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Search results for: lucigenin [Bis N methylacridinium nitrate]

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#27072911   2016/04/01 To Up

2,6-Bis(benzimidazol-2-yl)pyridine as a potent transmembrane anion transporter.

2,6-Bis(benzimidazol-2-yl)pyridine was shown to exhibit potent anionophoric activity via a process of both Cl(-)/NO3(-) antiport and H(+)/Cl(-) symport. This is in sharp contrast to the finding that its corresponding N-methylated analog exhibited negligible activity and reveals the importance of the imidazolyl-NH fragments in the anion-transport process.
Chen-Chen Peng, Zhi Li, Li-Qun Deng, Zhuo-Feng Ke, Wen-Hua Chen

1084 related Products with: 2,6-Bis(benzimidazol-2-yl)pyridine as a potent transmembrane anion transporter.

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#23978851   2013/08/16 To Up

In vivo imaging method to distinguish acute and chronic inflammation.

Inflammation is a fundamental aspect of many human diseases. In this video report, we demonstrate non-invasive bioluminescence imaging techniques that distinguish acute and chronic inflammation in mouse models. With tissue damage or pathogen invasion, neutrophils are the first line of defense, playing a major role in mediating the acute inflammatory response. As the inflammatory reaction progresses, circulating monocytes gradually migrate into the site of injury and differentiate into mature macrophages, which mediate chronic inflammation and promote tissue repair by removing tissue debris and producing anti-inflammatory cytokines. Intraperitoneal injection of luminol (5-amino-2,3-dihydro-1,4-phthalazinedione, sodium salt) enables detection of acute inflammation largely mediated by tissue-infiltrating neutrophils. Luminol specifically reacts with the superoxide generated within the phagosomes of neutrophils since bioluminescence results from a myeloperoxidase (MPO) mediated reaction. Lucigenin (bis-N-methylacridinium nitrate) also reacts with superoxide in order to generate bioluminescence. However, lucigenin bioluminescence is independent of MPO and it solely relies on phagocyte NADPH oxidase (Phox) in macrophages during chronic inflammation. Together, luminol and lucigenin allow non-invasive visualization and longitudinal assessment of different phagocyte populations across both acute and chronic inflammatory phases. Given the important role of inflammation in a variety of human diseases, we believe this non-invasive imaging method can help investigate the differential roles of neutrophils and macrophages in a variety of pathological conditions.
Jen-Chieh Tseng, Andrew L Kung

1095 related Products with: In vivo imaging method to distinguish acute and chronic inflammation.

16 Arrays/Slide1 mg4 Sample Kit32-50 Sample Kit96 wells (1 kit)4 Membranes/Box8 Sample Kit48 samples16 Arrays/Slide

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#22999887   // To Up

In vivo imaging of inflammatory phagocytes.

Inflammation contributes to the pathophysiology of many diseases. In this report, we present noninvasive bioluminescence imaging methods that distinguish acute and chronic inflammation in mouse models. Systemic delivery of luminol (5-amino-2,3-dihydro-1,4-phthalazinedione) enables detection of acute inflammation largely mediated by tissue-infiltrating neutrophils, whose myeloperoxidase (MPO) activity is required for luminol bioluminescence. In contrast, bioluminescence from injection of lucigenin (bis-N-methylacridinium nitrate) closely correlates with late phase and chronic inflammation. Lucigenin bioluminescence is independent of MPO and, instead, requires phagocyte NADPH oxidase (Phox) activity in macrophages. We are able to visualize tissue inflammation resulting from wound healing, bacterial infection, foreign substance implantation, and antitumor immune responses. Given the central role of inflammation in a variety of disorders, we believe these noninvasive imaging methods can help dissect the differential roles of neutrophils and macrophages in a variety of pathological conditions.
Jen-Chieh Tseng, Andrew L Kung

2518 related Products with: In vivo imaging of inflammatory phagocytes.

5ug0.1 mg5ug2ug96 tests2ug2ug5ug1 mg48 samples2ug

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#22340120   2012/01/04 To Up

Solid-phase spectrophotometric and test determination of silicate in natural water.

Quaternary ammonium salts (QAS) of aliphatic (tetradecylammonium nitrate) and heterocyclic (lucigenine) nature immobilized onto silica surface have been proposed as effective anion-exchangers for the adsorptional extraction of silicate in the form of the reduced molybdo-silicic heteropoly anion for the successive determination in the solid phase by using spectrophotometric and visual test techniques. The interface interaction has been investigated. On the basis of the results obtained the new solid-phase spectrophotometric and visual test techniques for the direct silicon determination in the rage of its concentrations 14-400 μg L(-1) have been proposed. The tolerance limits of the major components in natural waters and other ions capable of producing heteropoly anions in the silicate determination have been reported. The techniques have been successfully applied for the silicate determination in natural waters.
Olga A Zaporozhets, Julia P Bas, Igor A Kachan, Lionel S Zinko, Valentyn I Davydov

2307 related Products with: Solid-phase spectrophotometric and test determination of silicate in natural water.

500 tests1 mg50μl96 tests500 tests

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#18568337   2008/06/21 To Up

Toxic-dose warfarin-induced apoptosis and its enhancement by gamma ionizing radiation in leukemia K562 and HL-60 cells is not mediated by induction of oxidative stress.

The purpose of this study was to test the hypothesis that warfarin may enhance free radical production and oxidative damage on cancer cells. We examined the possible concentration-dependent effect of warfarin on cytotoxicity with respect to oxidative stress on leukemia cell lines (K562 and HL-60) and normal human peripheral blood mononuclear cells (PBMC). Gamma radiation was used as a positive control agent for oxidative stress. At all concentrations of warfarin (5-200 muM), 5-amino-2,3-dihydro-1,4-phthalazinedione (luminol)- and bis-N-methylacridinium nitrate (lucigenin)-amplified chemiluminescence responses and lipid peroxidation and protein oxidation were stable after 72 h incubation at 37 degrees C. However, The 2',7'-dichlorofluorescein diacetate (DCFH-DA) oxidation was increased when cells were incubated with high concentrations (50-200 muM) of warfarin. In these concentration ranges, warfarin reduced cell growth in a dose-dependent manner, producing apoptosis. Our results also revealed that at concentrations above 5 muM, warfarin had a potentiating effect on radiation-mediated growth inhibition and apoptosis. Furthermore, marked effects were observed on leukemic cells compared with PBMC. We report here that the increase of DCFH oxidation might be due to the increase in the release of cytochrome C caused by warfarin, as cytosolic cytochrome C content was significantly elevated in the warfarin-treated cells compared with control cells, and because cotreatment with antioxidants N- acetylcysteine or 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron) was unable to prevent cytochrome C release and DCFH oxidation induced by the drug. Taken together, these results suggest that high warfarin concentrations may be toxic to leukemic cells in vitro through apoptosis, although at the pharmacological concentrations (<50 muM), warfarin has no prooxidant or cytotoxic effect on PBMC, K562, and HL-60 cells. In addition, when the treatment of leukemic cells with warfarin at concentrations above 5 muM is combined with radiation, we observed an increase in radiation-induced cytotoxicity. The mechanism by which warfarin potentiates this cytotoxicity is unclear, but it may not be directly due to toxic damage induced by warfarin-generated free radicals.
Ilhan Onaran, Sevide Sencan, Halil Demirtaş, Birsen Aydemir, Turgut Ulutin, Murat Okutan

1629 related Products with: Toxic-dose warfarin-induced apoptosis and its enhancement by gamma ionizing radiation in leukemia K562 and HL-60 cells is not mediated by induction of oxidative stress.

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#17007989   2006/09/01 To Up

(+/-)-2-Chloropropionic acid elevates reactive oxygen species formation in human neutrophil granulocytes.

(+/-)-2-Chloropropionic acid (2-CPA) is a neurotoxic compound which kills cerebellar granule cells in vivo, and makes cerebellar granule cells in vitro produce reactive oxygen species (ROS). We have studied the effect of 2-CPA on ROS formation in human neutrophil granulocytes in vitro. We found an increased formation of ROS after 2-CPA exposure using three different methods; the fluorescent probe DCFH-DA and the chemiluminescent probes lucigenin and luminol. Four different inhibitors of ROS formation were tested on the cells in combination with 2-CPA to characterize the signalling pathways. The spin-trap s-PBN, the ERK1/2 inhibitor U0126 and the antioxidant Vitamin E inhibited the 2-CPA-induced ROS formation completely, while the mitochondrial transition permeability pore blocker cyclosporine A inhibited the ROS formation partly. We also found that 2-CPA induced an increased nitric oxide production in the cells by using the Griess reagent. The level of reduced glutathione, measured with the DTNB assay, was decreased after exposure to high concentrations of 2-CPA. Western blotting analysis showed that 2-CPA exposure led to an elevated phosphorylation of ERK MAP kinase. This phosphorylation was inhibited by U0126. Based on these experiments it seems like the mechanisms for 2-CPA induced toxicity involves ROS formation and is similar in neutrophil granulocytes as earlier shown in cerebellar granule cells. This also implies that 2-CPA may be immunotoxic.
B B Aam, F Fonnum

2460 related Products with: (+/-)-2-Chloropropionic acid elevates reactive oxygen species formation in human neutrophil granulocytes.

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#15604302   2004/12/16 To Up

Systemic arterial pressure response to two weeks of Tempol therapy in SHR: involvement of NO, the RAS, and oxidative stress.

The roles of nitric oxide (NO) and plasma renin activity (PRA) in the depressor response to chronic administration of Tempol in spontaneously hypertensive rats (SHR) are not clear. The present study was done to determine the effect of 2 wk of Tempol treatment on blood pressure [mean arterial pressure (MAP)], oxidative stress, and PRA in the presence or absence of chronic NO synthase inhibition. SHR were divided into four groups: control, Tempol (1 mmol/l) alone, nitro-L-arginine methyl ester (L-NAME, 4.5 mg x g(-1).day(-1)) alone, and Tempol + L-NAME or 2 wk. With Tempol, MAP decreased by 22%: 191 +/- 3 and 162 +/- 21 mmHg for control and Tempol, respectively (P < 0.05). L-NAME increased MAP by 16% (222 +/- 2 mmHg, P < 0.01), and L-NAME + Tempol abolished the depressor response to Tempol (215 +/- 3 mmHg, P < 0.01). PRA was not affected by Tempol but was increased slightly with L-NAME alone and 4.4-fold with L-NAME + Tempol. Urinary nitrate/nitrite increased with Tempol and decreased with L-NAME and L-NAME + Tempol. Tempol significantly reduced oxidative stress in the presence and absence of L-NAME. In conclusion, in SHR, Tempol administration for 2 wk reduces oxidative stress in the presence or absence of NO, but in the absence of NO, Tempol is unable to reduce MAP. Therefore, NO, but not changes in PRA, plays a major role in the blood pressure-lowering effects of Tempol. These data suggest that, in hypertensive individuals with endothelial damage and chronic NO deficiency, antioxidants may be able to reduce oxidative stress but not blood pressure.
Licy Yanes, Damian Romero, Radu Iliescu, Valeria E Cucchiarelli, Lourdes A Fortepiani, Francisco Santacruz, William Bell, Huimin Zhang, Jane F Reckelhoff

2368 related Products with: Systemic arterial pressure response to two weeks of Tempol therapy in SHR: involvement of NO, the RAS, and oxidative stress.

100 UG1 mg 1 G1mg25 100 μg

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#14564738   // To Up

[Effect of azole derivatives on lucigenin-dependent microsome chemiluminescence].

Both metronidazole and aminotriazole increased while sanazole (drug AK-2123) decreased the NADPH/lucigenin-dependent chemiluminescence of liver microsomes of phenobarbital-treated rats. Sanazole strongly inhibited the lucigenin-dependent chemiluminescence in the enzyme system of xanthine-xanthine oxidase. Aminotriazole and metronidazole were less potent inhibitors of chemiluminescence less than sanazole. All these azole derivatives did not absorb light in the region of light emission of lucigenin. Both lucigenin and sanazole increased the rate of cytochrome c reduction by microsomes in case of using NADPH as a donor of electrons, whereas no effect of metronidazole and aminotriazole on this rate was found. The sanazole inhibition of lucigenin-dependent chemiluminescence could reflect competition between sanazole and lucigenin for electrons in the active centre of flavin reductases. Thus, microsomal NAD(P)H-reductases can be potentially involved in a bioactivation of sanazole. Lucigenin-dependent chemiluminescence cannot be used for measuring the modulating action of agents on reactive oxygen species production in the microsomes, but it may be used for luminometrical studies of enzyme complex NAD(P)H-reductases/cytochrome P450 in model systems.
I A Shchepetkin, R R Akhmedzhanov, V T Kagiia

2966 related Products with: [Effect of azole derivatives on lucigenin-dependent microsome chemiluminescence].

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#11275372   // To Up

Different kinds of reactive oxygen and nitrogen species were detected in colon and breast tumors.

Several studies have shown the involvement of reactive oxygen species (ROS; O2*-, hypochlorite, hydroxyl radical, hydrogen peroxide) in carcinogenesis. With certain pathologies, nitric oxide (NO) is formed and can interact with superoxide radical (O2*-) resulting in the propagation of the highly reactive species, peroxynitrite. In order to study the molecular mechanisms underlying the ability of reactive oxygen and nitrogen species (RONS) to mediate carcinogenesis, we have measured ROS, NO, and peroxynitrite content of cancerous tissues obtained from colon and breast carcinoma cases by chemiluminescence technique. All ROS were significantly increased in cancerous colon tissues with hypochlorite making the most important contribution and suggesting the role of inflammatory cells. NO was also increased and the peroxynitrite concentration was higher in cancerous samples. For breast carcinoma cases, only O2*- was significantly increased. Hypochlorite was not detected excluding the contribution of inflammatory cells. NO concentrations were not significantly different, therefore, ROS might originate by change in the redox state of the tissue.
G Haklar, E Sayin-Ozveri, M Yüksel, A O Aktan, A S Yalçin

1160 related Products with: Different kinds of reactive oxygen and nitrogen species were detected in colon and breast tumors.

50 ug 50 ug 50 ug 1 mg96T10 ug

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