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At least 757 records · Page 42Linked to original sources
PubMed2000

Indanocine, a microtubule-binding indanone and a selective inducer of apoptosis in multidrug-resistant cancer cells.

BACKGROUND: Certain antimitotic drugs have antitumor activities that apparently result from interactions with nontubulin components involved in cell growth and/or apoptotic cell death. Indanocine is a synthetic indanone that has been identified by the National Cancer Institute's Developmental Therapeutics Program as having antiproliferative activity. In this study, we characterized the activity of this new antimitotic drug toward malignant cells. METHODS: We tested antiproliferative activity with an MTT [i.e., 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay, mitochondrial damage and cell cycle perturbations with flow cytometry, caspase-3 activation with fluorometry, alterations of the cytoskeletal components with immunofluorescence, and antimicrotubule activity with a tubulin polymerization assay. RESULTS/CONCLUSIONS: Indanocine is a cytostatic and cytotoxic indanone that blocks tubulin polymerization but, unlike other antimitotic agents, induces apoptotic cell death in stationary-phase multidrug-resistant cancer cells at concentrations that do not impair the viability of normal nonproliferating cells. Of the seven multidrug-resistant cell lines tested, three (i.e., MCF-7/ADR, MES-SA/DX5, and HL-60/ADR) were more sensitive to growth inhibition by indanocine than were their corresponding parental cells. Confluent multidrug-resistant cells (MCF-7/ADR), but not drug-sensitive cancer cells (MCF-7) or normal peripheral blood lymphocytes, underwent apoptotic cell death 8-24 hours after exposure to indanocine, as measured by sequential changes in mitochondrial membrane potential, caspase activity, and DNA fragmentation. Indanocine interacts with tubulin at the colchicine-binding site, potently inhibits tubulin polymerization in vitro, and disrupts the mitotic apparatus in dividing cells. IMPLICATIONS: The sensitivity of stationary multidrug-resistant cancer cells to indanocine suggests that indanocine and related indanones be considered as lead compounds for the development of chemotherapeutic strategies for drug-resistant malignancies.

Antineoplastic Agents↗
PubMed1977

Fluorometric studies on the light chains of skeletal muscle myosin. I. Effects of temperature, ionic strength, divalent metal ions, and nucleotides.

Light chains of skeletal muscle myosin were studied through the reactivity of their SH groups with a fluorescent thiol reagent, N-(7-dimethylamino-4-methylcoumarinyl) maleimide (DACM). The experiments were carried out by reacting the reagent with myosin for a short time and measuring the amounts of reacted dye by fluorometry after separating light chains by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The two classes of light chains, alkali light chains and DTNB light chain, were clearly distinguished by their manner of reactivity change, and differences in their environment and in their function were suggested. Although we found that the SH groups of the DTNB light chain were susceptible to very low concentrations of Mg ions (of the order of 10-5 M), we could not observe Ca2+-induced conformational change by our technique. We also estimated the stoichiometry of light chains in skeletal muscle myosin to be 1.37 mol alkali light chain 1, 1.95 mol of DTNB light chain and 0.77 mol of alkali light chain 2 per mole of myosin from the total amounts of our reagent that reacted with each light chain.

Adenine Nucleotides↗
PubMed1995

Effects of midazolam on intracellular Ca2+ and tension in airway smooth muscles.

BACKGROUND: It has been demonstrated that a group of minor tranquilizers, benzodiazepines, are able to relax airway smooth muscles. To determine the underlying mechanisms of this phenomenon, the effects of midazolam on the intracellular Ca2+ concentration ([Ca2+]i) and tension in airway smooth muscles were investigated. METHODS: Using front-surface fluorometry and fura-2-loaded porcine tracheal smooth muscle strips, both [Ca2+]i and isometric tension developments were simultaneously recorded. RESULTS: When the tracheal strips were exposed to a high external K(+)-solution (40 mM) or 10(-7) M carbachol containing 1.25 mM Ca2+, both [Ca2+]i and tension increased rapidly until they reached a plateau (the steady state). During steady-state contraction induced by K(+)-depolarization or carbachol, the cumulative application of midazolam (10(-7) approximately 10(-4) M) caused decreases in both [Ca2+]i and tension, in a concentration-dependent manner. During 40 mM K(+)-induced depolarization, the stepwise increases in the extracellular Ca2+ concentration induced the stepwise increases in [Ca2+]i and tension. Midazolam (3 x 10(-5) M) inhibited these increases in [Ca2+]i and tension, but had no effect on the [Ca2+]i-tension relationship. In the presence of 3 x 10(-3) M NiCl2 (a nonselective cation channel blocker), midazolam (3 x 10(-5) M) did not cause any additional reduction of [Ca2+]i or tension during the contraction induced by carbachol (10(-7) M). In the absence of extracellular Ca2+, midazolam (3 x 10(-5) M) had no effect on the transient increases in either [Ca2+]i or the tension induced by carbachol (10(-7) M) or caffeine (20 mM). Pretreatment with both 10(-5) M flumazenil (a specific central antagonist of benzodiazepines) and 10(-5) M PK11195 (a specific peripheral antagonist of benzodiazepines) did not influence the effect of 10(-5) M midazolam on [Ca2+]i or tension during the contractions induced by carbachol. CONCLUSIONS: Midazolam directly relaxes airway smooth muscles by decreasing [Ca2+]i; this can be attributed to the inhibition of the influx of extracellular Ca2+. Midazolam has no effect on the release of stored Ca2+. In addition, midazolam has no effect on Ca2+ sensitivity of the contractile apparatus. Finally, benzodiazepine antagonists, flumazenil and PK11195, have no effect on this mechanism of direct action of midazolam on airway smooth muscles.

Animals↗
PubMed1986

Intravenous nitroglycerin as a means of improving ischemic tissue hemodynamics and survival.

The effects of intravenous nitroglycerin infusion on experimental skin flap survival and fluorescein dye kinetics were studied in animals. Perfusion fluorometry was utilized to examine changes in flap hemodynamics and viability. An improvement in skin flap survival was found in the nitroglycerin-infused animals, whether the nitroglycerin was initiated 30 minutes before or 30 minutes after flap elevation. Dye elimination in the flap appeared to be significantly improved with the drug therapy, indicating an improvement in flap blood flow with nitroglycerin.

Animals↗
PubMed1977

A fluorometric study of oxidative metabolism in the in vivo canine heart during acute ischemia and hypoxia.

Optical techniques for monitoring the fluorescence of intramitochondrial nicotinamide adenine dinucleotide (NADH) were employed to allow an on-line, non-invasive study of the metabolic state of healthy and ischemic cardiac tissue in the intact dog. Acute interruption of blood flow to the area of myocardium studied resulted in an immediate rise in NADH, indicating impairment of oxidative metabolism due to limitation of oxygen availability. Release of the coronary artery occlusion resulted in an oxidation of NADH to preocclusion baseline and signaled repayment of incurred O2 debt. Collateral flow produced a spontaneous fall in NADH levels towards preocclusion baseline. Hypoxic tissue was recognized by an oxidation of NADH on ventilation with 100 per cent O2, while in normal hearts no oxidation indicated the O2 was not rate limiting. Ischemic NADH increases preceded the onset of epicardial EKG changes, suggesting that an inability to rephosphorylate ADP to ATP is the primary cause of the EKG changes. Fluorometry of the in vivo heart provides a sensitive, continuous technique of monitoring cardiac cellular mitochondrial NAD;NADH redox levels and, therefore, the adequacy of high energy phosphate production and allows localization of cardiac tissue with marginal oxygen supply.

Animals↗
PubMed1984

Comparison of early lung clearance of yellowcake aerosols in rats with in vitro dissolution and IR analysis.

The lung retention of uranium was determined in rats that inhaled aerosols of commercial yellowcake powders obtained from two mills (Mill A and Mill D) and whose chemical composition and solubilities in vitro were significantly different. Analysis by IR absorption indicated Mill A yellowcake contained 82% ammonium diuranate (ADU) and 18% U3O8. The Mill D powder contained 25% ADU and 75% U3O8. In vitro dissolution studies indicated for the Mill A sample, approximately 85% of the uranium had a dissolution half-time (T 1/2) of less than one day, with the remainder dissolving with a half-time of 500 days. For the Mill D sample, 25% had T 1/2 less than one day and 75% had T 1/2 of 300 days. Groups of 50 rats were exposed by nose-only inhalation to aerosols of either the Mill A or the Mill D yellowcake. Rats were sacrificed in groups of five at intervals through six months after exposure. Selected tissues and excreta samples were assayed by fluorometry to determine their uranium contents. For the Mill A yellowcake, 78% initial lung (broncho-alveolar) burden cleared with T 1/2 of 0.5 days, and 22% with T 1/2 of 240 days. For the Mill D yellowcake, 25% initial lung burden cleared with T 1/2 of 3.5 days and 75% with T 1/2 of 110 days. Thus, the lung clearance of uranium in the rat mimicked the in vitro dissolution data and supported the contention that ADU should be considered as a Class D compound (T 1/2 = 0.5 days) and U3O8 behaves in the lung as a Class Y (T 1/2 greater than 100 days) material.

Aerosols↗
PubMed1997

Resting load and modulation of the myofilament Ca2+ sensitivity in rabbit cerebral arteries.

The effect of preload on myofilament Ca2+ sensitivity was examined using alpha-toxin permeabilization and fura-2 fluorometry in rabbit cerebral arteries. The [Ca2+]i-force curves shifted leftward at a high preload, with a decrease in median effective concentration of Ca2+ in the permeabilized artery. In the fura-2-loaded artery, the preload modulated the force without affecting [Ca2+]i levels during K+ depolarization, and a high preload moved the [Ca2+]i-force curve upward and to the left. It is thus concluded that the preload regulates the Ca2+ sensitivity of the myofilament and, therefore, may play a role in the regulation of cerebral arterial tonus and blood flow.

Actin Cytoskeleton↗
PubMed2001

Protective effects of FK409, a novel nitric oxide donor, against postischemic myocardial dysfunction in guinea-pig hearts.

Effects of FK409 were investigated in perfused guinea-pig Langendorff hearts subjected to ischemia and reperfusion. Nitric oxide electrode, fluorometry, and 31P nuclear magnetic resonance imaging were used to monitor changes in cellular high-phosphorous energy and nitric oxide and Ca2+ content in the heart together with simultaneous recordings of left ventricular developed pressure. After cardioplegic arrest with St. Thomas' Hospital solution, normothermic (37 degrees C) global ischemia was induced for 40 min, and hearts were reperfused for 40 min. FK409 at 10(-8) M, which has a minimum inotropic effect on nonischemic hearts, was added to the cardioplegic solution. Treatment with FK409 reduced left ventricular developed pressure during and after ischemia and improved postischemic recovery of left ventricular developed pressure from 55.4% at 40 min of reperfusion in FK409-free hearts up to 80.4% in hearts treated with FK409 (p < 0.01). Flow rate at 1.5 min after treatment with the cardioplegic solution was 27.7 ml/min in hearts treated with FK409 compared with 21.2 ml/min in drug-free hearts (p < 0.01). Treatment with FK409 significantly effected preservation of tissue level of beta-adenosine triphosphate at the end of ischemia or reperfusion. During ischemia, arrested with the cardioplegic solution, intracellular Ca2+ accumulation and nitric oxide release were reduced. At the end of ischemia in FK409-treated hearts, nitric oxide release was 86% greater than in drug-free hearts without reference to the Ca2+ concentration. In cardiac surgery, normothermic arrested hearts are subject to damage by oxygen free radicals in reperfusion injury. Therefore, nitric oxide exogenously supplied by FK409 was responsible for the cardioprotective action, presumably by acting directly as an oxygen radical scavenger during reperfusion. A specific nitric oxide donor, like FK409, may have therapeutic use as a nitric oxide-mediated vasorelaxant and additional protective action for reperfusion-injury hearts.

Actin Cytoskeleton↗
PubMed1991

Fluorometric determination of isoniazid and its metabolites in urine by high-performance liquid chromatography using in-line derivatization.

A rapid, simple, and accurate method has been developed for the determination of isoniazid and its metabolites (isonicotinic acid, isonicotinylglycine, and acetylisoniazid) in human urine by high-performance liquid chromatography. Isoniazid and its metabolites are separated by reversed-phase ion-exchange chromatography with a mobile phase containing hydrogen peroxide as a fluorogenic reagent and butanesulfonate as a hydrophobic ion exchanger, and are detected by fluorometry (excitation at 317 nm and emission at 415 nm) using in-line derivatization at high temperature (160 degrees C). The detection limits are isonicotinic acid, 0.5 mumol/L; isonicotinylglycine, 1 mumol/L; acetylisoniazid, 1 mumol/L; and isoniazid, 1.5 mumol/L. This method can be applied for acetylator phenotyping.

Chromatography, High Pressure Liquid↗
PubMed2001

Relationship between nucleic acid ratios and growth in Listeria monocytogenes.

Listeria monocytogenes is a pathogen whose distribution in a range of foodstuffs requires the development of methods for sensitive and rapid detection. Molecular biological methods usually rely on specific detection of L. monocytogenes rDNA directly amplified by the application of PCR to DNA extracts. Information on the metabolic status of L. monocytogenes populations would be valuable and can, in theory, be provided by quantitative detection of rRNA itself. Both fluorometry and oligonucleotide probe assays were applied to L. monocytogenes cultures to quantify RNA and DNA and produced more meaningful data than previous estimates for bacteria based on eukaryotic nucleic acid standards. In batch culture, the RNA-DNA ratio was found to be greatest at the end of exponential growth, after which RNA became degraded in accordance with the rapid decrease in viability. When the pH of the medium was controlled at neutrality, culture viability was dramatically extended and although RNA was degraded, intact DNA was maintained for the duration of the experiment. Ribosome numbers per cell were estimated to decrease from about 25000 observed during mid-exponential growth to about 600 during stationary phase, under pH-controlled conditions. Like Escherichia coli, therefore, L. monocytogenes loses viability and rRNA rapidly once exponential growth has ceased in batch culture. However, much improved survival of a culturable L. monocytogenes population when pH is controlled has clear implications for the persistence of this species in buffered environments such as dairy products.

Culture Media↗
PubMedDate not supplied

Release of DNA from dead and dying lymphocyte and monocyte cell lines in vitro.

DNA is a nuclear macromolecule that circulates in the blood where its levels can reflect the activity of inflammatory and malignant diseases. While dead and dying cells have usually been considered the source of blood DNA, the mechanisms for its release during apoptosis and necrosis are not well defined. To elucidate DNA release, an in vitro model system was used, assessing DNA in the media of living, apoptotic or necrotic Jurkat and U937 cells. Apoptosis was induced by etoposide, camptothecin or staurosporine, while necrosis was induced by heating at 56 degrees C. DNA release was measured by fluorometry with the dye PicoGreen while the extent of death was measured by fluorescence-activated cell sorter analysis with propidium iodide and annexin. Apoptotic Jurkat cells released significantly more DNA in the media than untreated cells while necrotic cells did not show significant DNA release. U937 cells showed similar findings. Pretreatment of Jurkat cells with z-VAD-fmk, a caspase inhibitor, reduced both apoptosis and DNA release. By gel electrophoresis, extracellular DNA from apoptotic cells showed laddering with low molecular weight fragments. These studies suggest that extracellular release of DNA is a consequence of apoptosis and may account for some of the DNA in the blood.

Amino Acid Chloromethyl Ketones↗
PubMed1982

Kinetic studies of proton transfer in the microenvironment of a binding site.

Excitation of 8-hydroxypyrene 1,3,6-trisulfonate to its first electronic singlet state converts the compound from weak base (pK degrees = 7.7) into a strong acid (pK* = 0.5). The dissociation of the proton in water or dilute salt solution is a very fast reaction, K12 = 1 X 10(10) S-1. In concentrated salt solutions the dissociation is slowed as an exponential function of the chemical activity of the water in the solution. This kinetic parameter has been used to gauge the properties of the microenvironment of the binding sites of bovine serum albumin at which this compound is bound. Time-resolved fluorometry reveals two distinct steps: a rapid dissociation of the proton with tau = 300 +/- 40 ps which lasts approximately 0.5 ns, followed by a slower reaction with tau = 3.3 ns. The first rapid phase represents proton dissociation taking place in the binding site. From the rate constant K = 3.3 X 10(9) s-1 we estimate that the ability of the water molecules in the site to hydrate the ejected proton is equivalent to a salt solution with water activity of 0.85. The slow phase represents the escape of the proton from the binding site. The rate of the escape, 1.4 X 10(8) s-1, is significantly slower than diffusion-controlled dissociation. It is concluded that the shape of the site or its lowered proton conductivity do not allow a rapid escape of the proton to the bulk. Still it should be remembered that the escape of the proton is 10(5)-10(6)-times faster than a typical turnover of an enzyme.U

Arylsulfonates↗
PubMed2000

Stimulation of Ca(2+)-independent exocytosis in rat pituitary gonadotrophs by G-protein.

We employed the whole-cell recording technique in conjunction with fluorometry to measure cytosolic Ca(2+) concentration ([Ca(2+)](i)) and exocytosis (capacitance measurement) in single, identified rat gonadotrophs. Direct activation of G-protein (via intracellular dialysis of non-hydrolysable analogues of GTP, but not of GDP) triggered a slow rise in capacitance even in the presence of a fast intracellular Ca(2+) chelator. The broad-spectrum kinase inhibitors H7 and staurosporine did not prevent this Ca(2+)-independent exocytosis, ruling out the involvement of the cAMP and PKC pathways. AlF(4)(-), a potent stimulator of heterotrimeric G-proteins, failed to stimulate any exocytosis when the intracellular Ca(2+) store was depleted, implicating the involvement of AlF(4)(-)-insensitive G-protein(s). Maximal stimulation of Ca(2+)-independent exocytosis by GTP analogues did not reduce the number of readily releasable granules that were available subsequently for Ca(2+)-dependent release. The last finding raises the possibility that the G-protein-stimulated Ca(2+)-independent exocytosis may regulate a pool of granules that is distinct from the Ca(2+)-dependent pool.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2005

Ozone foliar symptoms in woody plant species assessed with ultrastructural and fluorescence analysis.

This paper compares the responses to ozone in five woody species: Fagus sylvatica (FS), Acer pseudoplatanus (AP), Fraxinus excelsior (FE), Viburnum lantana (VL) and Ailanthus altissima (AA). The hypothesis being tested was that the strategies that plants adopt to resist oxidative pressure are species-specific. The study was carried out on field grown plants in an area in Northern Italy characterized by elevated levels of ozone pollution. The observations were made both at ultrastructural (using light and electronic microscopy) and physiological (using chlorophyll a transient fluorescence and microspectral fluorometry) level. Common responses were: the hypersensitive response (i.e. the death of palisade mesophyll cells) and the formation of callose layers separating injured from healthy cells. FS and AP were capable of thickening the palisade mesophyll cell walls. This thickening process involved changes in cell wall chemical structure, evidenced by the accumulation of yellow autofluorescence compounds. Species-specific behaviours were observed with the fluorescence analysis, with special reference to the photochemical de-excitation constant (Kp). This value increased in FE and AP, and decreased in AA. The observed responses are interpreted as adaptative strategies against the ozone stress. The increase of Kp indicates that the reaction centres were working as more effective quenchers.

Chlorophyll↗
PubMed1992

A highly sensitive assay for histamine using ion-pair HPLC coupled with postcolumn fluorescent derivatization: its application to biological specimens.

A simple and highly sensitive method for the determination of histamine (HA) was developed using ion-pair, reversed-phase HPLC coupled with postcolumn o-phthalaldehyde derivatization fluorometry, and it was applied to the unpurified extracts of human and rat plasma, and brains of rats and mice. The HA concentrations both in the plasma and brains determined by the present method were well consistent with the values obtained by cation-exchange HPLC with postcolumn fluorescent derivatization currently in use. The present method was more advantageous than the assay using cation-exchange HPLC: (1) it was three to four times more sensitive (the detection limit was 0.5 pg of HA), and (2) it enabled the measurement of HA in samples containing (R)alpha-methylhistamine, a potent and specific H3-receptor agonist, which could not be separated from HA by cation-exchange chromatography. Using the present method coupled with intracerebral microdialysis, we found in the rat hypothalamus that (R)alpha-methylhistamine (5 mg/kg i.p.) markedly decreased the extracellular concentration of HA with a maximal effect (83% reduction) during 30-60 min after injection, suggesting that most of HA in the microdialysate fraction is neuronal in origin.

Animals↗
PubMed2005

Methadone increases intracellular calcium in SH-SY5Y and SH-EP1-halpha7 cells by activating neuronal nicotinic acetylcholine receptors.

(-)-Methadone acts as an agonist at opioid receptors. Both (+)- and (-)-enantiomers of methadone have been suggested to be potent non-competitive antagonists of alpha3beta4 neuronal nicotinic acetylcholine receptors (nAChRs). In the present study, we have examined interactions of methadone with nAChRs by using receptor binding assays, patch-clamp recording and calcium fluorometry imaging with SH-SY5Y cells naturally expressing alpha7 and alpha3* nAChR subtypes and SH-EP1-halpha7 cells heterologously expressing human alpha7 nAChRs. Methadone potently inhibited binding of [3H]methyllycaconitine to alpha7 nAChRs and that of [3H]epibatidine to alpha3* nAChRs. Methadone pretreatment induced up-regulation of epibatidine binding sites in SH-SY5Y cells. Using whole-cell patch-clamp recording, both isomers of methadone activated cation currents via mecamylamine-sensitive nAChRs in SH-SY5Y cells. Nicotine and both (+)- and (-)-methadone evoked increases in [Ca2+]i in both fluo-3AM loaded cell lines, and these effects were blocked by mecamylamine and by the alpha7 selective antagonist methyllycaconitine, suggesting effects of methadone as alpha7-nAChR agonist. Sensitivity of sustained nicotine and methadone effects to blockade by CdCl2, ryanodine and xestospongin-c implicates voltage-operated Ca2+ channels and intracellular Ca2+ stores as downstream modulators of elevated [Ca2+]i. Collectively, our results suggest that methadone engages in complex and potentially pharmacologically significant interactions with nAChRs.

Analgesics, Opioid↗
PubMed2006

Potential inplications of endogenous aldehydes in beta-amyloid misfolding, oligomerization and fibrillogenesis.

Aldehydes are capable of inducing protein cross-linkage. An increase in aldehydes has been found in Alzheimer's disease. Formaldehyde and methylglyoxal are produced via deamination of, respectively, methylamine and aminoacetone catalyzed by semicarbazide-sensitive amine oxidase (SSAO, EC 1.4.3.6. The enzyme is located on the outer surface of the vasculature, where amyloidosis is often initiated. A high SSAO level has been identified as a risk factor for vascular disorders. Serum SSAO activity has been found to be increased in Alzheimer's patients. Malondialdehyde and 4-hydroxynonenal are derived from lipid peroxidation under oxidative stress, which is also associated with Alzheimer's disease. Aldehydes may potentially play roles in beta-amyloid aggregation related to the pathology of Alzheimer's disease. In the present study, thioflavin-T fluorometry, dynamic light scattering, circular dichroism spectroscopy and atomic force microscopy were employed to reveal the effect of endogenous aldehydes on beta-amyloid at different stages, i.e. beta-sheet formation, oligomerization and fibrillogenesis. Formaldehyde, methylglyoxal and malondialdehyde and, to a lesser extent, 4-hydroxynonenal are not only capable of enhancing the rate of formation of beta-amyloid beta-sheets, oligomers and protofibrils but also of increasing the size of the aggregates. The possible relevance to Alzheimer's disease of the effects of these aldehydes on beta-amyloid deposition is discussed.

Aldehydes↗
PubMed1989

Intrathoracic microvascular circulation in haemorrhagically shocked rats. Studies by fluorescence techniques.

The microvascular circulation in the heart, lung and thymus was studied by fluorometry in 32 haemorrhagically shocked rats. Exsanguination to a blood pressure of 35 mmHg for 180 min did not result in any reduction of this circulation in the heart or lung, but in the thymus it was reduced by 52%. Retransfusion of shed blood caused no change in cardiac microcirculation, whereas the microcirculation in the thymus was increased by 59%. In the lungs a heterogeneous fluorescence pattern was observed after retransfusion, with large dark areas alternating with normal fluorescent ones and even some small intensively fluorescent areas. After retransfusion, maldistribution of blood flow seems to be a phenomenon of haemorrhagic shock in the lungs.

Animals↗