Ascites sarcoma-7 cells

ShimoyamaM (1975) The cytocidal action of alkylating agents and anticancer antibodies against in-vitro cultured Yoshida ascites sarcoma cells. J Jpn Soc Cancer Ther 10 63-72... 

Following the early observation of Klenk and Yamakawa and their associates, the presence of sialic acid residues at the surface of numerous cells was established, either by action of neuraminidase followed by determination of the cell electrophoretic mobility or by determination of the sialic acid released. For example, sialic acid residues were detected at the surface of EMich ascites tumor cells (Wallach and Eylar, 1961 Cook et aL, 1962), hamster kidney fibroblasts transformed by polyoma virus (Forrester et aL, 1964), squamous epithelial cells (Berwick and Coman, 1962), solid and ascites sarcoma cells (Cook et aL, 1963 Wallach and de Perez Esandi, 1964), normal and malignant rat liver cells (Kalant et aL, 1964), cells from human bronchial carcinoma, cells from rat myeloma, HeLa cells, and L-strain mouse fibroblasts (Fuhrmann etaL, 1962). 

Literature data on cytotoxic effects of photoexcited fullerene C60 are controversial. In the studies on transformed B-lymphocytes of Raji fine, phototoxic action of water-soluble carboxy-C60 was not revealed even upon its concentration of 5 x 10 5 M (Irie et al., 1996). In the study (Kamat et al., 2000) damaging effect of fullerenes C60 in dependence on intensity of irradiation toward CHO cells has been demonstrated. Using microsomal fraction of rat liver that was treated with C -cyclodextrin complex, it was shown that already in 5-30 min after UV-irradiation the accumulation of LPO products occurs that is suppressed by antioxidants like ascorbic acid and a-tocopherol. Similar effect of fullerenes C60 has been revealed in microsomal fraction of the cells of ascitic sarcoma 180 (Kamat et al., 2000). 

Beside this dermatoxic activity pederin (147) has various biological activities (92). When administered in appropriate doses to partially hepatectomized rats, this compound stimulates development of hepatic tissues. The inhibitory effect at the cellular level has been found in chicken heart fibroblast cultures, and mice embryo, dog kidney, HeLa, and KB cell lines. In plants, root growth of Lupinus albus is inhibited and mitosis in Allium cepa blocked at the metaphasic stage. Also, pederin (147) inhibits protein synthesis and growth of yeast cells. In addition, the treatment of rat ascites sarcoma with purified extracts of P. fuscipes produces almost complete regression. 

Fig. 6. The growth of Ascites Sarcoma-180 tumor cells in untreated ICR mice (solid line) and in treated mice (dashed line). The treatment consisted of five injections of 1.5 mg kg-1 given on day 1 after inoculation of 4 000 000 tumor cells on day 0. The number of cells continues to increase by repeated cell division up to day 4 and then slowly decreases to zero cells...

The nucleosides 236 were evaluated for cytotoxicity on mouse lymphoid leukemia cells (84JMC1358). Compounds 242 were screened for their anticancer or anti-AIDS activities (91JHC1417). Anticarcinogen activity against sarcoma 180 ascite tumor cells in mice was shown by 90 [84JAP(K) 5962593]. 

Early in vivo experiments (1913) showed that garlic and its compounds acted against mmors in mice, with similar results obtained by others (Reuter, Koch, and Lawson, in Garlic, pp. 178-186). Not only could mmor growth be inhibited, but alliin as freshly obtained from garlic bulbs and directly injected into rat sarcomas, resulted in reduction and dissipation. Similar results were obtained for intramuscular injections. Others, however, reported otherwise. On the other hand, allicin deactivated ehrlich ascites mmor cells, and also deactivated cells of Yoshida sarcoma (a mammary tumor). Other examples are described in the reference, with the note that fresh garlic neutralizes cancer cell virulence without compromising the immune response, whereby atumals at least become immune to untreated mmor cells. 

Romert, L., Jansson, T. Jenssen, D. 1994. The cytotoxicity of 50 chemicals from the NEIC study determined by growth inhibition of Ascites Sarcoma BPS cells A comparison with acute toxicity data in man and rodents. Toxicology Letters 71 39-46. 

Bekesi, J. G., and Winzler, R. J. The effect of D glucosamine on the adenine and uridine nucleotides of Sarcoma 180 ascites tumor cells. J. Biol. Chem., 244 5663-5668, 1969. 

Ascites sarcoma 180 cells (10 ) were implanted in the armpit of ICR-JCL mice. The polysaccharide solution, with a concentration of 1-10 mg/kg mouse, was injected intraperitoneally for ten days, starting 24 hr after the im.plantation of the ascites tumor. All mice were kept under observation for 5 weeks and then sacrificed for the evaluation of the effect of the treatment on the tumor growth. The inhibition ratios were calculated by the following equation, where A is the average tumor weight of the control groups and B is that of the treated groups. 

The effect of 6-mercaptopurine on the incorporation of a number of C-labelled compounds into soluble purine nucleotides and into RNA and DNA has been studied in leukemia L1210, Ehrlich ascites carcinoma, and solid sarcoma 180. At a level of 6-mercaptopurine that markedly inhibited the incorporation of formate and glycine, the utilization of adenine or 2-aminoadenine was not affected. There was no inhibition of the incorporation of 5(or 4)-aminoimidazole-4(5)-carboxamide (AIC) into adenine derivatives and no marked or consistent inhibition of its incorporation into guanine derivatives. The conversion of AIC to purines in ascites cells was not inhibited at levels of 6-mercaptopurine 8-20 times those that produced 50 per cent or greater inhibition of de novo synthesis [292]. Furthermore, AIC reverses the inhibition of growth of S180 cells (AH/5) in culture by 6-mercaptopurine [293]. These results suggest that in all these systems, in vitro and in vivo, the principal site at which 6-mercaptopurine inhibits nucleic acid biosynthesis is prior to the formation of AIC, and that the interconversion of purine ribonucleotides (see below) is not the primary site of action [292]. Presumably, this early step is the conversion of PRPP to 5-phosphoribosylamine inhibited allosterically by 6-mercaptopurine ribonucleotide (feedback inhibition is not observed in cells that cannot convert 6-mercaptopurine to its ribonucleotide [244]. 

The significance of these in vitro enzyme inhibition studies is uncertain, in view of the evidence that has been presented concerning the sensitivity of cancer cells to feedback inhibition by these nucleotides. On the other hand, 6-chloropurine inhibits the de novo biosynthesis of nucleic acid guanine but not of nucleic acid adenine in sarcoma 180 ascites cells [319],... 

In die peripheral blood system, crocetin derivatives prevent an elevation in bilirubin levels [3] and also reduce elevated levels of serum cholesterol and triglyceride [4]. Anti-tumor activity of saffron is observed in mice transplanted with several types of tumor cell lines including sarcoma 180, Ehrlich ascites carcinoma, and Dalton s lymphoma ascites... 

In addition to the (antimicrobial, enzyme and endocrine related) properties mentioned above, it is interesting that many labdane type diterpenes also exhibit significant properties against cancer cells. A number of labdane type diterpenes tested exhibited remarkable antiproliferative and cytotoxic activities. Itokawa et al. [193] found that extracts from the rhizomes of Hedychium coronarium (Zingiberacae), cause growth inhibition of Chinese hamster V-79 cells and sarcoma 180 ascites in mice. Chemical analysis led to the isolation of 8 (17), 12 (E)-labdadiene-15, 16-dial along with four new coronarins (A-D). All of the compounds exhibited... 

Some synthetic lapachol derivatives have also showed cytotoxic activity. Burton et al have prepared mono(arylimino) derivatives of P-lapachone. Some of these derivatives had good scores with net cell kills in preliminary in vivo testing hollow fiber assays against a standard panel of 12 human tumor cell lines [160].Twelve substituted 1,4-naphthoquinones were tested against the ascitic form of sarcoma 180 in Swiss mice. Statistical analysis showed that the most important molecular parameter determining their effectiveness in prolonging the life of mice bearing this tumor is their redox potentials [161]. Zalkow et al have synthesized a monoimine quinone, namely 2-methyl-(Z)-4-phenylimino)naphth[2,3-d]oxazol-9-one, which in in vitro tests showed a selective activity for some solid cancer tumors [162]. Enamine derivatives of lapachol were... 

Several techniques have been developed for producing ascites fluid in mice. In addition to the original adjuvant technique, a modification used in our laboratory involves injecting the antigen in complete Freund s adjuvant intraperitoneally followed by an injection 3 days later of 0.5 ml of pristane. Mice are boosted 7-10 days later and again after another 7-10 days. Another effective method is to administer intraperitoneal injections of Sarcoma 180 cells subsequent to several intraperitoneal injections of complete Freund s adjuvant. Distension of the abdomen is indicative of ascites development. The amount of ascites fluid that can be obtained at each tapping varies from 0.25 ml to 20 ml. 

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