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PubMed1978

Carcinostatic effect of aliphatic aldehydes and aldehyde dehydrogenase activity in Ehrlich carcinoma, Sarcoma 180, and Yoshida AH 130 hepatoma.

The antitumor activity of 2,3-dihydroxybutyraldehyde on Ehrlich carcinoma, Sarcoma 180, and Yoshida AH 130 hepatoma, as well as the aldehyde dehydrogenase activity in these tumors, was studied. 2,3-Dihydroxybutyraldehyde at nontoxic doses (500 mg/kg body weight i.p. daily for 7 days) slowed down the growth of solid and ascites tumors in mice. The treatment completely prevented the development of Yoshida ascites hepatoma in several rats. 2,3-Dihydroxybutyraldehyde, although it did not influence the growth of Ehrlich carcinoma transplanted in the brain of mice, significantly decreased in the lungs of these animals the number of viable tumour cells that derived from the primary tumor. All the tested tumors, which were sensitive to the action of 2,3-dihydroxybutyraldehyde, were virtually devoid of aldehyde dehydrogenase activity. These results suggest a possible relationship between the lack of this enzyme activity and the antitumor activity of aliphatic aldehydes.

Aldehyde Oxidoreductases↗
PubMed1981

Tumor-associated serum proteins in rats as detected by two-dimensional gel electrophoresis.

The sera from normal and tumor-bearing rats were separated by polyacrylamide gel disc isoelectric electrophoresis and then in a perpendicular dimension by polyacrylamide gel slab electrophoresis with a gradient from 4% to 20%. When the gel was stained with Coomassie brilliant blue, 100-150 components were separately observable with normal serum. With the sera from Rhodamine sarcoma-bearing rats, three more components were detected with a high reproducibility. They were of pI (isoelectric point) 4.5 and Rm (relative mobility) 0.63, of pI4.8 and Rm 0.63 and of pI 4.9 and Rm 0.75. The 4.5/0.63 (pI/Rm) and the 4.8/0.63 components appeared soon after transplanting the tumor, whereas the 4.9/0.75 component appeared at the late stage of its growth. Upon surgical removal of the grown tumor, the former two components disappeared rapidly, while the latter component disappeared gradually. Similar results were obtained with Yoshida sarcoma, and ascites hepatoma AH66 and AH130. A 3rd polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate revealed that the 4.5/0.63 and the 4.8/0.63 components were each composed of a single polypeptide of approximately 64,000 daltons, and that the 4.9/0.75 component was composed of two different polypeptides of approximately 33,000 daltons and approximately 10,000 daltons. It was confirmed by an immunodiffusion experiment that none of these three proteins was alpha-fetoprotein.

Animals↗
PubMed2001

Glutamine supplementation in cancer patients.

OBJECTIVES: Three series of studies investigated whether 1) glutamine deficiency occurs in tumor-bearing rats, 2) glutamine supplementation improves protein metabolism during chemotherapy in tumor-bearing rats, and 3) oral glutamine supplement improves systemic immune and gut-barrier function in patients with esophageal cancer receiving radiochemotherapy. METHODS: In the animal studies, AH109A hepatoma cells or Yoshida sarcoma cells were inoculated into male Donryu rats to induce tumors. Glutamine production was measured by U-14C-glutamine infusion and the conversion of arginine to glutamine was measured by infusion of U-14C-arginine. The effect of glutamine on protein metabolism was investigated by 1-14C-leucine infusion. In the clinical study, 13 patients with esophageal cancer were randomized into two groups, control and glutamine supplemented (30 g/d), for 4 wk. RESULTS: Glutamine levels in plasma and skeletal muscle were decreased in tumor-bearing rats, although glutamine production and the conversion of arginine to glutamine were increased. Glutamine-supplemented total parenteral nutrition reduced whole-body protein breakdown rate during chemotherapy in tumor-bearing rats. Oral supplementation of glutamine to the patients with esophageal cancer enhanced lymphocyte mitogenic function and reduced permeability of the gut during radiochemotherapy. CONCLUSIONS: Glutamine depletion in host tissues occurs in tumor-bearing rats. Glutamine supplementation can attenuate loss of protein in the muscle in tumor-bearing animals and protect immune and gut-barrier function during radiochemotherapy in patients with advanced cancer.

Animals↗
PubMed1978

New microbial secondary metabolites under preclinical development for cancer treatment.

Limitless numbers of various genetic structures have been formed in chromosomes and plasmids and numerous bioactive compounds are produced by microorganisms. Therefore, it may be said that compounds useful in treatment of cancer will be found more and more in microbial secondary metabolites and more effective antitumor antibiotics and their derivatives, or more effective products producing immune resistance to cancer, will be discovered. In these studies, as discussed in this paper, the most urgent problem is to establish a rational screening principle or system to select compounds worth clinical examination. This is particularly important in the analog area. Bleomycin is an analog of phleomycin chosen because of lower renal toxicity. It has become an antitumor agent of significant value. Macromycin is a new structure which has been found to bind with animal cells and inhibit growth. Neothramycin is a new benzodiazepine antibiotic which has lower toxicity than other structures studied in this class and is active against L1210, Yoshida sarcoma, and Sarcoma 180. Aclacinomycin A is an analog of adriamycin chosen for clinical study based on its low cardiac toxicity and high distribution in mouse lung and spleen. Coriolins are another new structural class. Diketocoriolin B has activity in L1210 leukemia and has been shown to inhibit Na-K-ATPase. Bestatin is a compound which inhibits aminopeptidase B and leucine aminopeptidase has been shown to increase delayed hypersensitivity. Bestatin also increases the effects of other antitumor agents such as adriamycin, and bleomycin.

Animals↗
PubMed1978

Clinical investigations of neocarzinostatin in Japan.

Neocarzinostatin (NCS) is an antibiotic from streptomyces carzinostaticus which inhibits DNA synthesis. Clinical trials in Japan began in 1971. NCS is active against S-180, Ehrlich tumor, L1210, Yoshida sarcoma, and a range of ascitic hepatomas. In rabbit NCS is distributed at high concentrations in the kidney, skin, stomach, pancreas, lung, and muscles. The high distribution in the pancreas and the stomach suggested possible effectiveness in human tumors at these sites. In clinical studies NCS has been shown to be active against acute leukemia. As a single agent 9 out of 51 obtained a CR with 9 more achieving a PR. Anorexia, nausea, and vomiting were the most frequent side effects. NCS has been tried in combination with Ara-C, daunorubicin and prednisolone and CR was ssen in 11 out of 14. In stomach cancer responses of some kind were observed in 12 out of 141 cases, while in the case of pancreatic tumors there were 10 out of 68.

Antibiotics, Antineoplastic↗
PubMed1980

Review of a new antimetabolic agent, 1,3-bis(tetrahydro-2-furanyl)-5-fluoro-2,4-pyrimidinedione (FD-1).

FD-1, a new anticancer drug, is a fluorinated pyrimidine derivative that has shown less acute toxicity than 5-FU and FT-207, and higher antitumor activity than FT-207 in Ehrlich carcinoma, S-180, AH-130, Yoshida sarcoma, and Walker 256. A principal feature of FD-1 is that, in comparison with FT-207, in oral administration it can maintain a higher concentration of 5-FU both in plasma and in tumor tissues. FD-1 is considered to be activated into 5-FU by a drug-metabolizing system in liver microsomes. In the plase I study of FD-1, the maximum tolerated dose was greater than 20 mg/kg in a single administration. The dose-limiting factor in FD-1 administration is gastrointestinal toxicity that causes side effects such as nausea and vomiting. The recommended dosage for daily oral administration of FD-1 is 6-12 mg/kg/day. In the phase I study of the sustained released form of FD-1 (FD-1-S), frequency of nausea and vomiting could be definitely reduced by the oral administration of FD-1-S, which showed higher tolerability. FD-1-S can be continuously administered at a dose ranging from 600 mg to 1200 mg/body/day for for 4 weeks and can be expected to have higher efficacy. In further studies on the long-term administration of FD-1-S, CNS toxicity has been reported in some cases.

Adult↗
PubMed1986

Analysis of the lodgement and extravasation of tumor cells in experimental models of hematogenous metastasis.

This review summarizes our experiments on the metastatic distribution patterns of Yoshida sarcoma and several strains of rat ascites hepatomas. These dissemination patterns cannot be explained entirely by either anatomical-mechanical considerations or by the seed-and-soil hypotheses for metastatic localization. In some experimental situations, anatomical-mechanical factors seem more important, but in others the seed-and-soil hypothesis offers a more compelling interpretation. Lodgement of tumor cells in the microcirculation of different organ vascular beds can occur by three non-exclusive mechanisms: direct attachment to vascular endothelial cells; direct adhesion to exposed vascular basement membrane components or by entrapment in thrombi. Similarly, extravasation can also occur via several mechanisms. The first, involves infiltration of tumor cells into perivascular tissues via their own movement. A second mechanism involves sequestration of tumor cells beneath vascular endothelial cells where they are separated from the blood stream. The third option for extravasation involves 'explosive' displacement in which the blood vessel wall swells as a result of intracapillary growth of tumor emboli causing the vessel to rupture.

Animals↗
PubMed1982

Interference of anti-tumor and immunosuppressive effects of cyclophosphamide in tumor-bearing rats. Analysis of factors determining resistance or susceptibility to a subsequent tumor challenge.

Adult rats were given 10(5) or 10(6) Yoshida ascites sarcoma (YAS) cells IP and were treated with cyclophosphamide (CY) given IP in single doses of 20 mg/kg or 100 mg/kg, 2 or 5 days after YAS inoculation. Both the curative effect of CY and subsequent resistance to tumor challenge in rats that survived depended on the dose of injected tumor cells and on the dose and time of administration of CY. These three factors determined whether the host's immune response to tumor antigens would develop and contribute to the overall anti-tumor effects of the chemotherapy. The curative effects of CY were significantly less pronounced in T-cell-deficient than in normal rats. Anti-tumor and immunosuppressive activities of CY exerted opposite influences on the ultimate result of the chemotherapy. Adverse immunosuppressive effects prevailed when the drug was administered early (2 days) after YAS inoculation. In this case the chemotherapy was less efficient and the surviving rats were susceptible to a subsequent tumor challenge. Further analysis showed that the injection of CY 2 days after inoculation of YAS antigens induced strong and specific immunologic tolerance to the tumor. In contrast, when a sufficient amount of tumor antigens (higher dose of tumor cells injected and CY injection delayed) elicited an anti-YAS immune response that was not suppressed by early injection of CY (CY administered 5 days after the tumor) effective eradication of tumor cells and anti-YAS resistance in cured animals were observed.

Animals↗
PubMed1977

[Studies on the thymidine-triphosphate synthesis in malignant tumors. I. Effects of thymidine on deoxyribonucleoside triphosphate pools and deoxyribonucleic acid synthesis (author's transl)].

Measurements of the deoxyribonucleoside triphosphate (dNTP) contents, the [14C] thymidine and deoxyuridine incorporation and the "key enzymes" of the thymidine triphosphate (dTTP) synthesis, thymidine kinase and ribonucleotide reductase, in diploid Ehrlich-ascites carcinoma, in Yoshida sarcoma-ascites cells and to a smaller extent in surgically removed malignant human tumours show 1. A distinctly increased dTTP content compared with the remaining dNTP is not a characteristic of tumour cells generally but a peculiarity of sarcoma and a sign of differentiation of a malignant tumour. 2. With simultaneous linear deoxyribonucleoside incorporation the dTTP content and the mix-proportion of [14C] dTTP to total dTTP in ascites tumour cells in short-term in-vitro incubation (120 min) remain constant. 3. Thymidine addition to the medium leads to a distinct rise of dTTP concentration even at a dosage of 3 X 10(-5) M. 4. The dNTP contents of ascites tumour cells are within the range of the endproduct-inhibiting concentrations of thymidine kinase and ribonucleotide reductase.

Animals↗
PubMed1977

[Partial synchronization of tumor cells in vivo with hydroxyurea (author's transl)].

For the partial synchronization of tumor cells, Yoshida ascitic sarcoma bearing rats were treated with Hydroxyurea using two methods, one in the form of a single intraperitoneal injection (0.5 mg/g body weight) and the other by continuous intraascitic infusion over a period of 12h (1.428 mg/g body weight total dose). The synchronization obtained by continuous infusion of Hydroxyurea is superior to that by a one time injection with respect to cell accumulation in one phase of the cell cycle and in the duration of synchronous proliferation. The degree of cell loss caused by infusion depends on the concentration of Hydroxyurea. Concentrations of slightly more than the minimal inhibitory concentration of DNA synthesis cause the least damage to the tumor cells.

Animals↗
PubMed1977

The influence of N-methyl-N-beta-chloroethyl hydrazines on the mitotic index of Ehrlich ascites tumor cells and the leukopoiesis of the mouse.

The cytostatic activity of N'-methyl-N'-beta-chloroethylbenzaldehyd hydrazone (B1) is at least equal to that of procarbazine when its effect is tested with the Ehrlich ascites tumor cells of the mouse and the Yoshida sarcoma of the rat. B1 causes a slighter decrease of mitotic cells and no shift from prophase to metaphase. These results suggest that the cytostatic effect of B1 is due to interference with cell metabolism or an effect at the cell membrane and not to an effect on cell proliferation. This assumption is supported by a considerable depression of lymphocytes and a minor effect on granulopoiesis, which is especially sensitive towards proliferation toxins. All these findings suggest a different mechanism of action of B1 and procarbazine.

Animals↗
PubMed1996

Is control of distribution of liposomes between tumors and bone marrow possible?

The objective of this study is to clarify to what extent the accumulation of liposomes from the blood into the tumor and bone marrow can be controlled by liposome size and membrane fluidity. Liposomes with different diameters (50-400 nm) and different membrane fluidity were prepared from hydrogenated egg phosphatidylcholine (HEPC) or egg phosphatidylcholine (EPC), cholesterol (Ch) and dicetylphosphate in various molar ratios. These liposomes were injected intravenously into rats bearing Yoshida sarcoma, and the ratios of the accumulation of liposomes in the tumor to those in the bone marrow, liver and spleen were compared. The tumor-to-bone marrow accumulation ratio increased with the decrease in liposome size from 400 to 50 nm. This ratio was greater than those for the liver and spleen at all sizes. Although tumor-to-liver accumulation ratios of 50- and 100-nm HEPC-containing liposomes were higher than those of EPC-containing liposomes, no obvious difference in tumor-to-bone marrow or tumor-to-spleen accumulation ratios was found between these liposomes. Tumor-to-bone marrow accumulation ratio of HEPC-containing liposomes increased remarkably with the decrease in Ch content from 40 to 30 or 20 mol% compared with ratios for the liver and spleen. Interestingly, the tumor uptake clearance of liposomes of the same size was constant regardless of their membrane fluidity. These findings show that the increases in these accumulation ratios are due to their decreased uptake clearance by the bone marrow. Furthermore, the uptake of 50-nm HEPC-containing liposomes by the bone marrow was specifically inhibited by preinjection of other liposomes, but not when they were exposed in advance to in vivo components. These observations suggest the involvement of in vivo component(s) in the uptake of these liposomes by the bone marrow. We conclude that small HEPC-liposomes with low Ch content show their significantly decreased uptake by the bone marrow due to their decreased recognition by this tissue.

Animals↗
PubMed1982

Potentiation of cell killing by inhibitors of poly(ADP-ribose) polymerase in four rodent cell lines exposed to N-methyl-N-nitrosourea or UV light.

The sensitivities (Do-values) of the cytotoxic effect of MNU on four rodent cell lines were: mouse L1210, 0.07 mM; rat Yoshida sarcoma, 0.52 mM; Chinese hamster V79A, 0.70 mM and the UV sensitive, X-ray sensitive V79/79, 0.35 mM. The abilities of maximum non-toxic doses of the poly-(ADP-ribose) polymerase inhibitors, 5-methyl nicotinamide (5MeN), 3-methoxybenzamide (3MBA) and caffeine to potentiate this cytotoxicity and that of UV light in V79A and V79/79 was measured. The degree of potentiation (ratio Do without inhibitor/Do with inhibitor) was both agent and cell line dependent. In general the lymphoid cell lines L1210 and YS showed greater potentiation, up to 4-fold, than did the fibroblast lines V79A and V79/79. The use of inhibitors in pairs suggested that 5MeN and 3MBA affect one process whereas caffeine affects additional processes. The data provide further support for a role for poly(ADP-ribose) in DNA repair, but indicate that metabolic factors may modify the effectiveness of individual inhibitors of poly(ADP-ribose) polymerase in different cell lines.

Animals↗
PubMed1982

Structure-antitumour activity relationships for new platinum complexes.

Fourteen platinum (Pt) coordination complexes with different ligands, which include both Pt(II) and Pt(IV) complexes, were prepared, characterized and tested for their in vitro cytotoxic effects on KB cells and for their antitumour activity against some tumour systems (L1210 and P388 leukaemia, ADJ/PC6A plasma cell tumour and Yoshida sarcoma). The majority of the ligands were derivatives of aniline or pyridine, but complexes with tranylcypromine, guanethidine and octodrine were also synthetized. Depending on cytotoxicity the Pt-compounds could be divided into 3 groups. The compounds with a high cytotoxicity (ED50 = 0.1-1 microgram/ml) were also active against L1210 and P-388 leukaemia; a correlation between cytotoxicity and antitumour activity was not always observed. In these complexes the oxidation state of the Pt appears to be critical for their activity.

Animals↗
PubMed1983

Isolation and characterization of DNA-binding proteins of Yoshida ascites tumour cells.

DNA-binding proteins from the cytosol and nuclei of Yoshida ascites sarcoma cells were isolated by affinity chromatography on native and denatured DNA-cellulose columns. The proteins that were retained in the columns were eluted by increasing concentrations of NaCl and analysed by electrophoresis in polyacrylamide gels. Two proteins with approximate molecular weights (MW) of 38 000 (38K) and 34 000 (34K) D showed high affinity for denatured DNA and eluted in large quantities from denatured DNA-cellulose columns. In contrast, only small amounts of 38 000 and 34 000 D proteins were found to be associated with native DNA and the native DNA-associated 38K and 34K proteins showed higher rate of phosphorylation than the corresponding denatured DNA-binding proteins. The 38 000 and 34 000 D DNA-binding proteins were present both in nuclei and cytoplasm. These two proteins together comprised over 70% of the total DNA-binding proteins present in the 0.4 M NaCl eluate of the cytoplasmic extracts. DNA-binding proteins of MW 38 000 and 34 000 D were also present in a methylcholanthrene-induced fibrosarcoma, although in smaller amounts.

Animals↗
PubMed1981

Differential inducibility of chromosome aberrations and sister-chromatid exchanges by indirect mutagens in various mammalian cell lines.

A total of 17 cultured mammalian cell lines of various types was investigated for the inducibility of chromosome aberrations (CAs) and sister-chromatid exchanges (SCEs) after exposure to 3 direct mutagens, cyclophosphamide (CP), dimethylnitrosamine (DMN) and benzo[a]pyrene (BP), without extrinsic metabolizing factors. The following cell lines were highly sensitive to CP as estimated by the dose-dependent increase of either CAs or SCEs, or both: 4 rat ascites hepatomas (AH66-B, AH66-C, AH70B, AH109A), 3 rat esophageal tumors (R1, R2, R3), the Yoshida sarcoma (YS), a Chinese hamster embryonic cell line (B-13), and a human embryonic (HE2236) cell line. 1 golden-hamster embryonic (GHE), 1 human embryonic (HE2144) and 1 human esophageal tumor (TH) cell line were moderately sensitive to CP in terms of the yield of SCEs, though they showed rather low sensitivity when measured by the frequency of CAs. 2 Chinese hamster (CHO-K1, CHL) and 1 human lymphoma (P3HR-1) cell lines were much less sensitive or almost insensitive with respect to the yield of both CAs and SCEs. Considering the above results and taking some other experimental conditions into account, 7 cell lines, including another Chinese hamster cell line (Don 6), were similarly investigated with DMN and BP. The results indicated that AH66-B, which was highly sensitive to CP, was also sensitive to DMN and BP, and that the CP-sensitive R1 and R3 were responsive to DMN. While YS, B-13, Don 6 and P3HR-1 did not show any significant response to DMN, a considerable increment of SCEs was noted in B-13 after treatment with BP, GHE was also notable for its high sensitivity to BP, showing an apparently dose-dependent increase of both CAs and SCEs. HE2144 exhibited a slightly increased rate of SCEs after exposure to BP.

Animals↗
PubMed1989

The hypercalcemic Walker carcinosarcoma 256 of the rat causes an increase in serum 1,25-dihydroxyvitamin D3.

We have studied vitamin D metabolism in rats with the transplantable hypercalcemic Walker carcinosarcoma 256, which is a well characterized animal model for humoral hypercalcemia of malignancy. 25-Hydroxyvitamin D3 (25(OH)D3) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) concentrations were determined in blood samples obtained from parathyroidectomized (PTX) female rats at different time intervals after intramuscular tumor cell inoculation. We observed a dramatic increase in serum 1,25(OH)2D3 (280 +/- 184 vs. 98 +/- 31 pmol/l) 6 days after tumor cell injection and 4 days after the initial rise of serum calcium, whereas 25(OH)D3 tended to decrease. In a separate control experiment we compared this to the effect of exogenous parathyroid hormone in PTX rats and found similar results. In contrast, rats exhibited no change in vitamin D metabolite blood concentration after inoculation of the normocalcemic Yoshida sarcoma, which obviously does not interfere with vitamin D metabolism. We conclude that the humoral bone-resorbing agent produced by the Walker tumor cells causes elevation of serum 1,25(OH)2D3 concentration by this fulfilling an additional criterion of PTH-like activity.

Animals↗