Antitumor effect of Bothrops jararaca venom.

Expression and Function of β1 Integrins on Adherent and Nonadherent Ehrlich Ascites Tumor Cells

Evidence for a hsp25-Specific Mechanism Involved in Transcriptional Activation by Heat Shock

Systemic Cancer Gene Therapy Using Adeno-associated Virus Type 1 Vector Expressing MDA-7/IL24

Both pre-activated and phorbol ester tetradecanoyl phorbol myristate acetate (TPA) activated reactive oxygen species (ROS) generation were inhibited by dexamethasone in vivo. Time kinetics on influence of dexamethasone on cytosolic phosphoprotein phosphatase activity revealed that, when compared to phosphatase activity in cytosol of control Ehrlich ascites tumor (EAT) cells, a 5-fold increase in specific activity is seen in the cytosol of EAT cells treated (in vivo, 0-90 min. 1 mg/kg body weight) with dexamethasone. Dexamethasone induced phosphatase was partially purified by conventional ion-exchange and gel filtration column chromatographic techniques. Purified phosphatase had a molecular weight of 70 KDa by SDS-PAGE. A dose-dependent inhibition of TPA activated ROS generation by partially purified phosphatase in permeabilized EAT cells suggested that dephosphorylation is a major regulatory mechanism in "switching off" of the respiratory burst. Anti-phosphatase antibodies were raised, purified and were used to quantitate cytosolic phosphatase by ELISA, which revealed that dexamethasone induces 6-fold increase in expression of phosphatase in EAT cells by 120 min. The expression of phosphatase in EAT cell cytosol was further confirmed by immunostaining using anti-phosphatase antibodies, the results of which showed intense blue staining on development with BCIP/NBT.

We have found that Ehrlich ascites tumour (EAT) cells, deprived of any carbon source, and suspended at a density of 2 X 10(5) cells/cm3, begin to die only after 12 h of starvation, though it is known that under these conditions they lose over 80% of their ATP within 30 min. Moreover, we have found that the viability of the cells incubated in the absence of any substrate for energy metabolism is strongly dependent on the density of the cell suspension, and can be significantly improved simply by increasing the suspension density. This prompted us to investigate the density dependence of the maintenance of EAT cell viability in the presence of various substrates for energy metabolism and metabolic intermediates. It was found that: Glucose ensures 48 h viability of EAT cells irrespective of suspension density. Fatty acids and pyruvate as sole carbon source do not improve EAT cell survival. In the presence of glutamine as sole carbon source the EAT cell survival shows dependence on cell-suspension density. At densities of 1.6 X 10(6) to 3.2 X 10(6) cells/cm3 the cell viability is maintained at least as well as in the presence of glucose, but at low cell-suspension densities glutamine does not support cell viability. In the presence of glutamine, addition of 1 mM-inosine and 1 mM-uridine ensures high cell survival irrespective of the cell-suspension density. In the presence of inosine or uridine (10 mM) as sole carbon source, the EAT cell survival is the same as in the presence of glucose and does not depend upon cell-suspension density. Guanosine is less effective, whereas adenosine has no effect at all on the maintenance of EAT cell viability for 48 h. There is no correlation at all between EAT cell survival and the rate of lactic acid production. At a cell-suspension density of 1.6 X 10(6) cells/cm3 the cell survival is of the same order in the presence of glutamine as in the presence of glucose, in spite of the fact that in the first case the rate of lactic acid production is more than 20 times lower. There is no correlation between the capacity of particular nucleosides to support EAT cell survival and their effects on glycolysis and oxygen consumption.

A simple method of analytical subcellular fractionation, combined with a sensitive computational method for data analysis and presentation, has been used to reinvestigate the distribution and relative amounts of several enzymes in the cytoplasmic and plasma membranes of two different cell types: one is a neoplastic, transformed cell type (Ehrlich ascites tumour cells), the other an untransformed, highly differentiated cell type (liver hepatocytes plus Kupffer and endothelial cells). In general the distribution of the enzymes in particular membranes is similar in the two cell types, however the relative amounts differ. Ehrlich ascites tumour cells have a higher specific activity of galactosyltransferase and ouabain-sensitive (Na,K)ATPase, while liver cells have higher glucose-6-phosphatase, 5'-nucleotidase and succinate dehydrogenase activity. These differences appear to be correlated with morphological and, in some cases, functional differences between the two cell types.

Aging and sister chromatid exchange. VIII. Effect of the aging environment on sister chromatid exchange induction and cell cycle kinetics in Ehrlich ascites tumor cells. A brief note

Induction of caspase-3 activated DNase mediated apoptosis by hexane fraction of Tinospora cordifolia in EAT cells

The biologic effects and the underlying mechanisms of Ehrlich ascitic tumor (EAT) cells induced by ultrasound were investigated in this study. Cells were subjected to ultrasonic irradiation with a frequency of 2.17 MHz and an intensity of 3 W/cm(2) for variable periods of time. Trypan blue exclusion was used to detect the integrity of cellular membrane; the membrane permeability was investigated by the incorporation of fluorescein isothiocyanate dextran during ultrasound exposure; and the cell membrane ultrastructure changes were observed under a scanning electron microscope. The potential mechanism was estimated from the generation of hydroxyl radicals, the lipid peroxidation levels, and intracellular reactive oxygen radicals production. The cell membrane damage effects induced by ultrasound increased with a prolonged exposure time; the fluorescent rates of the cells irradiated with ultrasound for 30 and 60 seconds were 11.46% and 18.50%, respectively; the amount of hydroxyl radicals in 30 (26.10 U/mL) and 60 seconds (28.47 U/mL) were significantly enhanced, compared with the control group (24.44 U/mL); then, the level of lipid peroxidation was also changed from 0.27 to 0.54 (30 seconds) and 1.21 nmol/mL (60 seconds). Shear forces and free radicals produced by acoustic cavitation may play important roles in these actions.

Glucose uptake study plays a major role in diabetes research. Impaired glucose uptake has been implicated in the development of hyperglycemia during diabetes. Banana plant is known for its anti-diabetic properties and our earlier report revealed that banana flower and pseudostem of Musa sp. cv. elakki bale is beneficial during diabetes in rat models. The present study was designed to evaluate the potential effect of banana flower and pseudostem extracts on glucose uptake in Ehrlich ascites tumor (EAT) cells using 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG), a fluorescent analogue of 2-deoxyglucose. Methanol and aqueous extracts of banana flower and pseudostem were more potent in promoting glucose uptake in EAT cells, in comparison to acetone and ethanol extracts. At 20 µg dosage, highest net glucose uptake was observed in aqueous extracts of banana flower (18.17 ± 0.43 nmol L⁻¹) and pseudostem (19.69 ± 0.41 nmol L⁻¹). Total polyphenol content was higher in methanol (9.031 ± 0.036 g kg⁻¹) and aqueous (6.862 ± 0.024 g kg⁻¹) extracts of banana flower compared to pseudostem, which were 0.442 ± 0.006 and 0.811 ± 0.011 g kg⁻¹, respectively. Banana flower and pseudostem extracts are able to promote glucose uptake into the cells, presumably through glucose transporters 1 and 3, which could be beneficial in diabetes. Glucose uptake is likely promoted by phenolic acids besides other bioactives. It can be hypothesized that consumption of nutraceutical-rich extract of banana flower and pseudostem could replace some amount of insulin being taken for diabetes.

69] Enzymatic synthesis of (2′-5′)-linked oligoadenylates on a preparative scale

Effect of tumour necrosis factor on growth of Ehrlich ascites tumour cells in vitro and in vivo

Introduction: Cancer is the second most common cause of death in the world. Several natural products have been studied for anticancer activity and for prevention or repair of oxidative injury. Curcumin is one of the natural products of high medicinal interest. This study was performed to investigate effects of curcumin on lipid peroxidation and antioxidant enzymes in tissues of mice bearing Ehrlich solid tumor. Materials and Methods: Forty mice were distributed to four groups as healthy control and treatments that received 1x106 Ehrlich ascites tumor (EAT) cells and EAT cells plus 25 mg/kg/day or 50 mg/kg/day curcumin with a single subcutaneous injection. The liver, kidney, brain and testis tissues were collected for the MDA, SOD and CAT analyses. Results: Tumor development increased MDA levels in liver (p=0.001), kidney (p<0.001) and testis (p<0.01) and curcumin reduced liver MDA. Liver and kidney SOD activities were increased by both levels of curcumin (p=0.001) but 50 mg/kg/day curcumin increased brain SOD activity (p<0.001). The kidney CAT activity was increased by 50 mg/kg/day curcumin (p<0.001). Discussion: This study showed that curcumin suppresses tumor progression, and alleviates the lipid peroxidation and improves antioxidant status in the tissues of solid tumor-bearing mice.

K24 capsular polysaccharide (K24-CPS), with a known structure of a repeating unit, was isolated from the capsule of Klebsiella pneumoniae serotype K24. The polysaccharide was found to suppress the proliferation of Ehrlich ascites tumour (EAT) cells in vitro, but did not alter the cell cycle distribution of cells. K24-CPS treatment reduced the tyrosine phosphorylation of some proteins in EAT cells. Furthermore, the treatment also decreased the expression of c-JUN, but had no effect on the levels of c-FOS and c-MYC. It is speculated that the growth suppression effect of K24-CPS may be related to its effect in down-regulating c-JUN expression.

Genetic constraints in the induction of the immune response to ehrlich ascites tumor in mice