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The chemiluminescence of the luminol-H2O2 system is found for the first time to be remarkably enhanced by the Ce(IV) complexes of cyclodextrin dimers.
Two lignans of the tetrahydrofuran type, di-O-methyltetrahydrofuroguaiacin B (1) and (+)-veraguensin (2) were isolated from fruits and leaves of Illicium floridanum Ellis (Illiciaceae). These compounds are the first genuine lignans isolated from the genus Illicium. We investigated their radical scavenging potency towards 1,1-diphenyl-2-picrylhydrazyl radical reagent and their influence on luminol enhanced chemiluminescence (CHL) induced by different stimuli in human polymorphonuclear neutrophils (PMN). Both compounds were inactive in the TLC assay for chemical radical scavenge. In the PMN assay, the symmetric lignan 1 at concentrations below 1.0 microM displayed a strong inhibition of CHL induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP). At concentrations above 5 microM, 1 led to a pronounced increase of fMLP induced CHL. When CHL was stimulated with opsonized zymosan, both compounds were completely inactive. Thus, 1 must interfere selectively with a step in the signal cascade evoked by fMLP. In addition to their known PAF-receptor antagonism tetrahydrofuran lignans may thus also interfere with inflammatory responses by inhibition of free radical formation.
1. The metabolism and disposition of Luminol (LMN, 3-aminophthalhydrazide), a widely used forensic and laboratory reagent that chemiluminesses upon oxidation, was determined as part of its overall toxicological characterization. 2. Radiolabelled LMN was well absorbed, metabolized and excreted following p.o. administration of a range of doses. About 90% of the total dose was recovered within 24 h of administration in urine in the form of two metabolites identified as LMN N8-glucuronide and LMN N8-sulphamic acid. 3-Aminophthalic acid, the oxidative product of LMN in the light-emitting reaction, was apparently not formed in vivo. 3. Metabolism and disposition of an i.v. administered dose was similar to that following gavage. Little or no LMN-derived radioactivity was present in tissue within 12 h post-dosing. Excretion of radioactivity in bile following i.v. injection was minimal (approximately 8% of the total dose in 6 h) and consisted of the same urinary-excreted glucuronide and sulphate conjugates. 4. LMN was not absorbed dermally in rat, potentially a major route of exposure to human. If the fate of LMN is similar between species, this compound should have little potential for either dermal absorption, bioaccumulation in tissues following other routes of exposure or chronic toxicity in humans.
Increased colonic cell proliferation (CCP) has been reported in patients with colonic neoplasia. Previous studies in rats suggest that increased CCP is closely related to increased reactive oxygen metabolite (ROM) production. We hypothesized that, in humans, ROM production is also involved in increased CCP. Using a chemiluminescence probe, we estimated the levels of ROMs in the rectal mucosa of 37 patients who previously had colonic neoplasia (14 with cancer and 23 with polyps) and 20 control subjects who had normal colonoscopic examination and no history of colonic neoplasia. Normal-appearing rectal mucosa of patients with colonic neoplasia contained significantly higher levels of luminol-enhanced chemiluminescence (LECL) than rectal mucosa of control subjects (p < 0.01). There was no difference in LECL levels between patients with polyps and patients with cancer. Four of 20 controls and 31 of 37 patients had LECL levels 1,000 cpm/mg protein (positive and negative predictive values of 89% and 73%, respectively). Addition of indomethacin, a specific cyclooxygenase inhibitor, to the tissue suspension significantly decreased LECL levels. These preliminary data suggest that 1) ROMs may be involved in both the rate of CCP and the process of malignant cellular transformation, 2) oxidation of arachidonic acid via the cyclooxygenase pathway significantly contributes to the production of ROMs in rectal mucosa, and 3) measurement of the levels of LECL produced by the rectal mucosa may be a sensitive marker to screen for colonic neoplasia.
Aqueous extracts of cotton bracts inhibited luminol-dependent chemiluminescence of phagocytosing alveolar macrophages. The inhibitory compounds were partitioned into organic solvents. Chromotographic analysis indicated that these compounds were either lacinilene C or its 7-methyl ether and scopoletin. The fact that the inhibitory activity of these compounds was always less than that of the total extract suggests synergistic action. These compounds may function as etiological agents of byssinosis.
The effect of electron-beam intraoperative radiotherapy (IORT) with radiosensitizer sanazole (drug AK-2123) on the functional activity of neutrophils and monocytes in patients with gastric cancer was studied with the use of luminol-amplified chemiluminescence. Sanazole was administered intravenously in a dose of 1.2 g/m2, 30 min before IORT. After resection of the tumor a single dose of 10 Gy was given to the field of regional lymph collectors and the bed of the removed tumor applying a small-size betatron MIB-6E. Cells were separated and chemiluminescence was estimated on the 1-st day before and on the 3-d day and 2-d week after IORT with sanazole. Insignificant effect on the zymosan- or phorbol-12 -myristate-13-acetate (PMA)-stimulated chemiluminescence was observed in this group, although there was found a considerable increase of chemiluminescence of neutrophils in response to zymosan and PMA in 5 from 8 patients, and chemiluminescence of monocytes--in 3 from 8 patients. Correlation between individual indices of zymosan- and PMA-stimulated chemiluminescence of neutrophils before IORT with sanazole was not high, r = 0.71, but it increased significantly to r = 0.91 on the 3-d day and to r = 0.96 on 2-d week after treatment. Correlation between individual indices of stimulated chemiluminescence of monocytes before IORT with sanazole was r = 0.90, and increased to r = 0.99 on the 3-d day and to r = 0.96 on the 2-d week after treatment. So, it is indicative of a correcting effect of the combined treatment including IORT with sanazole administration on the functional activity of neutrophils and monocytes, and the absence of functional disturbances of these cells.
The effect of interferon-alpha (rIFN-alpha 2) on modulating the luminol-dependent chemiluminescence (CL) response evoked by Zymosan or phorbol myristate acetate (PMA) has been studied in heparinized whole blood as well as isolated peripheral blood leukocytes derived from cancer patients and healthy blood donors. The cancer patients, diagnosed with chronic leukemia or lymphoma or solid cancer, were under rIFN-alpha 2 therapy. The CL emission to both Zymosan or PMA was enhanced in the whole blood of the patient's group in comparison to whole blood of healthy blood donors. CL reactivity induced in Dextran-sedimented leukocytes derived from neoplasia patients and healthy blood donors did not differ in the two groups. CL reactivity to Zymosan or PMA could be potentiated when whole blood samples or isolated leukocytes of patients or healthy blood donors were incubated in vitro with rIFN-alpha 2 in the range of 0.001-1000 U/ml prior to addition of CL-stimulating agents. rIFN-alpha 2 itself without adding further agents did not stimulate CL reactivity. Therefore, enhanced CL reactivity to PMA or Zymosan observed in the whole blood of the patients' population appears to be due to the presence of interferon in serum blood components as a consequence of IFN-infusion rather than to other symptoms or treatments of the neoplastic diseases, since the relative CL enhancement in patients is abrogated when isolated blood leukocytes are used for CL assay.
A luminol-enhanced chemiluminescence (CL) assay was developed to evaluate type III group B streptococcal opsonins. Sera from 11 adults that contained high (greater than 25 microgram/ml), intermediate (3-24 microgram/ml), or low (less than 2 microgram/ml) antibody concentrations were assessed by CL, indirect immunofluorescence (IF), and bactericidal assays. Total CL activity correlated with antibody concentration (P less than 0.005), IgG- and C3-IF values, and phagocytic and bactericidal indices. Heat-stable CL activity correlated with antibody concentration (P less than 0.0001) and was related to IgG-IF values and phagocytic indices. Significant bactericidal activity was demonstrated in all sera containing greater than 2 microgram of antibody/ml, but no bactericidal activity was observed in heat-inactivated sera. Adsorption of heated sera with type III group B Streptococcus abolished CL activity, whereas CL values of MgEGTA-chelated sera were approximately 80% of untreated sera. Thus, type-specific antibody in addition to heat-labile serum factors, including those of the alternative complement pathway, contribute to opsonization of type III group B Streptococcus.
The factors involved in the in vitro interaction of two strains of Chlamydia trachomatis with polymorphonuclear leukocytes were studied by employing the technique of luminol-dependent chemiluminescence. Unopsonized, partially purified elementary bodies of chlamydia failed to induce a significant chemiluminescence response when compared with serum-activated zymosan (less than 90%). Opsonization of the chlamydia with human sera greatly enhanced the chemiluminescence response. This enhancement was independent of the presence or absence of antibody specific for chlamydia or of complement. Primate serum had 77% of the activity of human serum; nonprimate sera (sheep, cow, horse, and rabbit) demonstrated substantially less activity. The magnitude of the chemiluminescence response observed with opsonized chlamydia was also dependent on the chlamydia-to-polymorphonuclear leukocyte ratio, with the greatest effect seen at 10:1. Chlamydia opsonized with human sera containing less than 100 mg of IgG/dl did not stimulate chemiluminescence more than did unopsonized chlamydia. These results suggest that human IgG may interact with C. trachomatis independent of specific antibody-binding sites.
When human polymorphonuclear leukocytes (PMN) were attached to glass coverslips, cells always spread and formed reactive oxygen species prior to any experimental stimulation. To avoid this, a polyvinylidine chloride film was used as an inactive substance to place the cells. Cells engaged in phagocytosis on the film exhibited a specific H2O2-mediated luminol chemiluminescence (LCL) at the cell-particle interface; the cells stimulated with 12-O-tetradecanoylphorbol-13-acetate became aggregated and the LCL was observed at the cell-cell contact. These results corresponded well with those obtained by an electron microscopic H2O2-demonstration method.
When mouse polymorphonuclear leukocytes (PMNs) sensitized with rabbit antibody to mouse Ehrlich ascites tumor cells were stimulated by Staphylococcus aureus Cowan I cells, a conspicuous luminol-dependent chemiluminescence was observed in the absence of opsonin. The profile of the chemiluminescence (CL) response evoked by staphylococcal cells from antibody-sensitized PMNs had two peaks. An initial peak, observed within 1 min after stimulation, was sharp and high and a second peak, observed about 5 min after stimulation, was low and extended. The CL response of antibody-sensitized PMNs stimulated by S. aureus Cowan I cells was dose-dependently blocked by preincubation with soluble SpA. Cells of a mutant derived from S. aureus Cowan I strain with trace amounts of cell-bound SpA failed to stimulate the antibody-sensitized PMNs to generate the CL response. The antibody-sensitized PMNs were found to phagocytize SpA-bearing S. aureus cells even in the absence of opsonic serum. These results suggest that the observation presented here might provide a useful tool for the investigation of CL response of PMNs.
We compared the luminol-dependent chemiluminescence (CL) response of peripheral blood from severely burned patients with that from normal controls to evaluate the primary defense level against bacterial infection in the patients. The CL was measured upon addition to diluted whole blood of a soluble stimulus, phorbol myristate acetate (PMA) or particulate stimuli such as bacteria or zymosan without special opsonization. In the early post-burn days, the initial rate of whole blood CL induced with the particulate stimulus was much lower than that in the normal controls, whereas the rate was higher when PMA was used as a stimulus. The number of granulocytes in the patients' blood had increased and isolated polymorphonuclear leukocytes (PMNs) from the patients exhibited higher CL responses to the particulate or soluble stimulus as compared with those of normal controls. The results suggest that the PMNs in burn patients were activated and normally mobilized in the early post-burn period but the opsonizing capacity in the blood decreased. In fact, the serum levels of complement, immunoglobulins and fibronectin were found to be lower in the blood from the patients than those from normal controls and a supplement of freshly frozen plasma of human immunoglobulin preparations restored the initial rate of the whole blood CL upon phagocytosis. The prognosis is still poor when severe infection occurs in the patients with decreased CL response of whole blood. Recombinant human granulocyte colony-stimulating factor (rh G-CSF) enhanced the CL response of PMNs from burn patients. The administration of rhG-CSF may be useful for decreasing the morbidity of severe infection following burn injury in the near future.
At concentrations of 10 micrograms/ml and greater, dithranol (anthralin) caused an intense, dose-related activation of luminol-enhanced chemiluminescence (LECL) of human neutrophils and also increased oxygen consumption by these cells. Activation of LECL, which was maximal with 40 micrograms/ml dithranol, occurred promptly, peaked at 3-5 min, then declined. Dithranol-mediated stimulation of LECL was inhibited by catalase and by the protein kinase C inhibitor, H-7. Neutrophils from individuals with chronic granulomatous disease were unresponsive to the pro-oxidative effects of dithranol. At concentrations of 2.5 micrograms/ml and less, dithranol did not directly activate the LECL responses of neutrophils. However pre-treatment of neutrophils with dithranol at concentrations of 0.5-2.5 micrograms/ml increased the LECL-responses of cells subsequently stimulated with calcium ionophore and opsonized zymosan. These observations demonstrate two distinct dose-related, pro-oxidative interactions of dithranol with human neutrophils: low-dose priming and high-dose activation of oxidant generation. Since phagocyte-derived reactive oxidants are immunosuppressive, these pro-oxidative interactions of dithranol with human neutrophils may contribute to the pharmacotherapeutic mechanisms of this agent.
The oxidative metabolic burst of blood monocytes and polymorphonuclear leukocytes (PMN) from 22 untreated patients with Hodgkin's disease (HD) and 18 healthy subjects were studied. Monocytes and PMN were enriched by density centrifugation and in vitro activated by zymosan. The oxidative metabolism was measured by luminol-enhanced chemiluminescence (CL). The CL of the patients' monocytes and PMN was higher than that of controls (P less than 0.01 and P less than 0.05, respectively). Patients with stage II-IV HD showed an increased blood monocyte CL as compared with stage I patients (P less than 0.05). Furthermore, patients with lymphocytic depletion or mixed cellularity subtype demonstrated an increased CL of PMN as compared with the remainder. Enhanced CL of phagocytes has been observed in chronic inflammatory disease and can be induced by various serum factors such as monokines and immune complexes. The present study demonstrates an increased CL of blood-borne phagocytic cells in untreated HD. Furthermore, CL of blood monocytes and PMN correlated to tumour burden and histologic subtype, respectively.
1. Formyl-methionyl-leucyl-phenylalanine (FMLP) or arachidonic acid (AA) induced luminol dependent chemiluminescence (LCL) response of rat polymorphonuclear leukocytes (PMNLs) was found to be inhibited by nitric oxide synthease inhibitors and their D-enantiomers. 2. Rat PMNLs LCL response was inhibited by NG-nitro-L-arginine methyl ester (L-NAME), D-NAME, NG-monomethyl-L-arginine (L-NMMA) or D-NMMA, in a concentration- and time-dependent manner. 3. It was observed that both L- and D-enantiomers of the arginine analogues (1000 microM) did not inhibit AA induced lucigenin-dependent chemiluminescence (LUCDCL) response and cytochrome c reduction, used for estimating the NADPH-oxidase activity in the cells and in the cell free system, respectively. 4. None of the L- and D-enantiomers had any effect on either rat basal PMNLs or AA-induced oxygen consumption. 5. In addition, neither the L nor D-enantiomers of NAME altered either AA-induced release or the activity of myeloperoxidase from rat PMNLs azurophilic granules. 6. The results obtained indicate that the attenuation of the LCL response by L- and D-enantiomers of arginine analogues, is a non-specific effect as there was no inhibition of NADPH-oxidase and MPO activity, MPO release or oxygen consumption. Therefore, the data obtained indicate that these agents should be used with caution to analyse the role of nitric oxide in rat PMNLs LCL response.
Listeria monocytogenes produces chemiluminescence in brain heart infusion broth at 37 degrees C in the presence of carbonate ions and acetaldehyde. This phenomenon can be enhanced by the use of luminol rather than acetaldehyde. Furthermore, there is direct relationship between the extent of growth and the level of luminescence which culminates at the end of the exponential growth. This property was used to study the susceptibility of this bacterium to two antiseptics, cetrimonium bromide and chlorhexidine, and to two antibiotics, ampicillin and chloramphenicol. Inhibition of chemiluminescence was proportional to the antimicrobial agents' concentrations and was complete at their minimal inhibitory concentrations.
The generation rate of free oxygen radicals as measured by maximal light intensity of luminol-enhanced chemiluminescence from peripheral blood granulocytes (PMN) stimulated with differently opsonized Staphylococcus aureus was studied in 13 patients with juvenile periodontitis (JP) and pair-matched, healthy controls. Plasma proteins related to inflammation were also assayed. When stimulated with bacteria opsonized with autologous serum, the PMN from the JP patients showed a more intensive chemiluminescence than did their pair-matched controls (p less than or equal to 0.0005). The difference was consistent but slightly reduced when using heat-treated serum (p less than or equal to 0.006) or heterologous gammaglobulin (p less than or equal to 0.19) for opsonization. When testing freeze preserved sera from 11 of the compared pairs, the sera from JP patients induced a slightly higher chemiluminescence in PMN from a healthy donor (p less than or equal to 0.031). Protein analysis of the patient sera revealed a slightly higher concentration of complement 4 (p less than or equal to 0.032) and IgM (p less than or equal to 0.030) when compared with their respective pair-matched healthy controls. The influence of other blood components contaminating our assay system was checked on healthy PMN cells. Lymphocytes, platelets, relevant amounts of ADP and serum had no effect on the chemiluminescence. In conclusion, the increased chemiluminescence of peripheral blood granulocytes from patients with juvenile periodontitis seems to be related mainly to the cells. The association with free oxygen radicals and their tissue-damaging potency might be a contributing factor in the pathogenesis of periodontal disease.
The granulocyte function in patients with juvenile periodontitis (JP) (eight men and six women, aged 13-33 yr) and sex and age matched controls was determined by the luminol enhanced chemiluminescence (CL) induced by opsonized and unopsonized bacteria or latex beads. Maximal CL induced by latex beads with or without autologus serum did not differ between the two groups. However, bacteria with or without autologous serum seemed to induce a higher maximal CL in the JP group. The difference was statistically significant for the results obtained with opsonized bacteria. Serum opsonized bacteria induced a much higher maximal CL than the unopsonized. The opsonin dependent reaction indicates a close association with the process of phagocytosis. The increased CL of granulocytes in JP could indicate the formation of extracellularly free oxygen radicals with the potential to damage tissue. These observations support a possible involvement of the granulocytes in the pathogenesis of JP.