scholarly journals Evolution of sarcoma 180 in mice treated with hyperchlorinated water

1983 ◽  
Vol 78 (2) ◽  
pp. 209-214
Author(s):  
Fausto Edmundo Lima Pereira ◽  
Fabio Benezath Chaves
Keyword(s):  
Weight Gain ◽  
Tumor Cells ◽  
Peritoneal Cavity ◽  
Tap Water ◽  
Bactericidal Effect ◽  
Peritoneal Macrophages ◽  
Tumor Evolution ◽  
Sarcoma 180 ◽  
Tumor Implantation ◽  
Effect Of Chlorine

Mice treated with hyperchlorinated water (50 ppm of chlorine) and control mice, drinking tap water (1-3 ppm of chlorine) were inoculated with 2.5 x 10 [raised to the power of 6] sarcoma 180 cells, by intraperitoneal route. Tumor evolution was measured by enumeration of tumor cells in peritoneal cavity and by evaluation of weight gain at different time intervals after tumor implantation. In mice treated with excessive amounts of chlorine there was enhancement of tumor growth demonstrated by: (a) shorter incubation period and increased weight gain (ascites formation) after tumor implantation; (b) increased number of tumor cells in the peritoneal cavity 2, 3 and 4 days after tumor challenge. The number of peritoneal cells exsudated after tumor implantation was lower in mice treated with hyperchlorinated water than in controls. The tumor enhancement observed after excessive chlorine ingestion would be due to: (a) reduction of the number of peritoneal macrophages that migrate to the peritoneal cavity and (b) reduction of the tumoricidal capacity of peritonela macrophages induced by the direct effect of chlorine or by the reduction of the amount of endogenous endotoxins due to the bactericidal effect of chlorine.

scholarly journals Evolution of sarcoma 180 in mice infected with Trypanosoma cruzi

1983 ◽  
Vol 78 (3) ◽  
pp. 237-244
Author(s):  
Fausto Edmundo Lima Pereira ◽  
William Assad Sassine ◽  
Dimith Chequer Bouhabib ◽  
Elton de Almeida Lucas
Keyword(s):  
Weight Gain ◽  
Trypanosoma Cruzi ◽  
Tumor Cells ◽  
Ascitic Fluid ◽  
Tumor Development ◽  
Sarcoma 180 ◽  
Tumor Inoculation ◽  
Time Intervals ◽  
Tumor Challenge ◽  
Ascites Formation

Mice infected with Trypanosoma cruzi were challenged with 2x10[raised to the power of 6] cells of sarcoma 180 (ascite tumor) by i.p. route, on day seven post infection. Tumor development was followed by evaluation of weight gain, by measurement of ascitic fluid produced and enumeration of tumor cells in ascitic fluid. Infected mice were more resitant to tumor development as demonstrated by reduction in ascites formation and by reduction in the number of tumor cells in ascitic fluid, at different time intervals after tumor challenge. The number of peritoneal cells exsudated after tumor inoculation was greater in infected mice than in controls. This increased resitance of mice infected with T. cruzi to tumor development could be due to the action of macrophages activated by the infection and by the action of endotoxins absorbed from the gut or produced by the own parasite.

scholarly journals Evolution of sarcoma 180 (ascitic tumor) in mice infected with Schistosoma mansoni

1986 ◽  
Vol 19 (1) ◽  
pp. 39-42
Author(s):  
Fausto Edmundo Lima Pereira ◽  
Pedro Raso ◽  
Paulo Marcos Zech Coelho
Keyword(s):  
Weight Gain ◽  
Schistosoma Mansoni ◽  
Infected Group ◽  
Sarcoma 180 ◽  
Ascites Tumor ◽  
Tumor Inoculation ◽  
Transplantable Tumor ◽  
Tumoricidal Activity ◽  
Tumor Implantation ◽  
Ascites Formation

Mice infected with 60 cercariae of Schistosoma mansoni were more resistant to the sarcoma 180 ascites tumor. Tumor inoculation was performed 50 days after schistosoma infection and the animals were observed and weighed at 48 hours intervals for development and progression of malignancy. In infected mice the weight gain (ascites formation) started later and was shorter than in uninfected Controls. Also, the number of tumor cells into the peritoneal cavity 72h after tumor implantation was shorter in infected group than incontrols. This in creased resistance against a transplantable tumor probably is related to the effect of endotoxin on tumoricidal activity of macrophages activated by the infection. The immunodepression induced by Schistosoma mansoni infection enhances the proliferation of endogenous bacteria increasing the amount of endotoxin absorbed from the gut.

scholarly journals Phosphorylation of Ribosomal Proteins in Sarcoma 180 Tumor Cells

1972 ◽  
Vol 247 (17) ◽  
pp. 5345-5350
Author(s):  
Lawrence Bitte ◽  
David Kabat
Keyword(s):  
Tumor Cells ◽  
Ribosomal Proteins ◽  
Sarcoma 180

Effect of Garlic, Chinese Medicinal Drugs and Amino Acids on Growth of Erlich Ascites Tumor Cells in Mice

1983 ◽  
Vol 11 (01n04) ◽  
pp. 69-73 ◽  
Author(s):  
Y.M. Choy ◽  
T.T. Kwok ◽  
K.P. Fung ◽  
C.Y. Lee
Keyword(s):  
Amino Acids ◽  
Tumor Cells ◽  
Peritoneal Cavity ◽  
Growth And Development ◽  
Ehrlich Ascites Tumor Cells ◽  
Ascites Tumor ◽  
Tumor Bearing ◽  
Ehrlich Ascites ◽  
Medicinal Drugs ◽  
Growth Of Tumor

A number of food materials or drugs have been screened for the effect on the growth and development of transplantable Ehrlich ascites tumor cells. Growth of tumor-bearing mice was significantly inhibited by feeding garlic as well as some amino acids. These materials significantly reduced the total number of free tumor cells growing in the peritoneal cavity of mice and prolonged significantly the length of time for 50% death of tumor-bearing mice.

scholarly journals Evaluation of (anti)genotoxic activities of Phyllanthus niruri L. in rat bone marrow using the micronucleus test

2013 ◽  
Vol 49 (1) ◽  
pp. 135-148 ◽  
Author(s):  
Fernando Márlisson de Queiroz ◽  
Kayo Wanderson de Oliveira Matias ◽  
Mylena Mylana Freire da Cunha ◽  
Aline Schwarz
Keyword(s):  
Bone Marrow ◽  
Body Weight ◽  
Weight Gain ◽  
Micronucleus Test ◽  
Body Weight Gain ◽  
Tap Water ◽  
Control Group ◽  
Cytotoxic Activities ◽  
Phyllanthus Niruri ◽  
Polychromatic Erythrocytes

Phyllanthus niruri L. (Euphorbiaceae), known as "quebra-pedra" (Portuguese for "stonebreaker"), is an herb used for kidney disorders. In light of its frequent use by the population, the present study aimed to investigate the genotoxic, antigenotoxic and cytotoxic activities of a standardized P. niruri extract in bone marrow rats. Three groups of 12 animals were treated daily by gavage over a period of 30 days, with 50, 150 or 250 mg/kg of P. niruri extract aqueous solution. The control group (n = 12) received tap water. At the end of treatment (day 31), groups were divided into two minor subgroups (n=6/group) and received cyclophosphamide (50 mg/kg, i.p.) or saline 0.9% (i.p.). After 24 hours, we evaluated the frequency of micronucleated polychromatic erythrocytes for each animal (MNPCE) at 1000 PCE. Cytotoxicity was evaluated with the PCE/NCE ratio (NEC = normochromatic erythrocytes). General toxicity was assessed during treatment using the parameters of body weight gain, ration and water consumption. The dry extract did not provoke changes in body weight, weight gain, ration and water intake or changes in the frequency of MNPCE or cytotoxicity in bone marrow. We propose that the P. niruri extract used here showed no genotoxic, antigenotoxic and cytotoxic activities under the experimental conditions.

Macrophage Antitumor Activity Induced by the Antigenic Lymphoma L5178Y/DTIC Subline

1982 ◽  
Vol 68 (5) ◽  
pp. 365-371 ◽  
Author(s):  
Ornella Marelli ◽  
Alberto Mantovani ◽  
Paola Franco ◽  
Angelo Nicotin
Keyword(s):  
Antitumor Activity ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Peritoneal Macrophages ◽  
Leukemic Cells ◽  
Target Cells ◽  
Tumor Target ◽  
Growth Inhibitory

Murine leukemic cells, after in vivo treatment with antineoplastic drugs, have been shown to express new antigenic specificities that were not detectable on parental cells and that were heritable after the withdrawal of drug treatment. A study was conducted of macrophage antitumor activity triggered by LY/DTIC cells, a subline of LY murine lymphoma, antigenically altered by the drug DTIC. In vitro non-specific inhibition of tumor cell growth was exhibited by spleen and peritoneal macrophages from mice previously challenged with viable LY/DTIC. Peritoneal macrophages from LY/DTIC immune animals showed moderate, although significant lytic activity against unrelated tumor target cells. Supernatants from mixed lymphocyte-tumor cell cultures, in which LY/DTIC immune lymphocytes and LY/DTIC tumor cells had been cultured, rendered normal macrophages non-specifically growth inhibitory for tumor cells.

scholarly journals Role of activated macrophages in antibody-dependent lysis of tumor cells.

1980 ◽  
Vol 152 (1) ◽  
pp. 183-197 ◽  
Author(s):  
C Nathan ◽  
L Brukner ◽  
G Kaplan ◽  
J Unkeless ◽  
Z Cohn
Keyword(s):  
Tumor Cells ◽  
Peritoneal Macrophages ◽  
Activated Macrophages ◽  
Fab Fragment ◽  
Bacille Calmette Guerin ◽  
Pharmacologic Agent ◽  
Peritoneal Cells ◽  
Specific Contact ◽  
Cytolytic Response

Treatment of mice with Bacille Calmette-Guérin (BCG) or C parvum activates their peritoneal macrophages to release increased amounts of H2O2, and thereby to lyse extracellular tumor cells, in response to a pharmacologic agent, phorbol myristate acetate (PMA) (1-3). In the present study, the same bacterial vaccines activated peritoneal cells to become cytolytic to lymphoma cells sensitized with alloantiserum, in the absence of PMA. Resident peritoneal cells, or those elicited with thioglycollate broth, were ineffective, not only in PMA-induced lysis, but also in antibody-dependent lysis of tumor cells. The cytolytic effect of BCG peritoneal cells toward sensitized tumor cells appeared to be mediated mostly by macrophages. Cytotoxicity was immunologically specific, contact dependent, rapid, and efficient. Phagocytosis of intact tumor cells was not involved. Alloantiserum-dependent cytolysis was specifically blocked by the Fab fragment of a monoclonal antibody directed against the trypsin-resistant macrophage Fc receptor (FcR II). Thus, tumor cells coated with homologous immunoglobulin interact with FcR II on activated macrophages to trigger an extra-cellular cytolytic response.

Coagulant And Procoagulant Factors In Ascitic Fluid.-About Etiology Of Dic Induced By Ascitic Fluid Infusion

1981 ◽  
Author(s):  
M Ojiro ◽  
M Takenoshita ◽  
M Nishi
Keyword(s):  
Tumor Cells ◽  
Ascitic Fluid ◽  
Peritoneal Cavity ◽  
Hepatic Cirrhosis ◽  
Vascular System ◽  
Vena Cava ◽  
Clotting Time ◽  
Fluid Infusion ◽  
Normal Plasma ◽  
Tissue Thromboplastin

We have experienced two cases of DIC following infusion of ascitic fluid from the peritoneal cavity to the vascular system. We have studied the etiology of this DIC. So, FDP, endotoxin, coagulant factors and procoagulant activity were investigated in ascitic fluid of 11 hepatic cirrhosis cases and 15 cancer cases.Method and Result; FDP in ascites were more included than in plasma. Endotoxin were positive in about 60% of ascitic fluid. The coagulant factors were recognized a littile except VUI-factor. Only ascitic fluid ded not clott the fibrinogen and did not affect the platlate aggregation. The procoagulant activities were measured by clotting times which the normal plasma (0.lcc) was added with the ascitic fluid or buffer (0.1cc), after 3 minutes incubation, and then added with 1/40 M Cacl2 (0.1cc).The clotting time was shortened in the ascitic fluid than buffer (buffer 120.7 ± 7.9 sec, Cancer 82 ± 23.8 sec., cirrhosis 91.4 ± 16.5 sec), and both VII and VIII deficient plasma was shortened too, but X dificient plasma was not coagulated. Also FDP and endotoxin did not shorten the clotting time of normal plasma. Experimentally, the ascitic fluid in dog by binding vena cava in ferior and the ascitic fluid in rat by transplantation of tumor cells shortened the clotting time. Conclusion; Coagulant, fibrinolytic and procoagulant factors were existed in ascitic fluid. We think that DIC induced by ascitic fluid are due to this procoagulant factor and this procoagulant factor may be not tissue - thromboplastin only.

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