida sarcoma cells and human erythrocytes demonstrate that whereas cytotoxin P6 was more active in lysing Yoshida sarcoma cells the order of activity was reversed in the human erythrocytes. Apparently these two cell systems respond differently to the action of the two polypeptides suggesting that they bind to different membrane receptors. The selectively displayed in changing the membrane permeability of different cells is probably dependent not ony on their basic charge but on the specificity of their protein structure.

Amino Acids↗
PubMed1986

Differential expression of fucosyl GM1 and a disialoganglioside with a NeuAc alpha 2-6GalNAc linkage (GD1e) in various rat ascites hepatoma cells.

A distinct difference in ganglioside composition among various rat ascites hepatomas and Yoshida sarcoma was observed on TLC-immunostaining with anti-fucosyl GM1 antibody, and chemical and enzymatic analyses. Yoshida sarcoma and ascites hepatomas, AH13, AH66F and AH66, but not the other 9 tumor cell lines investigated, specifically contained a disialoganglioside, NeuAc alpha 2-3Gal beta 1-3(NeuAc alpha 2-6)GalNAc beta 1-4Gal beta 1-4Glc beta 1-1ceramide (GD1e), whereas the 9 ascites hepatoma cells without GD1e contained fucosyl GM1. The differential expression of fucosyl GM1 and GD1e in various tumor cell lines indicates that different cell lineages express distinct metabolic pathways for gangliosides, and that the gangliosides are useful markers for distinguishing tumor cell lines.

Animals↗
PubMed1979

Serum Zn content in tumor-bearing rats treated with anticancer drugs.

The serum Zn content in rats bearing Yoshida-Sarcoma, AH 66F, AH 13 or AH 109A was found to be low as compared with that in normal controls. In the rats which had received intraperitoneal inoculum of Yoshida-Sarcoma, the effects of anticancer drugs were closely related to the changes in serum Zn content. Namely, serum Zn content increased and approached the normal range almost parallel with the prolongation of survival time by anticancer drugs. As the causes responsible for the reduction in quantity of serum Zn in the tumor-bearing rats, the reduction of serum albumin content and the accumulation of Zn in the tumor tissue and organs such as the liver and kidneys were suggested.

Animals↗
PubMed1991

[In-vivo 19F-MRS study of 5-fluorouracil (5-FU) metabolism on tumors].

5-Fluorouracil (5-FU) metabolism on tumors was studied by in-vivo 19F-MRS (magnetic resonance spectroscopy). In this study, two kinds of tumors were used, i.e., Yoshida sarcoma implanted subcutaneously to the abdomen of rats and drug-induced tumors in the rats livers. Sequential 19F spectra were obtained just after 150 mg/kg 5-FU injected intravenously. In Yoshida sarcoma, the accumulation of 5-FU was observed and disappearance of 5-FU was slower compared to the normal tissue. However, synthesis of fluoronucleotides (Fnct) could not be detected. In drug-induced liver tumors, the peak of fluoro-beta-alanine (FBAL) was observed. Disappearance of 5-FU and catabolism to FBAL in the liver tumors group were slower compared to the normal liver. Synthesis of Fnct did not increase in the liver tumor group. The results in the liver tumor group are considered to be the confined result of the hepatocytes and tumors cells. It was considered that the delayed catabolism to FBAL in the liver tumor group showed metabolic dysfunction of the liver. Also the synthesis of Fnct in tumors could not be detected by in-vivo 19F-MRS. 19F-MRS method could not detect Fnct in tumors in-vivo. However, the accumulation of 5-FU could be assessed by this method. It is expected that the evaluation of 5-FU pooling in tumors could be used for the index of chemotherapeutic effect.

Animals↗
PubMed1996

[Hypoxyradiotherapy: changes in the oxygen partial pressure distribution in the tumor and in the healthy tissue under acute respiratory hypoxia].

PURPOSE: Based on the oxygen effect a new therapeutic modality has been developed to protect healthy tissues while breathing hypoxic gas mixture during irradiation. MATERIAL AND METHODS: The effect of breathing hypoxic gas mixture (8.1% O2) on pO2 in Yoshida sarcoma and muscle was studied using rats of Wistar strain. Different fractionation schedules were used: 10 x 3 Gy, 6 x 5 Gy and 3 x 10 Gy. Tissue oxygenation was assessed with a polarographic electrode system. RESULTS: The median pO2 in Yoshida sarcoma was 10 mm Hg. 21% of pO2-values were lower than 5 mm Hg. During breathing of hypoxic gas mixture no significant changes in median tumor pO2 or radiobiologic hypoxic values (< or = 5 mm Hg) were recorded. The median pO2 in muscle was 30 mm Hg. During breathing of gas hypoxic mixture a significant decrease of the median to the value 12 mm Hg and an increase of the radiobiologic hypoxic values (p < 0.00001) were observed. The changes of pO2-values were constant independent from fractionation. CONCLUSIONS: Between tumor and healthy tissue exists a significant difference regarding changes in the radiobiologic fraction during breathing of hypoxic gas mixture. This fact explains the experimental and clinical experience, that the breathing hypoxic gas mixture protects the healthy tissue without changes in the radiosensibility of chronic hypoxic tumor tissue.

Acute Disease↗
PubMed1978

Cellular factors for stimulation of nucleosomal template activity for in vitro DNA synthesis.

Nucleosomes isolated from Yoshida sarcoma chromatin by micrococcal nuclease treatment were relatively inactive as templates for in vitro DNA synthesis. However, the template activity increased by trypsin digestion of nucleosomes or addition of heparin to the reaction mixture. This indicates that the nucleosomal template activity is masked. A crude extract of Yoshida sarcoma cells stimulated the nucleosomal template activity. The stimulatory factor was separated into three peaks by DEAE cellulose column chromatography. The same three peaks were observed in normal rat liver extract with much lower activities, but enhanced in regenerating liver. The factors seem to stimulate DNA synthesis by activating DNA template in nucleosomes without degrading histones or changing the primary structure of nucleosomal DNA.

Animals↗
PubMed1979

Metabolism of 5-fluorouracil in sensitive and resistant tumor cells.

Thymidine kinase, dTMP kinase, and DNA polymerase activities were determined in cell lines of AH hepatoma, L1210 leukemia, and Yoshida sarcoma that were sensitive and resistant to 5-fluorouracil (5-FU). It was found that the levels of these enzymes in tumor cells were not consistently related to the property of sensitivity to 5-FU. A marked difference was observed between sensitive and resistant cell lines of L1210 leukemia and Yoshida sarcoma in the uptake of labeled 5-FU into the acid-soluble, nucleotide, and RNA fractions, the rate of incorporation of 5-FU into these fractions being 3 to 5 times greater in sensitive tumor cells than in resistant tumor cells. The radioactivities in the acid-soluble fractions of AH44 (sensitive) and AH109A (resistant) were similar after incubation of these cells with labeled 5-FU in vitro. However, a smaller volume of ascites and lower cell number were observed in AH44 (sensitive)-bearing rats than in AH109A (resistant)-bearing rats. These in vivo results indicate that the 5-FU injected intraperitoneally was diluted by ascites more in AH109A (resistant)-bearing rats than in AH44 (sensitive)-bearing rats.

Animals↗
PubMed1982

Growth factor from tumor cells.

Suitable conditions for assay of the growth factor from Yoshida sarcoma and AH-130 tumor cells were investigated using three different cell lines: baby hamster kidney cells, human embryonic lung cells and Swiss Albino mouse 3T3 embryo fibroblast cells. The results indicated that the 3T3 cell line was more sensitive to the growth stimulating activity than the other two lines. A fraction of Yoshida sarcoma tumor cells containing the growth factor showed less growth stimulating activity than a fraction of AH-130 tumor cells prepared by the same method. Using the 3T3 cell line for assay of activity, the growth factor was partially purified from AH-130 tumor cells by ammonium sulfate fractionation, DEAE-cellulose column chromatography and gel filtration on a Sephacryl S-300 column. It appeared to be thermolabile, and its molecular weight was estimated as about 80,000 by gel filtration on Sephacryl S-300. These findings suggest that it is a high-molecular-weight substance.

Animals↗
PubMed2002

Renal chemoembolization with mitomycin c/Ethibloc: pharmacokinetics and efficacy in an animal model.

BACKGROUND AND PURPOSE: Arterial embolization can be an alternative treatment for kidney malignancy. We investigated the efficacy of renal embolization with a combination of an occlusive agent (Ethibloc) and the cytotoxic substance mitomycin C (MMC) in an animal model. MATERIALS AND METHODS: In 32 rats with implanted Yoshida sarcoma, nephrectomy was carried out 15, 30, 60, or 90 minutes after chemoembolization (1 mg v 2 mg of MMC/mL of Ethibloc) or chemoperfusion (1 mg of MMC/mL of NaCl) of the tumor-bearing kidney. The MMC tissue concentration was measured in the kidney specimens. Six dogs also underwent chemoembolization or chemoperfusion with monitoring of MMC serum concentration at the same intervals. We compared the survival time of rats with Yoshida sarcoma after chemoembolization (N = 15), chemoperfusion (N = 18), embolization (N = 18), nephrectomy (N = 21), and no treatment (N = 25). RESULTS: The MMC tissue concentration in the rat model was much higher after chemoembolization than after chemoperfusion for at least 1.5 hours. The MMC serum concentration in the dogs showed a high initial peak (0.6 mg/L) after chemoperfusion, then dropped quickly to the same level seen 30 minutes after chemoembolization with 1 mg of MMC/mL of Ethibloc (0.15 mg/L). The MMC serum concentration following chemoembolization with 2 mg of MMC/mL of Ethibloc stayed higher (0.3-0.25 mg/L) for 60 minutes. The survival rates after nephrectomy were equal to those after chemoembolization (80% survival after 30 days), with poorer survival being seen after embolization (75%) and chemoperfusion (70%). In the control group, all rats were dead at the 27th day. CONCLUSION: Chemoembolization produces persistently high tissue concentrations of MMC and avoids toxic peak serum levels. It improves the efficacy of organ ablative vasoocclusion in renal malignancies.

Animals↗
PubMed1977

Relationship between transcerebral passage of tumor cells and brain metastasis.

Quantitative study was carried out on transcerebral passage of tumor cells using Yoshida sarcoma and 6 strains of rat ascites hepatoma. The counting was done every second for 40 sec. In relation to the results obtained, histological study was made on the cerebral metastasis of these tumor cells. Metastatic foci in the brain parenchyma, except the meninges and choroid plexus, were formed by island-forming strains (AH-130, AH-272, and AH-7971) which showed comparatively low passage rate and not be single-cell strains (Yoshida sarcoma, AH-7974F, AH-66F, and AH-13) which showed comparatively high rates. Accordingly, it is obvious that there is a correlation between transcerebral passage rates and brain metastasis formation. The mechanisms of metastasis formation were discussed with special reference to arrest of tumor cells in blood vessels.

Animals↗