Inhibition of Transfer Ribonucleic Acid Nucleotidyl Transferase (EC 2.7.7.25) from Ehrlich Tumor Cells by Proflavine Sulfate and Ethidium Bromide

Enzyme ◽  
1976 ◽  
Vol 21 (3) ◽  
pp. 225-231 ◽  
Author(s):  
Anthony J. Girgenti ◽  
Theodore W. Whitford, jr. ◽  
Joseph G. Cory
Keyword(s):  
Tumor Cells ◽  
Ethidium Bromide ◽  
Ribonucleic Acid ◽  
Ehrlich Tumor ◽  
Nucleotidyl Transferase ◽  
Ehrlich Tumor Cells

scholarly journals The Ehrlich Tumor Induces Pain-Like Behavior in Mice: A Novel Model of Cancer Pain for Pathophysiological Studies and Pharmacological Screening

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Cassia Calixto-Campos ◽  
Ana C. Zarpelon ◽  
Mab Corrêa ◽  
Renato D. R. Cardoso ◽  
Felipe A. Pinho-Ribeiro ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cancer Pain ◽  
Tumor Cells ◽  
Tricyclic Antidepressant ◽  
Mechanical Hyperalgesia ◽  
Cyclooxygenase Inhibitor ◽  
Paw Edema ◽  
Ehrlich Tumor ◽  
Novel Model ◽  
Ehrlich Tumor Cells

The Ehrlich tumor is a mammary adenocarcinoma of mice that can be developed in solid and ascitic forms depending on its administration in tissues or cavities, respectively. The present study investigates whether the subcutaneous plantar administration of the Ehrlich tumor cells induces pain-like behavior and initial pharmacological susceptibility characteristics. The Ehrlich tumor cells (1 × 104–107cells) induced dose-dependent mechanical hyperalgesia (electronic version of the von Frey filaments), paw edema/tumor growth (caliper), and flinches compared with the saline group between days 2 and 12. There was no difference between doses of cells regarding thermal hyperalgesia in the hot-plate test. Indomethacin (a cyclooxygenase inhibitor) and amitriptyline hydrochloride (a tricyclic antidepressant) treatments did not affect flinches or thermal and mechanical hyperalgesia. On the other hand, morphine (an opioid) inhibited the flinch behavior and the thermal and mechanical hyperalgesia. These effects of morphine on pain-like behavior were prevented by naloxone (an opioid receptor antagonist) treatment. None of the treatments affected paw edema/tumor growth. The results showed that, in addition to tumor growth, administration of the Ehrlich tumor cells may represent a novel model for the study of cancer pain, specially the pain that is susceptible to treatment with opioids, but not to cyclooxygenase inhibitor or to tricyclic antidepressant.

scholarly journals Immunodetection of RNA on ultra-thin sections incubated with polyadenylate nucleotidyl transferase.

1993 ◽  
Vol 41 (5) ◽  
pp. 657-665 ◽  
Author(s):  
M Thiry
Keyword(s):  
Divalent Cations ◽  
Ultrastructural Level ◽  
Ehrlich Tumor ◽  
Precise Location ◽  
Great Precision ◽  
Thin Sections ◽  
Nucleotidyl Transferase ◽  
Ehrlich Tumor Cells ◽  
Labeling Pattern

A new method is described for locating RNA on ultra-thin sections. Sections of aldehyde-fixed, plastic-embedded cells were incubated in a medium containing polyadenylate nucleotidyl transferase (PnT) and biotinylated ATP. The labeled nucleotides bound to RNA at the surface of the ultra-thin sections were than visualized by an indirect immunogold labeling technique. The resulting labeling pattern was dependent on the presence of divalent cations in the PnT medium. The method revealed with great precision the specific RNA-containing structures within Ehrlich tumor cells. The method is applicable to Epon sections. However, the labeling intensity varies according to the fixation used. Best results were obtained on acetylated cell sections. The method can be combined with EDTA regressive staining. The in situ PnT method provides a very useful tool for pinpointing the precise location of RNA within biological material at the ultrastructural level.

scholarly journals Mechanisms of Anthracycline-Enhanced Reactive Oxygen Metabolism in Tumor Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
James H. Doroshow
Keyword(s):  
Tumor Cells ◽  
Superoxide Anion ◽  
Oxygen Metabolism ◽  
Oxygen Radical ◽  
Ehrlich Tumor ◽  
Anthracycline Antibiotics ◽  
Superoxide Anion Production ◽  
Superoxide Formation ◽  
Anion Production ◽  
Ehrlich Tumor Cells

In this investigation, we examined the effect of anthracycline antibiotics on oxygen radical metabolism in Ehrlich tumor cells. In tumor microsomes and nuclei, doxorubicin increased superoxide anion production in a dose-dependent fashion that appeared to follow saturation kinetics; the apparent Km and Vmax for superoxide formation by these organelles was 124.9 μM and 22.6 nmol/min/mg, and 103.4 μM and 4.8 nmol/min/mg, respectively. In both tumor microsomes and nuclei, superoxide formation required NADPH as a cofactor, was accompanied by the formation of hydrogen peroxide, and resulted from the transfer of electrons from NADPH to the doxorubicin quinone by NADPH:cytochrome P-450 reductase (NADPH:ferricytochrome oxidoreductase, EC 1.6.2.4). Anthracycline antibiotics also significantly enhanced superoxide anion production by tumor mitochondria with an apparent Km and Vmax for doxorubicin of 123.2 μM and 14.7 nmol/min/mg. However, drug-stimulated superoxide production by mitochondria required NADH and was increased by rotenone, suggesting that the proximal portion of the electron transport chain in tumor cells was responsible for reduction of the doxorubicin quinone at this site. The net rate of drug-related oxygen radical production was also determined for intact Ehrlich tumor cells; in this system, treatment with doxorubicin produced a dose-related increase in cyanide-resistant respiration that was enhanced by changes in intracellular reducing equivalents. Finally, we found that in the presence of iron, treatment with doxorubicin significantly increased the production of formaldehyde from dimethyl sulfoxide, an indication that the hydroxyl radical could be produced by intact tumor cells following anthracycline exposure. These experiments suggest that the anthracycline antibiotics are capable of significantly enhancing oxygen radical metabolism in Ehrlich tumor cells at multiple intracellular sites by reactions that could contribute to the cytotoxicity of this class of drugs.

Swim training suppresses tumor growth in mice

2009 ◽  
Vol 107 (1) ◽  
pp. 261-265 ◽  
Author(s):  
Pedro William M. Almeida ◽  
Ary Gomes-Filho ◽  
Anderson J. Ferreira ◽  
Carlos Eduardo M. Rodrigues ◽  
Marco Fabrício Dias-Peixoto ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Cancer Progression ◽  
Macrophage Infiltration ◽  
Neutrophil Accumulation ◽  
Ehrlich Tumor ◽  
Exercise Time ◽  
Clinical Observations ◽  
Important Approach ◽  
Ehrlich Tumor Cells ◽  
Maximal Capacity

The present study was designed to determine the effects of physical training on the development of cancer induced by the injection of Ehrlich tumor cells in mice. Male Swiss mice were subjected to a swim training protocol (5 days/wk for 6 wk, 1 h at 50% of maximal capacity-trained groups) or remained sedentary in their cages (sedentary groups). The inoculation of Ehrlich tumor cells was performed at the end of the fourth week, and animals were killed after 6 wk of training. Heart and solid tumor weights were recorded, and tumor volumes were calculated. Portions of the tumors were used for the evaluation of macrophages and neutrophil accumulation or fixed in neutral 10% buffered formalin for histological analysis. The tumor volume and weight were, respectively, ∼270% and 280% greater in sedentary mice than in trained mice. Macrophage infiltration in the tumor tissue was significantly lower in trained mice (0.65 ± 0.16 vs. 1.78 ± 0.43 macrophages × 103 in the sedentary group). Moreover, neutrophil accumulation in tumors was slightly reduced after exercise training, and the amount of tumor cells was reduced in trained mice. Exercise capacity was substantially increased in trained mice, as determined by a 440% increase in the exercise time at 50% of maximal capacity. In summary, swim training retarded the development of Ehrlich tumors in mice, accompanied by a reduction in macrophage infiltration and neutrophil accumulation. These findings provide conceptual support for clinical observations that controlled physical activities may be a therapeutically important approach to preventing cancer progression and may improve the outcome of cancer treatment.

scholarly journals Entry of diphtheria toxin into cells: possible existence of cellular factor(s) for entry of diphtheria toxin into cells was studied in somatic cell hybrids and hybrid toxins.

1984 ◽  
Vol 98 (2) ◽  
pp. 466-472 ◽  
Author(s):  
Y Kaneda ◽  
T Uchida ◽  
E Mekada ◽  
M Nakanishi ◽  
Y Okada
Keyword(s):  
Tumor Cells ◽  
Binding Sites ◽  
Diphtheria Toxin ◽  
Human Fibroblasts ◽  
Ehrlich Ascites Tumor Cells ◽  
Ehrlich Tumor ◽  
Ehrlich Ascites ◽  
Group A ◽  
Group B ◽  
Ehrlich Tumor Cells

Ehrlich ascites tumor cells were found to be very insensitive to diphtheria toxin. We formed 37 hybrids from Ehrlich tumor cells and diphtheria toxin-sensitive human fibroblasts. The effects of diphtheria toxin on protein synthesis in those hybrids were examined. The hybrids were divided into three groups on the basis of toxin sensitivity. Group A hybrids were as sensitive to diphtheria toxin as human fibroblasts, Group C were as resistant as Ehrlich tumor cells, and Group B had intermediate sensitivity. Group A hybrids had diphtheria toxin-binding sites but Group B and C had no detectable binding sites. Elongation factor-2 of all the hybrids was susceptible to ADP-ribosylation by fragment A of diphtheria toxin. Cells of Group A and B became more sensitive to CRM 45 (cross-reacting material 45 of diphtheria toxin) after they were exposed to low pH (pH = 4.5). The resistance of Group C to CRM 45 was not affected by the same treatment. Group A and B hybrids and human fibroblasts had similar sensitivities to a hybrid toxin composed of wheat germ agglutinin and fragment A of diphtheria toxin, but Group C and Ehrlich tumor cells were resistant to this hybrid toxin. All the hybrids and Ehrlich tumor cells were more sensitive to a hybrid toxin composed of wheat germ agglutinin and subunit A of ricin than were human fibroblasts. On subcloning of Group B hybrids, one Group C hybrid was obtained, but no Group A hybrid. These facts suggest that Ehrlich ascites tumor cells differ from human fibroblasts in the expression of a factor(s) that is involved in entry of fragment A of diphtheria toxin into the cytoplasm after the toxin binds to its surface receptors.

cis -[RuCl(BzCN)(bipy)(dppe)]PF6 induces anti-angiogenesis and apoptosis by a mechanism of caspase-dependent involving DNA damage, PARP activation, and Tp53 induction in Ehrlich tumor cells

2017 ◽  
Vol 278 ◽  
pp. 101-113 ◽  
Author(s):  
Lorena Félix Magalhães ◽  
Francyelli Mello-Andrade ◽  
Wanessa Carvalho Pires ◽  
Hugo Delleon Silva ◽  
Paula Francinete Faustino da Silva ◽  
...  
Keyword(s):  
Dna Damage ◽  
Tumor Cells ◽  
Ehrlich Tumor ◽  
Parp Activation ◽  
Ehrlich Tumor Cells
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