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At least 217 records · Page 12Linked to original sources
PubMed2004

Flow-injection inhibition chemiluminescence determination of indapamide based on luminol-ferricyanide reaction.

A novel and sensitive chemiluminescence (CL) method for the determination of indapamide coupled with flow-injection analysis (FIA) technique is developed in this paper. It is based on the inhibition effect of the studied drug on the chemiluminescence emission of luminol-potassium ferricyanide system. Under the optimum conditions, the decreased CL intensity is proportional with the concentration of indapamide in the range of 1 x 10(-8) to 1.0 x 10(-6) g ml(-1). The detection limit is 3.4 x 10(-9) g ml(-1) (3sigma). A complete analysis could be performed in 45 s including washing and sampling, giving a throughout of about 90 h(-1). The relative standard deviation (R.S.D.) for 11 parallel measurements of 1.0 x 10(-7) g ml(-1) indapamide is 3.0%. The proposed method has been applied for the determination of indapamide in its pharmaceutical formulations. The results obtained compared well with those by an official method. The possible inhibition mechanism of indapamide on luminol-potassium ferricyanide CL system was discussed briefly.

Antihypertensive Agents↗
PubMed1999

Indirect determination of paracetamol in pharmaceutical formulations by inhibition of the system luminol-H2O2-Fe(CN)3-(6) chemiluminescence.

After a large drug scanning, the system Luminol-H2O2-Fe(CN)6(3-) is proposed for first time for the indirect determination of paracetamol. The method is based on the oxidation of paracetamol by hexacyanoferrate (III) and the subsequent inhibitory effect on the reaction between luminol and hydrogen peroxide. The procedure resulted in a linear calibration graph over the range 2.5-12.5 microg ml(-1) of paracetamol with a sample throughput of 87 samples h(-1). The influence of foreign compounds was studied and, the method was applied to determination of the drug in three different pharmaceutical formulations.

Acetaminophen↗
PubMed2002

In vitro monitoring sub-nanogram amounts analgin in human urine by its inhibitory of the luminol-periodate chemiluminescence reaction using reagent immobilization release technique.

A selective and sensitive as well as rapid chemiluminescence (CL) flow sensor for the determination of analgin is described. The analytical reagents involved in chemiluminescence reaction, luminol and periodate, were both immobilized on an anion-exchange column. The CL signals produced by the reaction between luminol and periodate, which were eluted from the column through water injection, were decreased in the presence of analgin. Analgin was sensed by measuring the decrement of CL intensity, and which was observed linear over the logarithm of analgin concentration range of 0.1 to 50.0 ng mL(-1), and the limit of detection was 0.04 ng mL(-1) (3ó). At a flow rate of 2.0 mL min(-1), including sampling and washing, the detection could be performed in 0.5 min with a relative standard deviation of less than 3.0%. The proposed procedure was applied successfully in the monitoring of analgin in human urine samples without any pre-treatment process. It was found that the analgin concentration reached its maximum after being orally administrated for 4 h, and the analgin metabolism ratio in 10 h was 9.28% in the body of volunteers. The flow sensor offered reagentless procedures and remarkable stability in determination of analgin, and could be easily reused over 80 h.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Detection of nitric oxide production from a perfused organ by a luminol-H2O2 system.

Nitric oxide, thought to be the endothelium-derived relaxing factor (EDRF), is involved in intra- and intercellular signalling in various tissues. A system for the continuous detection of NO in the picomolar range from a perfused organ is described. The detection is based upon the chemiluminescence reaction between NO and the luminol (5-amino-2,3-dihydro-1,4-phthalazinedione)-H2O2 system. The chemiluminescence is due to the formation of peroxynitrite from NO and H2O2. The luminol-H2O2 system is specifically reactive to NO, so that other nitrogen-containing compounds, (organic nitrite, organic nitrate, and thio-nitroso compounds) or endothelium-derived compounds do not interfere. The limit of determination was approximately 100 fM. This system has been used to measure continuous NO release from isolated perfused rat kidney and the simultaneous changes of perfusion pressure. In Wistar rats basal NO release was 85 +/- 11 fmol/min-1 (g of kidney weight)-1 (39 pM in the perfusate), and acetylcholine increased NO release dose dependently with a concomitant pressure reduction. The changes in NO release were always associated with mirror image changes in the perfusion pressure. Simple pressure reduction did not interfere with the chemiluminescence. Precise titration data as well as results of some preliminary experiments using this method are presented.

Animals↗
PubMed2005

Soybean peroxidase-catalyzed oxidation of luminol by hydrogen peroxide.

Anionic soybean peroxidase Glycine max (SbP) is shown to efficiently catalyze luminol oxidation by hydrogen peroxide. Contrary to horseradish peroxidase, the presence of p-iodophenol in the reaction medium affects slightly the efficiency of SbP catalysis. A maximal intensity of chemiluminescence, produced through this enzymatic reaction, was detected at pH 8.4-8.6. Contrary to anionic palm tree peroxidase, in the presence of SbP, chemiluminescence intensity increases with the reaction buffer concentration. The detection limit of SbP in the reaction of luminol oxidation is 0.3 x 10(-12) M. Therefore, high sensitivity in combination with the long-term chemiluminescent signal is indicative of good prospects for application of this enzyme in enzyme immunoassay with chemiluminescent detection.

Catalysis↗
PubMed1984

Luminol-dependent chemiluminescence produced by neutrophils stimulated by immune complexes.

The origin of luminol-dependent chemiluminescence (CL) in neutrophils stimulated by immune complexes (IC) was investigated. It was found that CL induced by soluble IC and aggregated human gamma globulin (AHG) was glucose-independent, while insoluble IC-induced CL was diminished in the absence of glucose. AHG-induced CL was not inhibited by superoxide dismutase, catalase or 2,5-dimethyl furan, but was suppressed in the presence of phenol, sodium benzoate, sodium formate and mannitol. The CL was also inhibited by inhibitors of arachidonic acid (AA) metabolism including 5,8,11,14-eicosatetraynoic acid, nordihydroguaiaretic acid, quinacrine, indomethacin and aspirin, and by prostaglandins E1 and E2, theophylline and dibutyryl cyclic AMP. Luminol-dependent CL was also studied in cell-free systems including AA plus soybean lipoxygenase, hydroperoxyeicosatetraenoic acid plus peroxidase and xanthine oxidase plus xanthine. Our results indicate that, in neutrophils exposed to soluble IC and AHG, CL is produced and this is closely linked to the formation of free radicals during the metabolism of AA. The radical(s) involved is likely to include the hydroxyl radical. In neutrophils stimulated by large aggregates of IC or micro-organisms, superoxide anion, H2O2 and singlet oxygen are also produced as a result of activation of NAD(P)H oxidase. These oxygen species function as oxidizing agents for AA metabolism and amplify the production of hydroxyl radical along the lipoxygenase (and possibly cyclooxygenase) pathway(s).

Antigen-Antibody Complex↗
PubMed1998

Comparison of antioxidant activities of aminoguanidine, methylguanidine and guanidine by luminol-enhanced chemiluminescence.

1. The objective of this study was to investigate the ability of aminoguanidine, methylguanidine and guanidine to inhibit free radicals or metabolites generated by either stimulated human leucocytes or cell-free systems using luminol-enhanced chemiluminescence (CL). 2. Aminoguanidine (0.1 microM-10 mM), methylguanidine (10 microM-10 mM) and guanidine (10 microM-10 mM) produced concentration-dependent inhibition (96+/-0.1%, n=7, 59+/-1.3%, n=6, and 62+/-3%, n=6, P<0.05 at 10 mM, respectively) in FMLP-stimulated leucocytes CL. 3. In cell-free experiments, hydrogen peroxide (H2O2), hypochlorous acid (HOCl), hydroxyl radical and peroxynitrite-induced CL responses were initiated by hydrogen peroxide (3.5 mM), NaOCl (50 microM), FeSO4 (40 nM) and peroxynitrite (20 nM), respectively. Aminoguanidine, methylguanidine and guanidine produced concentration-dependent inhibition in H2O2-(69+/-0.7%, n=7, 26+/-1%, n=6, and 15+/-0.5%, n=6, at 1 mM, respectively) and HOCl-(84+/-0.3%, n=6, 50+/-1%, n=6, and 29+/-1%, n=7, at 1 mM, respectively) induced luminol CL. Peroxynitrite-induced CL was markedly attenuated in a concentration-dependent manner by aminoguanidine (99+/-0.1%, n=6, at 10 mM), methylguanidine (5+/-0.2%, n=6, at 10 mM) and guanidine (27+/-0.4%, n=7, at 10 mM). However, inhibition with aminoguanidine was found to be more marked than with methylguanidine and guanidine. Aminoguanidine (95+/-0.5%, n=6, at 1 mM) and methylguanidine (25+/-1%, n=6, at 1 mM), but not guanidine (2+/-1%, n=6, at 1 mM), significantly decreased ferrous iron-induced CL. 4. Collectively, these data suggest that aminoguanidine and a high concentration (> or = 0.1 mM) of methylguanidine have direct scavenging activities against H2O2, HOCl, hydroxyl radical and peroxynitrite. Guanidine, at a high concentration (> or = 0.1 mM), scavenges H2O2, HOCl and peroxynitrite, but not the hydroxyl radical. These direct scavenging properties may contribute to inhibitory effects of these compounds on human leucocyte CL.

Antioxidants↗
PubMed1995

Development of a novel luminol-related compound, 3-propyl-7,8-dihydropyridazino-[4,5-g]quinoxaline-2,6,9(1H)- trione, and its application to hydrogen peroxide and serum glucose assays.

Manual and flow injection methods with chemiluminescence detection were developed for the determination of hydrogen peroxide (H2O2) using a novel luminol-related compound, 3-propyl-7,8-dihydropyridazino[4,5-g]quinoxaline-2,6,9(1H)-trione (PDIQ), having a higher efficiency than luminol. The methods are based on the chemiluminescence produced by the reaction of H2O2 with PDIQ in the presence of microperoxidase in alkaline media. Detection limits for manual and flow injection methods are 13 pmol per 100 microliter of test solution and 1.3 pmol per 100 microliter injection volume, respectively, at a ratio of chemiluminescence intensities (or peak heights) of test to blank of 2. The manual method was applied to the determination of glucose in human serum. The method correlated well with the conventional spectrophotometric method (4 = 0.998).

Blood Glucose↗
PubMed2004

A general chemiluminescence method for the determination of surfactants based on its quenching effect on the luminol-NaIO4-cyclodextrin reaction.

Here we report that all types of surfactant could be simply and sensitively determined, by directly quenching the chemiluminescence (CL) between luminol and NaIO4 in a basic solution containing one polyhydroxyl compound such as cyclodextrin (CD), glucose or glycerol. This specific quenching effect was attributed to the change of the microenvironment of the CL reaction, caused by the addition of various surfactants. Based on this fact, the potential use of this CL reaction was exemplified by the cationic surfactant CTMAB, anionic surfactant SDS and non-ionic surfactant Triton X-100. It was found that the measurable range of CTMAB, SDS and Triton X-100 were 4.0 x 10(-6)-4.0 x 10(-4) M by using a basic CD-luminol-NaIO4 CL reaction. With our simple setup, CTMAB, SDS and Triton X-100 were detectable at a concentration as low as 2 microM. Overall, this new CL reaction is quite promising for the post-column determination of surfactant mixtures.

Animals↗
PubMed1981

Alloxan-induced luminol luminescence as a tool for investigating mechanisms of radical-mediated diabetogenicity.

Chemiluminescence of luminol in a cell-free system was used to investigate the mechanism of alloxan-dependent free-radical generation. In the presence of alloxan and reduced glutathione (GSH), luminescence was greatly stimulated by FeSO4. Replacing GSH by oxidized glutathione or NAD(P)(H), or replacing FeSO4 by CuSO4, ZNSO4 or FeCl3, did not yield chemiluminescence. The chemiluminescence of a mixture of alloxan. GSH, FeSO4 and luminol was inhibited by catalase, superoxide dismutase, scavengers of hydroxyl radicals (sodium benzoate, n-butanol, D-mannitol, dimethyl sulphoxide) or metal-ion chelators (EDTA, diethylenetriaminepenta-acetic acid, diethyldithiocarbamate. desferroxamine), D-glucose, L-glucose, D-mannose, D-fructose, 3-O-methyl-D-glucose, NAD+, NADH, NADP+ or NADPH, but not by urea or enzymically inactive superoxide dismutase. The results support the hypothesis that the diabetogenic action of alloxan is mediated by hydroxyl radicals generated in an iron-catalysed reaction. Protection against alloxan in vivo depends both on the chemical reactivity of protector with radicals or radical-generating systems and on the stereospecific requirement of some strategic site in the B-cell.

Alloxan↗
PubMed2004

Zymosan-induced luminol-dependent chemiluminescence response of circulating and extravasated leukocytes in experimental sepsis.

This study examines a concurrent profiling of circulating and extravasated polymorphonuclear leukocytes (PMNs) in a rat model of experimental sepsis. Fecal peritonitis was induced in Wistar male rats by intraperitoneal instillation of a fecal suspension in saline (1:1 w/v). Blood and peritoneal fluid were collected 8 h following fecal inoculation for the evaluation of inflammatory response of PMNs using zymosan-induced luminol-dependent chemiluminescence. Fifty microliters of pre-diluted blood or peritoneal fluid samples were mixed with 150 microl of reaction mixture (4 x 10(-4) M luminol+50 microg opsonized zymosan+0.1% gelatin in Hank's balanced salt solution) and the chemiluminescence signal was measured in a luminometer at 37 degrees C. Fecal peritonitis caused a significant leukocytopenia (3540+/-297 mm(-3) versus control value of 7525+/-711 mm(-3), p < 0.001) accompanied by massive infiltration of PMNs in the peritoneal cavity (34700+/-4006 versus 7325+/-425 mm(-3), p < 0.001). The phagocytic activity of circulating blood PMNs was down-regulated whereas a significant up-regulation was observed in the activity of PMNs from peritoneal fluid. In conclusion, this study clearly demonstrates sepsis-induced alterations in both blood and peritoneal fluid PMNs and their quantitative assessment may be helpful in disease evaluation and designing effective therapies.

Animals↗
PubMed2004

Detection of superoxide and peroxynitrite in model systems and mitochondria by the luminol analogue L-012.

In the present study we investigated the specificity and sensitivity of the chemiluminescence (CL) dye and luminol analogue 8-amino-5-chloro-7-phenylpyrido[3,4-d]pyridazine-1,4-(2H,3H) dione (L-012) to detect reactive oxygen species (ROS) such as superoxide, peroxynitrite and hydrogen peroxide in cell free systems as well as in isolated mitochondria. The results obtained by L-012 were compared with other CL substances such as luminol, lucigenin, coelenterazine and the fluorescence dye dihydroethidine. The results indicate that the L-012-derived chemiluminescence induced by superoxide from hypoxanthine/xanthine oxidase (HX/XO) or by 3-morpholino sydnonimine (SIN-1)-derived peroxynitrite largely depends on the incubation time. Irrespective of the experimental conditions, L-012-derived CL in response to HX/XO and SIN-1 was 10-100 fold higher than with other CL dyes tested. In a cell-free system, authentic peroxynitrite yielded a higher L-012-enhanced CL signal than authentic superoxide and the superoxide-induced signal in cell-free as well as isolated mitochondria increased in the presence of equimolar concentrations of nitrogen monoxide (NO). The superoxide signal/background ratio detected by L-012-enhanced CL in isolated mitochondria with blocked respiration was 7 fold higher than that obtained by the superoxide sensitive fluorescence dye dihydroethidine. We conclude that L-012-derived CL may provide a sensitive and reliable tool to detect superoxide and peroxynitrite formation in mitochondrial suspensions.

Animals↗
PubMed1998

Luminol luminescence induced by oxidants in antioxidant-deficient yeasts Saccharomyces cerevisiae.

Luminol chemiluminescence induced in the presence of yeast cells and yeast cell homogenates was significantly induced by exogenous oxidants (hydrogen peroxide and menadione). tert-Butyl hydroperoxide did not stimulate chemiluminescence by itself but augmented menadione-induced chemiluminescence. Comparison of yeast strains deficient in catalase, superoxide dismutase or glutathione showed that only glutathione-deficient strains showed elevated chemiluminescence in this system. These results support the idea that more reactive species than hydrogen peroxide and superoxide are critical in the induction of luminol chemiluminescence.

Acatalasia↗
PubMed1997

Influence of nitric oxide on luminol-enhanced chemiluminescence measured from porcine-stimulated leukocytes.

The influence of endogenous nitric oxide (NO) and NO-releasing compounds on free radical release from porcine leukocytes was investigated by luminol-enhanced chemiluminescence (CL). The direct free radical-scavenging activity of the compounds was determined by a cell-free system using xanthine plus xanthine oxidase (X + XO). The NO donor, N-(2-hydroxyethyl)nicotinumide nitrate (nicorandil), markedly inhibited CL generated by phorbol myristate acetate (PMA)-stimulated leukocytes. In addition, nicorandil and S-nitrozo-N-acetylpenicillamine (SNAP) both decreased CL generated by X + XO. Conversely, C87 3754, a NO-releasing sydnonimine, decreased free radical release from leukocytes only when preincubated with the cells and had no effects on the X + XO system. None of the NO donors inhibited peroxynitrite-generated CL. L-, but not D-, arginine inhibited PMA-activated free radical generation without affecting X + XO-induced CL. L-Canavanine, N omega-nitro-L-arginine (L-NNA), and L-nitro-arginine methyl ester (L-NAME), inhibitors of the NO pathway, augmented PMA-induced CL. However, L-canavanine, but not L-NNA and L-NAME, produced a significant inhibition of X + XO-induced CL. It is concluded that endogenous NO may play an important role in the measurement of free radicals released from porcine leukocytes, assessed by luminol-enhanced CL, and that compounds with NO-releasing properties decrease CL, possibly by interfering with free radical generation.

Animals↗
PubMed2003

Coenzyme Q1-catalyzed luminol chemiluminescent assay for rapid antimicrobial susceptibility testing of Mycobacterium bovis.

Coenzyme Q1 is herein proposed as the best catalyst among coenzymes Q and vitamins K for quinone-catalyzed luminol chemiluminescent assays applied to rapid determination of viability or rapid antimicrobial susceptibility tests of Mycobacterium bovis. Luminol chemiluminescence intensity (LCI) was determined 10 min after the incubation of M. bovis with coenzyme Q1, and was proportional to CFU (colony-forming unit)/ml in the range of 9,000 to 2,250,000. LCI depended on the the production of the superoxide anion (O2-) rather than H2O2 during a 10-min incubation of M. bovis with coenzyme Q1, as superoxide dismutase reduced LCI more effectively than catalase. The minimal inhibitory concentrations (MICs) of 10 kinds of antituberculous agents estimated on the basis of decrease in LCI after one or two days' cultivation were in good agreement with MICs determined by turbidity analysis, which requires upwards of 1 week to complete.

Antibiotics, Antitubercular↗
PubMed1983

Role of myeloperoxidase in luminol-dependent chemiluminescence of polymorphonuclear leukocytes.

When polymorphonuclear leukocytes (PMNL) and soluble or particulate matter interact, the cells produce chemiluminescence, linked to activation of the oxidative metabolism of the cells. PMNL isolated from a patient with a myeloperoxidase deficiency were found to produce almost no luminol-dependent chemiluminescence, despite a pronounced production of superoxide anions (O2-). The chemotactic peptide formylmethionyl-leucyl-phenylalanine induced a two-peak chemiluminescence response in control PMNL. The response was modified, both in magnitude and in time-course, when the cells were incubated at 22 degrees C for 120 min. Addition of purified myeloperoxidase to the PMNL lacking this enzyme, before stimulus addition, resulted in a chemiluminescence response. In the response to formylmethionyl-leucyl-phenylalanine, only one peak, corresponding to the initial peak of control PMNL, was found. This indicated that luminol-dependent chemiluminescence is dependent on and directly related to the presence of myeloperoxidase in PMNL and that both intra- and extracellularly located myeloperoxidase has to be taken into account when interpreting the cellular response assayed as chemiluminescence.

Cytochalasin B↗
PubMed1984

Intra- and extracellular events in luminol-dependent chemiluminescence of polymorphonuclear leukocytes.

When polymorphonuclear leukocytes (PMNL) and soluble or particulate matter interact, the cells produce chemiluminescence. Luminol-dependent light emission from PMNL is linked to the myeloperoxidase (MPO)-H2O2 system. Light emission from a cell-free MPO-H2O2 system was found to be totally inhibited by human serum albumin (HSA), and since HSA is a large molecular protein that does not readily gain access to intracellular sites of PMNL, it could be used to determine the importance of extra- and intracellular events in PMNL chemiluminescence. In studies with cells from an MPO-deficient patient, we found that HSA inhibited more than 90% of extracellularly produced chemiluminescence. The chemotactic peptide formylmethionyl-leucyl-phenylalanine induced a two-peak chemiluminescence response in normal PMNL, and addition of HSA reduced the first peak, whereas the second peak was unaffected. This result indicated that the first peak was a result of extracellular reactions and the second peak was a result of intracellular reactions of the MPO-H2O2 system. Most of the phorbol myristate acetate-induced response in normal PMNL was due to intracellular events. Furthermore, chemiluminescence of intracellular origin seems to be limited not by generation of oxidative metabolites but by diffusion of luminol into the cells.

Humans↗
PubMed1985

Pattern of formylmethionyl-leucyl-phenylalanine-induced luminol- and lucigenin-dependent chemiluminescence in human neutrophils.

The stimulation of neutrophils by formylmethionyl-leucyl-phenylalanine results in a bimodal luminol-dependent chemiluminescence pattern. We observed, however, only a single peak chemiluminescence pattern in the response to the peptide when we used lucigenin as an amplifying substance. We suggest that lucigenin, the larger molecule, (510 daltons; luminol is 177 daltons) only exerts an extracellular effect.

Acridines↗