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At least 955 records · Page 53Linked to original sources
PubMed2005

Gliosarcoma cell death after radiosurgery in a rat model.

Therapeutic radiation and subsequent detection of tumor cell death has been performed mainly in vitro systems, making it difficult to accurately characterize the mechanisms of tumor cell death after radiosurgery. To better characterize what occurs to glioma cells after radiation therapy, we developed a rat model using the 9L gliosarcoma cell line implanted reproducibly to the caudate nucleus in rats. After 1 Gy radiation, 9L tumors in vivo induced mainly necrosis (determined by trypan blue exclusion) of 10 - 74 % at 6 - 72 hours post-radiation. This is in contrast to a previous in vitro study which demonstrated that 18 Gy of radiation induces considerably less cell death as determined by trypan blue exclusion (approximately 20 - 25 % at 6 - 72 hours post-radiation). However, significant amounts of apoptosis were detected as early as 6 hours after radiation. Apoptosis determination was by annexin V (marker of early apoptosis) and propidium iodide (marker of membrane stability) staining followed by flow cytometry detection. When caspase 3 and caspase 8 enzymatic activities (mediators of apoptosis) were measured from freshly explanted tumor cells, peak activity was found 6 hours after 1 Gy radiation (p < 0.01). Taken together, these data indicate the presence of apoptosis early after radiation therapy (1 Gy) which progressed to necrosis in a unique in vivo model of gliosarcoma that may prove useful in determining new therapeutic approaches to radiation therapy and tumor cell biology.

Animals↗
PubMed2005

Citrate provides protection against oxalate and calcium oxalate crystal induced oxidative damage to renal epithelium.

PURPOSE: Oxalate and calcium oxalate (CaOx) crystals are injurious to renal epithelial cells. The injury is caused by the production of reactive oxygen species (ROS). Citrate is a well-known inhibitor of CaOx crystallization and as such it is one of the major therapeutic agents prescribed. Since citrate increases cellular reduced nicotinamide adenine dinucleotide phosphate and glutathione (GSH), we hypothesized that exogenously administered citrate should act as an antioxidant and protect cells from oxalate induced injury. MATERIALS AND METHODS: We exposed LLC-PK1 and MDCK cells to 500 microM/ml oxalate or 150 mug/cm calcium oxalate crystals for 30, 60 and 180 minutes with or without 3 mg/ml citrate in the medium. We determined cell viability by lactate dehydrogenase release and trypan blue exclusion, ROS involvement by changes in hydrogen peroxide and GSH, and lipid peroxidation by quantifying 8-isoprostane. RESULTS: The presence of citrate was associated with significant decrease in lactate dehydrogenase release (p <0.001) and staining with trypan blue (p <0.05). In addition, there was a significant increase in GSH (p <0.005) and a decrease in the production of hydrogen peroxide (p <0.05) and 8-isoprostane (p <0.0005) secretion into the culture medium when citrate was present in the medium. CONCLUSIONS: Citrate protects cells from oxalate and CaOx crystal induced injury by preventing lipid peroxidation through a decrease in ROS production. The results provide additional data for the beneficial role of citrate therapy for CaOx nephrolithiasis.

Calcium Oxalate↗
PubMed1988

The effect of fluorouracil on the corneal endothelium.

The utility of the antiproliferative agent fluorouracil has been demonstrated recently in glaucoma-filtering surgery and in the management of proliferative vitreoretinopathy after vitrectomy. Because of the potential for contact with the corneal endothelium, its toxicity to the endothelium is an important consideration. The effect of fluorouracil on corneal endothelial integrity in an in vitro animal model was studied. Freshly excised sheep corneal buttons were exposed to increasing concentrations of fluorouracil for four hours and were subsequently evaluated microscopically using vital staining with alizarin red and trypan blue. Exposure to normal saline and chlorhexidine gluconate was used to establish negative- and positive-staining controls. Corneal buttons exposed to normal saline or to 1.0 mg/mL or less of fluorouracil had intact endothelial monolayers that completely excluded trypan blue. Corneal buttons exposed to chlorhexidine gluconate or to 10 mg/mL of fluorouracil, however, had severely or totally disrupted endothelial monolayers in which the remaining cells, if any, all had blue-staining nuclei. These results suggest that the threshold concentration for fluorouracil toxicity to corneal endothelium lies between 1 and 10 mg/mL when exposure time is four hours.

Animals↗
PubMed1987

Fructose prevents hypoxic cell death in liver.

Perfusion of livers from fasted rats with nitrogen-saturated buffer caused hepatocellular damage within 30 min. Lactate dehydrogenase (LDH) was released at maximal rates of approximately 300 U . g-1 . h-1 under these conditions, and virtually all cells in periportal and pericentral regions of the liver lobule were stained with trypan blue. Infusion of glucose, xylitol, sorbitol, or mannitol (20 mM) did not appreciably change the time course or extent of damage due to perfusion with nitrogen-saturated perfusate. However, fructose (20 mM) completely prevented damage assessed by LDH release, trypan blue uptake, and ultrastructural changes for at least 2 h of perfusion. Neither glucose, xylitol, sorbitol, nor mannitol (20 mM) increased lactate formation above basal levels during hypoxia. On the other hand, fructose (0.4-20 mM) caused a concentration-dependent increase in lactate formation that reached maximal rates of approximately 180 mumol . g-1 . h-1. The dose-dependent increase in glycolytic lactate production from fructose correlated well with cellular protection reflected by decreases in LDH release. ATP:ADP ratios were also increased from 0.4 to 1.8 in a dose-dependent manner by fructose. The results indicate that fructose protects the liver against hypoxic cell death by the glycolytic production of ATP in the absence of oxygen.

Adenine Nucleotides↗
PubMed1982

Ca2+-tolerant adult canine myocytes: preparation and response to anoxia/acidosis.

A procedure is described for the production of large numbers of Ca2+-tolerant adult canine ventricular myocytes. Gentle tissue dissociation is achieved in Spinner flasks using 320 mosM enzyme buffer containing collagenase hyaluronidase, and trypsin in the presence of millimolar levels of Ca2+. The technique allows for the complete removal of erythrocytes, the gentle removal of closely adhering nonmuscle cells (less than 3% contamination), and the selective removal of damaged from nondamaged myocytes. Total myocyte yields averaged 4-6 x 10(6)/g wet wt; 61.0 +/- 6.5% of the cells have rod-shaped morphology and are "viable" based on trypan blue exclusion. Only 3.9 +/- 1.1% of the rod-shaped cells beat spontaneously when challenged with 2 mM Ca2+. Exposure to 2 mM Ca2+ at 37 degrees C results in minimal loss of viability (2.1 +/- 1.3%/h) based on both trypan blue uptake and creatine kinase release. Simulation of cellular (i.e., membrane) injury in vitro is performed by the separate application of the perturbations of anoxia, acidosis, and low glucose to the canine myocyte suspensions; the data suggest that these myocytes are affected independently by these perturbations and are in good agreement with the results obtained by others using the isolated rat myocyte system.

Acidosis↗
PubMed2005

[Effect of Bcl-2 antisense phosphorothioate oligodeoxynucleotides on bile duct carcinoma cell line QBC939].

OBJECTIVE: To investigate the effect of Bcl-2 antisense oligodeoxynucleotides (ASODN) on the cell proliferation and Bcl-2 expression in bile duct carcinoma cell line QBC939. METHODS: Bcl-2 ASODN and control sequence were transfected into cell line QBC939 by Lipofectamine 2000. The changes of Bcl-2 protein were detected by Western blot. The survival rate and colony formation rate of QBC939 cells incubating with Bcl-2 ASODN were evaluated by trypan blue staining assay and colony forming test. RESULTS: The densitometric analysis of Gel-photograph showed that the level of Bcl-2 protein expression in the ASODN transfected group was significantly lower than that in the controls (P < 0.01). Both trypan blue staining assay and colony forming test demonstrated that Bcl-2 ASODN could partially inhibit the growth of QBC939 cells. After incubating with Bcl-2 ASODN, the survival rate and colony formation rate of QBC939 cells were significantly lower than those of the controls (P < 0.05). CONCLUSION: Bcl-2 ASODN inhibits the cell proliferation in bile duct carcinoma cell line QBC939 by blocking the expression of bcl-2 gene.

Bile Duct Neoplasms↗
PubMed2003

Effects of GDNF on 6-OHDA-induced death in a dopaminergic cell line: modulation by inhibitors of PI3 kinase and MEK.

Parkinson's disease is a neurodegenerative disorder associated with the selective death of dopaminergic neurons. Glial cell line-derived neurotrophic factor (GDNF) can protect dopaminergic neurons in several parkinsonian models. We used the dopaminergic cell line MN9D to explore the mechanisms underlying GDNF-mediated protection against the neurotoxin 6-hydroxydopamine (6-OHDA). MN9D cell viability was decreased 24 hr after a 15-min exposure to 6-OHDA (50-1000 microM) as revealed by staining with Hoechst reagent and Trypan blue. The addition of GDNF (10 ng/ml) before, during, and after exposure to 6-OHDA significantly increased the number of viable cells as assessed by Hoechst staining. In contrast, 6-OHDA-induced cell membrane damage was unaffected as measured by Trypan blue exclusion. The PI3K specific inhibitor LY294002 (10-50 microM) blocked GDNF-mediated protection against nuclear condensation, as did the MAPK kinase (MEK) inhibitor U0126 (5- 20 microM). These studies suggest that GDNF can protect dopaminergic cells against some but not all aspects of 6-OHDA-induced toxicity by acting through both PI3K and MAPK signaling pathways.

Animals↗
PubMed1977

Intracellular uptake and alpha-amylase and lactate dehydrogenase releasing actions of the divalent cation ionophore A23187 in dissociated pancreatic acinar cells.

Intracellular uptake of A23187 and the increased release of amylase and lactate dehydrogenase (LDH) accompanying ionophore uptake was studied using dissociated acinar cells prepared from mouse pancreas. Easily detected changes in the fluorescence excitation spectrum of A23187 upon transfer of the ionophore from a Tris-buffered Ringer's to cell membranes were used to monitor A23187 uptake. Uptake was rapid in the absence of extracellular Ca2+ and Mg2+ (t1/2=1 min) and much slower in the presence of Ca2+ or Mg2+ (t1/2=20 min). Cell-associated ionophore was largely intracellular as indicated by fluorescence microscopy, lack of spectral sensitivity to changes in extracellular Ca2+ and Mg2+, and by equivalent interaction of ionophore with membranes of whole and sonicated cells. A23187 (10 micronm) increased amylase release 200% in the presence of extracellular Ca2+ and Mg2+. In the absence of Ca2+ (but in the presence of Mg2+) A23187 did not increase amylase release. A23187 (10 micronm) also produced Ca2+ -dependent cell damage, as judged by increased LDH release, increased permeability to trypan blue, and by disruption of cell morphology. The cell damaging and amylase releasing properties of A23187 were distinguished by their time course and dose-response relationship. A23187 (1 micronm) increased amylase release 140% without increasing LDH release or permeability to trypan blue.

Amylases↗
PubMed2003

HMG-CoA reductase inhibitors induce apoptosis in neointima-derived vascular smooth muscle cells.

In the context of atherogenesis and restenosis, vascular smooth muscle cell (SMC) proliferation and apoptosis play a crucial role. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins) have been shown to inhibit the migration and proliferation of SMC, and to induce apoptosis in different cell types including SMC. However, it is not known whether these agents induce apoptosis in neointimal SMC. We investigated the effects of statin treatment on neointimal SMC as compared to medial cells by using trypan blue counting, MTT test, Annexin V staining, cell cycle analysis and a co-culture model. The incubation of neointimal or medial SMC with lovastatin reduced the MTT activity as well as the total cell number, and increased the amount of trypan blue positive cells, indicative of cell death. We tested by staining with Annexin V/propidium iodide, specific antibodies to active caspase-3, TUNEL reaction, and by the appearance of a sub-G1 peak, whether the observed increase in cell death was due to apoptosis. After treatment with lovastatin, programmed cell death was slightly increased in medial SMC, while neointimal cells showed a pronounced rate of apoptosis. In an attempt to mimic early phases of restenosis in vitro by seeding low density neointimal cells onto high density medial cells, we found that statin treatment induced cell death preferentially in the neointimal SMC. Our results suggest that statins enhance the rate of apoptosis in neointimal SMC, which may be an interesting feature to reduce restenosis after successful angioplasty.

Animals↗
PubMedDate not supplied

Use of a simple light absorbance assay to measure lymphocyte proliferation.

The proliferative response of human lymphocytes to stimuli such as foreign histocompatibility antigens or mitogens is generally assessed by measuring the amount of tritiated thymidine which the cells incorporated in culture. In this paper, the possibility of assessing lymphocyte proliferation and viability by an empirical assay, using measurement of light absorbance on a ELISA reader in the yellow wave length (450 nm/air-550 nm/air), has been studied. The correlation of these measurements with a colormetric viability assay using MTS/PMS, with tritiated thymidine incorporation and with trypan blue exclusion viability counting, was determined. The results showed that the light absorbance assay correlated well with cell proliferation during 48-120 hours culture period and with cell viability after a 72 hour period. The MTS/PMS colormetric assay as well as trypan blue exclusion cell counting confirmed that the light absorbance assay was not merely caused by dead cells. This data confirm that the light absorbance assay is sufficiently sensitive to low levels of proliferation to allow detection of such responses at least as effectively as thymidine incorporation. The light absorbance assay procedure avoids the expense, time and hazards associated with scintillation counting, and is simple to perform without the necessity for reagents and preparative steps required by other assays.

Adolescent↗
PubMed2005

Evaluation of the inhibitory effect of antisense oligodeoxynucleotides on the growth of hepatitis C-associated hepatocellular carcinoma cells in vitro.

OBJECTIVE: Hepatitis C virus (HCV) RNA is invariably detected in the serum and tumor tissue of anti-HCV-positive patients with hepatocellular carcinoma (HCC). The inflammation and cirrhosis caused by HCV could be the promoter for development of HCC or HCC could be the consequence of HCV infection independent of the effect of cirrhosis. The ability of the core protein of HCV to modulate gene transcription, cell proliferation and cell death by interacting with cellular genes that regulate cell growth and differentiation is involved in the pathogenesis of HCC. HCV NS3 protease is an attractive target for antiviral agent development because it is required for viral replication. Recent studies that constructed an in vitro model of HCC demonstrated that antisense oligodeoxynucleotides (AS-ODN) interfered with NS3 translation in a dose-dependent fashion and significantly inhibited protease activity. We studied the in vitro effect of AS-ODN on the rate of growth of the HCC cells grown in culture associated with HCV. METHODS: Core biopsy was taken from 20 patients with HCC associated with HCV and each one was divided into two parts: group I to which antisense was added and group II which served as a control group. Comparison of cell viability between tubes with and without AS-ODN was done using MTT assay, LDH assay, cell cycle analysis, trypan blue exclusion test and colony formation in soft agar. RESULTS: Colony formation in soft agar was inhibited in group I compared with the control group and the inhibition was highly significant (P < 0.01). The LDH concentration in culture supernatant and the trypan blue exclusion test, both reflecting cellular death, was higher in group I than group II and the difference was highly significant (P < 0.01). MTT assay showed a highly significant decrease in cell activation in group I than in group II (P < 0.01). The percentage of cells in the G(0)/G(1) phase was higher in group I than in group II and the difference was significant (P = 0.04). There was an insignificant difference between both groups in the percentage of cells in S phase (P = 0.378). The inhibitory effect of AS-ODNs on tumor cells in G(2)/M phase was highly significant compared with the control group (P < 0.01). CONCLUSIONS: AS-ODN has a significant inhibitory effect on the growth of HCV-associated HCC cells grown in fluid culture, and there is potential for the use of AS-ODN as oncotherapy.

Aged↗
PubMed2000

Modulation of TNF-alpha-induced apoptosis in corneal fibroblasts by transcription factor NF-kappaB.

PURPOSE: Previous studies have suggested no role for tumor necrosis factor (TNF)-alpha in the modulation of apoptosis in corneal fibroblasts. However, recent investigations have demonstrated that nuclear factor (NF)-kappaB activation by TNF-alpha mediates negative apoptotic effects that must be blocked to unmask the apoptotic effects of TNF-alpha in vitro. The purpose of this study was to investigate the role of transcription factor NF-kappaB in the suppression of TNF-alpha-induced apoptosis of corneal fibroblasts. METHODS: mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) and RNase protection assay. Proteins were detected by immunocytochemistry and immunoprecipitation with Western blot analysis. Cell death was evaluated by trypan blue exclusion assay in corneal fibroblasts treated with TNF-alpha in presence or absence of the specific inhibitor of NF-kappaB activation, SN50, actinomycin D, or actinomycin D with dexamethasone, ketorolac tromethamine, or diclofenac sodium. Apoptosis was monitored by trypan blue exclusion, colorimetric cell assay, CPP32 activation assay, DNA fragmentation assay, and transmission electron microscopy. NF-KB activation was monitored using electrophoretic gel shift assay. RESULTS: TNF-alpha, TNF receptor (R)I, and TNFRII mRNAs were detected in all three cultured corneal cell types and in ex vivo corneal epithelium using RT-PCR. TNF-alpha mRNA was also detected in ex vivo corneal epithelium, corneal epithelial cells, and stromal fibroblasts with the RNase protection assay. TNF-alpha, TNFRI, and TNFRII proteins were detected by immunocytochemistry in all three major corneal cell types in human corneal tissue. TNF-alpha protein was also detected in ex vivo corneal epithelium, primary corneal epithelial cells, and primary stromal fibroblasts using immunoprecipitation and Western blot analysis. TNF-alpha stimulated corneal fibroblast cell death when NF-kappaB activation was blocked with actinomycin D or SN50. Enhanced cell death was noted with dexamethasone, ketorolac tromethamine, or diclofenac sodium when used in the presence, but not in the absence, of actinomycin D. A gel shift assay revealed induction of NF-KB by TNF-alpha and suppression of induction in the presence of actinomycin D or SN50, but not by the control peptide SN50M. CONCLUSIONS: The TNF-alpha receptor system is expressed in the cornea, and NF-kappaB activation is an important regulator of TNF-alpha-mediated corneal fibroblast apoptosis. Nonsteroidal anti-inflammatory agents or corticosteroids may potentiate corneal fibroblast apoptosis in response to cytokine stimulation.

Antigens, CD↗
PubMedDate not supplied

The effects of high molecular weight dextran on the preservation of human corneas.

Paired human corneas (48) were preserved at 31 degrees C for different periods of time up to 122 days in a modified MEM tissue culture medium free of or supplemented with 8% dextran T500. Cell density and vitality of the endothelial cells were analysed using morphometry, light microscopy after trypan blue staining, followed by sucrose provoked swelling and fine structural observations. Culturing for periods up to 7 weeks resulted in an endothelial cell loss of 11% of dextran-blue and of 15% in dextran-supplemented medium. For preservation periods between 9-13 weeks, these values were 43% and 36% respectively. The differences between dextran-free and dextran-supplemented preservation media were not significant. As deduced from trypan blue staining, sucrose provoked swelling and fine structural observations; the remaining cells were vital. Dextran was taken up by the endothelial cells. The practical consequences of endothelial cell loss and the toxic effects of dextran are discussed in relation to penetrating keratoplasty.

Aged↗
PubMed1986

Ion-sensitive microelectrode measurements of free intracellular chloride and potassium concentrations in hyperthermia-treated neuroblastoma cells.

Murine NG108-15 neuroblastoma cells were heated for times of 5-40 min at 45.5 degrees C, and survival ranged from 0.7-0.0015, respectively. Ion-sensitive microelectrodes (ISM) were used to measure the free intracellular concentrations of Cl- and K+ immediately after heating and up to 30 hr later. The free intracellular Cl- and K+ concentrations, [Cl-]i and [K+]i respectively, of the heated cells remained identical to those of the controls for the first 10 hr after heating. At later times, some cells had increased [Cl-]i values and decreased [K+]i values identical to those of the extracellular medium. These cells had a mottled morphology, no longer excluded the vital stain trypan blue, and had no membrane potential. The number of these dye-including, physiologically dead cells increased with time, and was always greater following longer heating times. No changes in mean cellular volume were observed until 25 hr after heating. All trypan-blue-excluding, physiologically live cells had the same [Cl-]i and [K+]i as the control cells, even when the majority of them were destined for clonogenic death.

Animals↗
PubMed2004

Effect of intracameral injection of lidocaine and carbachol on the rabbit corneal endothelium.

PURPOSE: To determine the effect of intracameral injection of preservative-free lidocaine 1% and carbachol 0.01% on corneal endothelial cells of rabbits. SETTING: Department of Ophthalmology, National Taiwan University Hospital, Taipei, Taiwan. METHODS: Forty eyes of 20 New Zealand White rabbits were divided into 2 equal groups. In the first group, 1 eye was injected with 0.02 mL of preservative-free lidocaine 1% and the fellow eye was injected with 0.02 mL of normal saline as a control. In the second group, 1 eye was injected with 0.02 mL of carbachol 0.01% and the fellow eye was injected with 0.02 mL of normal saline. Specular microscopy was used to evaluate corneal endothelial cell loss and corneal thickness 1 week and 1 month postinjection. For morphologic studies, corneal buttons were excised and stained with alizarin red with trypan blue. Scanning electron microscopy (SEM) examination was performed. RESULTS: Specular microscopy revealed no significant endothelial cell loss and normal endothelial thickness with the intracameral injection of preservative-free lidocaine 1% and carbachol 0.01% compared with the control eye. Alizarin red with trypan blue stain and SEM examinations revealed smooth, distinct, and intact intercellular borders and normal viability of corneal endothelial cells in both groups. CONCLUSIONS: Intracameral injections of preservative-free lidocaine 1% and carbachol 0.01% do not produce morphologic and functional changes in the corneal endothelial cells of rabbits.

Anesthetics, Local↗
PubMed1979

Lysosome stability during lytic infection by simian virus 40.

By 48 h postinfection, 40--80% of SV40-infected CV-1 cells have undergone irreversible injury as indicated by trypan blue staining. Nevertheless, at this time the lysosomes of these cells appear as discrete structures after vital staining with either acridine orange or neutral red. Lysosomes, vitally stained with neutral red at 24 h postinfection, were still intact in cells stained with trypan blue at 48 h. Acid phosphatase activity is localized in discrete cytoplasmic particles at 48 h, as indicated by histochemical staining of both fixed and unfixed cells.

Acid Phosphatase↗
PubMed1999

Gymnema sylvestre stimulates insulin release in vitro by increased membrane permeability.

To determine whether extracts of Gymnema sylvestre may have therapeutic potential for the treatment of non-insulin-dependent diabetes mellitus (NIDDM), we examined the effects of an alcoholic extract of G. sylvestre (GS4) on insulin secretion from rat islets of Langerhans and several pancreatic beta-cell lines. GS4 stimulated insulin release from HIT-T15, MIN6 and RINm5F beta-cells and from islets in the absence of any other stimulus, and GS4-stimulated insulin secretion was inhibited in the presence of 1 mM EGTA. Blockade of voltage-operated Ca(2+) channels with 10 microM isradipine did not significantly affect GS4-induced secretion, and insulin release in response to GS4 was independent of incubation temperature. Examination of islet and beta-cell integrity after exposure to GS4, by trypan blue exclusion, indicated that concentrations of GS4 that stimulated insulin secretion also caused increased uptake of dye. Two gymnemic acid-enriched fractions of GS4, obtained by size exclusion and silica gel chromatography, also caused increases in insulin secretion concomitant with increased trypan blue uptake. These results confirm the stimulatory effects of G. sylvestre on insulin release, but indicate that GS4 acts by increasing cell permeability, rather than by stimulating exocytosis by regulated pathways. Thus the suitability of GS4 as a potential novel treatment for NIDDM can not be assessed by direct measurements of beta-cell function in vitro.

Animals↗
PubMed1989

The toxicity of flavonoids to guinea pig enterocytes.

Flavonoids, a group of compounds found primarily in vegetables and fruits, are generally believed to be beneficial to biological systems. Isolated guinea pig enterocytes were exposed to three of these compounds (kaempferol, quercetin, and myricetin) in concentrations of 50-450 microM. Toxicity was examined using trypan blue exclusion and lactic dehydrogenase (LDH) leakage. All three flavonoids produced cellular damage at 450 microM: compared with a control incubation, cellular viability was 12-60% lower and LDH leakage 28-41% greater after a 3-hr incubation. In addition, as assessed by trypan blue exclusion, quercetin and myricetin, both of which produce superoxide on autoxidation, appeared to be more toxic than kaempferol. These results suggest that dietary flavonoids may have the potential for producing intestinal injury.

Animals↗