Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Luminol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

Detection of oxygen activation and determination of the activity of antioxidants towards reactive oxygen species by use of the chemiluminigenic probes luminol and lucigenin.

Reactive oxygen metabolites can transfer, via oxygenation, the chemiluminigenic probes luminol and lucigenin to an excited state and thus induce light emission from these probes. This technique has been applied to a study of the effect of common food antioxidants on the availability of reactive oxygen species in aqueous model systems and in microsomal preparations. In all systems tested, propyl gallate and its congener octyl gallate proved to be the most active scavengers of the oxygenating species involved in the chemiluminescence reaction. In aqueous model systems, butylated hydroxyanisole was 10 times less efficient than the gallic acid ester antioxidants. In biological material, the lower scavenger activity of butylated hydroxyanisole is further compromised by its ability to induce a marked increase in production of hydrogen peroxide in the endoplasmic reticulum. Butylated hydroxytoluene is only marginally active in aqueous media and in biological material. It is concluded that gallic acid ester antioxidants may possess a significant protective potential towards toxic and carcinogenic agents due to their ability to remove toxic oxygen metabolites.

Acridines↗

Inhibition by nonsteroidal antiinflammatory drugs of luminol-dependent human-granulocyte chemiluminescence and [3H]FMLP binding. Effect of sulindac sulfide, indomethacin metabolite, and optical enantiomers (+) and (-) MK830.

A system is described to evaluate for nonsteroidal antiinflammatory drugs by means of luminol-dependent human-granulocyte chemiluminescence (CL) is described. The CL is produced using either opsonized zymosan (yeast cells) or the soluble chemotactic peptide f-Met-Leu-Phe as the perturbant of the granulocyte membrane. Using either system, the following drug effects 2 x 10(-5) M were noted: only sulindac sulfide, and not sulindac sulfone or sulindac, displayed marked inhibition of chemiluminescence, following the in vivo data regarding inflammatory effects. The 5-OH indomethacin metabolite was likewise inactive as an inhibitor of CL mirroring in vivo effects. MK(+)410, MK(-)830 and MK835 all showed approximately 50% inhibition of CL, displaying deviation from in vivo data. MK(+)830 markedly stimulated CL, 4-6 times the control (without drug), which is clearly different from its enantiomer, MK(-)830. The reasons for this behavior are unclear. However, receptor binding studies with [3H]FMLP were accomplished in the presence and absence of the various drugs at 2 x 10(-5) M that were effective inhibitors of chemiluminescence (CL). Indomethacin, MK(-)830 and MK(+)410 had equivalent percent control binding and percent control CL. Sulindac sulfide and MK(+)835 both had higher percent control binding than percent control CL, with MK(+)835 displaying apparent increased numbers of available receptors relative to control. MK(+)830, which produces large increases in CL, produced a minor effect on percent control binding. A direct relationship between binding and CL does not exist with each drug. Chemiluminescence is dependent on ion movement and oxidative metabolism and is a secondary event to agonist-receptor occupation.

Anti-Inflammatory Agents↗

Antioxidation theory of non-steroidal anti-inflammatory drugs based upon the inhibition of luminol-enhanced chemiluminescence from the myeloperoxidase reaction.

The action of non-steroidal anti-inflammatory drugs (NSAIDS) has been ascribed to their ability to block the reaction of arachidonate with cyclooxygenase/peroxidase, thus inhibiting the cellular production of inflammation mediators such as prostaglandins and leukotrienes. However, this and other polymorphonuclear leukocyte (PMN) peroxidases such as myeloperoxidase (MPO) would still be capable of producing destructive oxidants which contribute to inflammation. Sulindac sulfide (Clinoril sulfide) has recently been shown to scavenge oxidant products of prostaglandin cyclooxygenase/peroxidase and MPO. The MPO-H2O2-Cl- reaction is a potent antimicrobial/cytotoxic system which produces HOCl, a strong oxidant. MPO itself has the ability to oxidize drugs and cellular components, and may be the main oxidant in PMN defenses. An antioxidant/free radical scavenger action of NSAIDs against the MPO system could be a primary mechanism of their anti-inflammatory effects. Other antioxidant/free radical scavengers have anti-inflammatory effects. MPO activity has previously been quantified using chemiluminescence (CL). In this study, NSAIDs from various classes were tested for their ability to inhibit luminol-enhanced CL from MPO. The most potent NSAIDs against MPO-CL were BW755C, phenylbutazone, indomethacin and sulindac sulfide. Salicylates and arylacetic acid derivatives, such as naproxen, also decreased MPO-CL. These drugs are also effective against CL from PMNs, of which MPO may be a main source. This effect of NSAIDs on MPO suggests that NSAIDs may impair the killing mechanism of the PMN, preventing cell destruction and release of inflammation mediators. PMN MPO appears to be a target for the antioxidant/free radical scavenging effects of NSAIDs.

Anti-Inflammatory Agents↗

Effects of histamine agonists and antagonists on luminol-dependent chemiluminescence of granulocytes.

Histamine inhibited luminol-dependent chemiluminescence (CL) of granulocytes in a dose-dependent manner, with an ID50 of about 3 X 10(-5) M. Dimaprit, a selective H2-agonist, produced a histamine-like effect. Furthermore, cimetidine, ranitidine, and TZU 0460, which are selective H2-antagonists, but not mepyramine, a selective H1-antagonist, blocked the inhibitory effect of histamine on CL. Thus it may be concluded that the inhibitory effect of histamine is mediated via histamine H2-receptors. H1- and H2-antagonists per se, except at extremely high concentrations, had no effect on CL of granulocytes.

Cimetidine↗

Luminol-enhanced, whole blood chemiluminescence of human neutrophils evaluated by means of an automated, computer-assisted, and high-sensitivity luminescence analyzer.

Luminol-enhanced whole blood chemiluminescence of human neutrophils was studied using opsonized zymosan as a stimulus. Heparinized blood (0.5 microliters) was used, and the chemiluminescence signals were recorded by a very sensitive, automated, and computer-assisted luminometer (LB 950, Berthold, Wildbad, Germany). The following parameters were provided: integral values over the total measuring time, peak values, the time to reach maximum value, and the time to reach half maximum value. Normal subjects, neutropenic patients, subjects with total or partial myeloperoxidase deficiency, patients with recurrent infections, phagocytic defects, thrombocythemic patients and those with non-Hodgkin's lymphomas undergoing therapy with recombinant human granulocyte colony-stimulating factor were studied. The integral response of chemiluminescence and the time of reach half maximal value were useful indicators of chemiluminescence defects; the assay, was able to detect chemiluminescence responses in neutropenic subjects with neutrophil levels as low as 0.6 x 10(9)/l; differences between cellular and plasma defects could be identified; the quenching effect exerted by erythrocytes was negligible.

Adolescent↗

Luminol-enhanced chemiluminescence of peripheral blood leukocytes as an early indicator of graft take after allogeneic bone marrow transplantation in patients with acute myelogenous leukaemia.

The luminol-enhanced chemiluminescence (CL) of peripheral blood leukocytes was studied daily in five patients with acute myelogenous leukaemia (AML) in first remission, who were undergoing allogeneic bone marrow transplantation (BMT). The CL was measured after stimulation of leukocytes with opsonized zymosan in highly diluted whole blood. All patients had an undetectable CL level on day +7, post BMT, simultaneously with severe pancytopenia caused by the pre-conditioning for BMT. Subsequently, CL started to rise, reaching the maximum level, twice that of healthy controls, on day +11. This preceded the rise of blood leukocytes above 1.0 x 10(9) l.-1 and that of neutrophils above 0.5 x 10(9) l.-1 by 3-14 days, but coincided with the appearance of large unstained cells (LUC; a parameter given by a Technicon H 6000 blood analyzer). One of the patients later had a transient decline of CL. This preceded the fall in white blood count and platelets by 7 days, suggesting marrow suppression. We conclude that in AML the measurement of leukocyte CL is a more sensitive test for prediction of graft take than the conventional blood counts.

Blood Cell Count↗

Sensitive flow-injection chemiluminescence determination of terbutaline sulfate based on enhancement of the luminol-permanganate reaction.

A novel and highly sensitive chemiluminescence (CL) method for the determination of terbutaline sulfate, coupled with flow-injection analysis (FIA), is described in this paper. The method is based on enhancement by terbutaline sulfate of the chemiluminescence emission of the luminol-permanganate system under alkaline conditions. Under the conditions selected the concentration of terbutaline sulfate is proportional to CL intensity in the range 5 x 10(-10)-5 x 10(-7) g mL(-1), with a detection limit of 1.7 x 10(-10) g mL(-1) (3 sigma). The relative standard deviation is 2.8% for 1 x 10(-8) g mL(-1) terbutaline sulfate ( n=11). Ninety samples can be determined per hour. The proposed method has been used to determine terbutaline sulfate in pharmaceutical preparations and in plasma and urine samples with satisfactory results. The possible mechanism of the chemiluminescence reaction is discussed briefly.

Calibration↗

Investigating the post-chemiluminescence behavior of phenothiazine medications in the luminol-potassium ferricyanide system: molecular imprinting-post-chemiluminescence method for the determination of chlorpromazine hydrochloride.

A new post-chemiluminescence (PCL) phenomenon was observed when phenothiazine medications were injected into the reaction mixture after the chemiluminescence (CL) reaction of luminol and potassium ferricyanide had finished. A possible reaction mechanism was proposed based on studies of the kinetic characteristics of the CL, CL spectra, fluorescence spectra, and on other experiments. The feasibility of determining various phenothiazine medications by utilizing these PCL reactions was examined. A molecular imprinting-post-chemiluminescence (MI-PCL) method was established for the determination of chlorpromazine hydrochloride using a chlorpromazine hydrochloride-imprinted polymer (MIP) as the recognition material. The method displayed high selectivity and high sensitivity. The linear range of the method was 1.0 x 10(-8) approximately 1.0 x 10(-6), with a linear correlation coefficient of 0.9985. The detection limit was 3 x 10(-9) g/ml chlorpromazine hydrochloride, and the relative standard deviation for a 1.0 x 10(-7) g/ml chlorpromazine hydrochloride solution was 4.0% (n = 11). The method has been applied to the determination of chlorpromazine hydrochloride in urine and animal drinking water with satisfactory results.

Animals↗

Applications of the luminol chemiluminescent reaction in analytical chemistry.

This critical review discusses the results published between 2000 and 2005 on the development of analytical systems based on the luminol chemiluminescent and electrochemiluminescent reactions. An increasing number of non-specific detection systems based on the enhancing, inhibiting or catalysing effect of a large range of compounds have been published. Possible detected compounds and their concomitant presence in samples are discussed. Chemiluminescent and electrochemiluminescent reactions were also found to merge in biochip and microarray development as a possible substitute to the well-established but hardly quantitative fluorescent detections.

Catalysis↗

Development of a novel luminol chemiluminescent method catalyzed by gold nanoparticles for determination of estrogens.

It has been found that gold nanoparticles (nano-Au) enhance the chemiluminescence (CL) of the luminol-hydrogen peroxide system and that estrogens inhibit these CL signals in alkaline solution. CL spectra, UV-visible spectra, X-ray photoelectron spectra (XPS), and transmission electron microscopy (TEM) were used to investigate the mechanism of the CL enhancement. On the basis of the inhibition, a flow-injection CL method has been established for determination of three natural estrogens. Under the optimized conditions, the linear range for determination of the estrogens was 0.07 to 7.0 micromol L(-1) for estrone, 0.04 to 10 micromol L(-1) for estradiol, and 0.1 to 10 micromol L(-1) for estriol. The detection limits were 3.2 nmol L(-1) for estrone, 7.7 nmol L(-1) for estradiol, and 49 nmol L(-1) for estriol, with RSD of 2.9, 2.6, and 1.8%, respectively. This method has been used for analysis of estrogens in commercial tablets and in urine samples from pregnant women.

Adult↗

Luminol assay for microdetermination of superoxide dismutase activity: its application to human fetal blood.

A microtechnique for determining the superoxide dismutase activity in erythrocytes is described. This technique involves the inhibition of luminol-enhanced chemiluminescence of superoxide anion generated by xanthine-xanthine oxidase. Measurements required a steady-state chemiluminescence whether superoxide dismutase was present or absent; the level of luminescence was correlated to enzyme activity. Superoxide dismutase activity measured by this technique was 836 +/- 112 micrograms/g of hemoglobin for whole blood and 834 +/- 109 micrograms/g of hemoglobin for erythrocytes. When the reference technique was applied to larger amounts of blood, the results were 862 +/- 58 and 858 +/- 116 micrograms/g of hemoglobin for whole blood and washed erythrocytes, respectively. The enzymatic activity of superoxide dismutase from fetal blood (obtained by venipuncture in utero and of 19-26 weeks gestational age) was similar to that of adult blood, when measured by the new technique.

Adult↗

Glucose determination in samples taken by microdialysis by peroxidase-catalyzed luminol chemiluminescence.

An automatic, luminometric assay of glucose in samples of the extracellular water space obtained by microdialysis is described. The assay involves oxidation by glucose oxidase (EC 1.1.3.4) and mutarotation of glucose by aldose mutarotase (EC 5.1.3.3.). The H2O2 formed is subsequently determined in a reaction catalyzed by horseradish peroxidase (EC 1.11.1.7) using luminol as electron donor. The assay is linear between 0.01 and 1 nmol in the cuvette. The detection limit, defined as 3 standard deviations of the reagent blank, was 0.008 mumol/liter in the cuvette. A complete oxidation of glucose is obtained within 4 min and 25 samples are automatically assayed within 75 min. Addition of microdialysate sample obtained from human adipose tissue in vivo did not interfere with the standard curves. Glucose added to microdialysate resulted in a complete recovery compared to a H2O2 standard. Analytical interference from different factors was investigated. No interference was observed up to the following concentrations: 5 mumol/liter epinephrine, 1 mumol/liter norepinephrine, 100 mumol/liter insulin, 500 mumol/liter pyruvate, 50 mmol/liter lactate, and 1 mumol/liter ascorbate. The glucose values with the present method correlated strongly (r = 0.984) with values obtained using a routine method involving glucose oxidase and peroxidase.

Adipose Tissue↗

Luminol chemiluminescence and active oxygen generation by activated neutrophils.

Upon stimulation by various ligands and membrane perturbers, neutrophils produce various active oxygen species. Since luminol chemiluminescence (LCL) in neutrophils can be blocked by azide, an inhibitor of myeloperoxidase, LCL has been believed to reflect mainly the myeloperoxidase-catalyzed reaction. When cells were stimulated by formyl-methionyl-leucyl-phenylalanine, LCL was strongly inhibited by superoxide dismutase (SOD) and uric acid, a scavenger for hydroxy radical (.OH) and singlet oxygen, whereas it was stimulated by azide. LCL was also inhibited by .OH scavengers, such as mannitol, ethanol, and dimethylsulfoxide. However, when stimulated by phorbol myristate acetate or opsonized zymosan, LCL was strongly inhibited by azide but not by uric acid, and the inhibitory action of SOD was low. Thus, the qualitative and quantitative aspects of reactive oxygen generation by activated neutrophils differ significantly from one ligand to another. These results suggest that the metabolic fate of active oxygens in neutrophils and, hence, their effect on microorganisms and the surrounding tissues might differ depending on the stimulus.

Animals↗

Stimulus-specific enhancement of luminol chemiluminescence in neutrophils by phosphatidylserine liposomes.

When stimulated with different stimuli, neutrophils generate various active oxygen species. These active oxygen molecules can be analyzed by luminol chemiluminescence (LCL). Phosphatidylserine (PS)-liposomes increased the formylmethionyl-leucyl-phenylalanine-induced LCL of guinea pig peritoneal neutrophils without affecting their oxygen consumption and superoxide (O2.-) generation. Similar effects of PS-liposomes were also observed in LCL of neutrophils stimulated by phorbol myristate acetate or arachidonic acid but not by opsonized zymosan. Kinetic analysis revealed that the PS-liposome-induced increase in LCL depended on extracellulary generated O2.-. Moreover, the stimulatory effect of PS could be seen only when it formed liposomal membranes. The effect of PS-liposomes was also inhibited by superoxide dismutase, catalase, and deferoxamine, an iron chelator, but not by azide, an inhibitor of myeloperoxidase. Similar enhancement of stimulation-dependent LCL response was also observed with Fe3+ and ADP-Fe3+, but the degree of enhancement was much greater with PS-liposomes than with iron and its complex. The increase in hydroxyl radical generation by PS-liposome-treated neutrophils was confirmed by experiments with EPR spectrometry using spin-trapping agents. These results suggested that the interaction of neutrophils with PS-containing membrane surface might generate reactive oxygen species that enhance the stimulus-dependent LCL response of neutrophils.

Animals↗

Thrombospondin-exposed human monocytes display augmented luminol-enhanced chemiluminescence upon receptor triggering.

It was tested whether the exposure to blood platelet thrombospondin (TSP) influences the function of monocytes. TSP-treated monocytes displayed luminol-enhanced chemiluminescence (CL) upon triggering with polyclonal or monoclonal anti-TSP. This response was mediated by an Fc receptor, since F(ab')2 fragments were without effect. Evidence is provided that a CL signal was induced only when antibodies bound to TSP and Fc receptors of the same monocyte. TSP-treated monocytes exerted enhanced CL to aggregated IgG when compared with untreated or albumin-treated cells, suggesting that TSP up-regulated the cells' capacity to mediate Fc receptor-dependent generation of reactive oxygen. A similar enhancement was observed when TSP-treated cells were stimulated with anti-CD36, or with fMLP. Upon stimulation of TSP-pretreated cells with monoclonal anti-fibrinogen (Fg), a much stronger enhancement was noted, which was similar in magnitude to that induced by anti-TSP. The effect of anti-Fg cannot be explained by a trace contamination of TSP with Fg alone. In contrast to receptor-mediated CL, PMA-induced and zymosan-induced CL were influenced little by TSP pretreatment. IgG-mediated phagocytosis was not enhanced in TSP-treated cells. Thus, TSP selectively modulates certain monocyte functions which could be of physiological relevance.

Antibodies↗

How flavonoids inhibit the generation of luminol-dependent chemiluminescence by activated human neutrophils.

The mechanism by which (a panel of) flanonoids inhibit the production of luminol-dependent chemiluminescence (CLlum) by activated human neutrophils is subject to this study. CLlum is frequently used as a bio-assay to quantify the effect of xenobiotics on the production of reactive oxygen species (ROS). Most of the flavonoids decreased CLlum by inhibition of ROS production by the cells. Four selected flavonoids (Taxifolin, Eriodictyol, Hesperetin and Luteolin), inhibited myeloperoxidase (MPO) release, while two of these (Taxifolin and Eriodictyol) strongly inhibited MPO activity. Because CLlum is a MPO-dependent process these activities might mask effects of the flavonoids on ROS production. Finally, our results provide evidence that essential determinants for inhibition of O2(-)-release are the OH-groups located in the B-ring of the flavonoid molecule. Flavonoids methylated at a single OH-group in the B-ring are only inhibitory when they react with activated neutrophils in the presence of myeloperoxidase.

Anti-Inflammatory Agents, Non-Steroidal↗

Chemiluminescent immunosorbent assay of serum myoglobin based on the luminol reaction.

A simple and sensitive method for the determination of serum myoglobin is described. Myoglobin was determined in the range of 10-500 micrograms/1 by the chemiluminescent luminol reaction after adsorption to anti-myoglobin IgG onto a solid phase. Only 50 microliter of serum has to be used and the luminescent immunoassay (LIA) has a better sensitivity and a wider linear range than the conventional radioimmunoassay (RIA). However, in its present form LIA has a higher imprecision than RIA. In clinical specimens the correlation between the two methods was excellent.

Antibody Specificity↗

Enhancement of hydrogen peroxide-induced luminol-dependent chemiluminescence by neopterin depends on the presence of iron chelator complexes.

We have previously shown that neopterin, 6-D-erythro-trihydroxypropyl-pteridine, synthesized by human monocytes/macrophages upon stimulation by interferon-gamma, enhances toxicity of reactive oxygen at neutral or slightly alkaline pH (7.5), but not at acidic pH (below 6.5). In the present study, we explored in more detail the necessary requirements for neopterin to modulate the effects of hydrogen peroxide in a luminol-dependent chemiluminescence assay. We demonstrate that neopterin enhances hydrogen peroxide effects only in the presence of iron chelator complexes like iron-(III)- or iron-(II)-EDTA or iron-(III)-DTPA. Thus, iron chelator complexes together with neopterin may play an important role in macrophage-mediated effector mechanisms.

Biopterins↗