Disease relevance of Quin 2

• Cytoplasmic free calcium concentration (Ca2+)i was measured in neutrophils from patients with the classical X-linked form of chronic granulomatous disease (CGD) by trapping the fluorescent calcium indicator Quin 2 in intact cells [1].
• We employed an intracellularly trapped fluorescent probe of Ca2+, Quin 2, to measure [Ca2+]i in GH3 cells, cloned rat pituitary tumor cells [2].
• Intradermal or spinal injection of intracellular calcium modulators (TMB-8 and Quin-2), which had no effect on nociception in control rats, significantly attenuated and together eliminated ddC and suramin-induced mechanical hypersensitivity [3].
• To test this hypothesis directly, we measured the cytosolic free Ca2+ concentration ([Ca2+]i) in two hormone-responsive human (SaOS-2 and G-292) and two rat osteosarcoma cell lines (Ros 25/1 and Ros 17/2.8) and in primary cultures of bone cells from neonatal mouse calvaria using the fluorescent Ca2+ indicator Quin 2 [4].
• These results suggest that Quin 2 causes toxicity by chelating iron or by activating some cellular process(es) that is dependent on the presence of iron or Ca++ [5].

High impact information on Quin 2

• A major requirement of any intracellular Ca2+ indicator is that it should not disturb intracellular Ca2+ homeostasis and Quin-2 is generally considered to be satisfactory in this respect [6].
• This constraint on cell size was removed by the development of the fluorescent Ca2+ -sensitive dye Quin-2 and its acetoxymethyl ester, which can be introduced into a wide range of cell types [6].
• Using the calcium-sensitive probe Quin 2/AM, FMLP induced an increase in fluorescence of up to 51% in adult PMN (10) [7].
• Using the fluorescent dye Quin 2, we have investigated the effects of 1,25(OH)2D and 24,25(OH)2D on cytosolic calcium levels in hepatocytes [8].
• The cytoplasmic ionized calcium was measured with the fluorescent probe, Quin 2, which indicated a resting level of 83 nM free calcium in unadhered monocytes [9].

Chemical compound and disease context of Quin 2

• This hyperalgesia is prevented by sympathectomy and suppressed by the calcium antagonists Quin 2 and verapamil [10].
• Using Fura-2 and Quin-2 loaded C6 rat glioma cells, it was shown that Cd2+ ions strongly interfered with the ET-1 induced Ca(2+)-influx in C6 glioma cells (IC50 approximately 10 microM) [11].

Biological context of Quin 2

• Prevention of the rise in cytosolic Ca2+ normally associated with platelet activation with the permeant Ca2+ chelator, Quin-2, inhibits formation of lamellipodial networks but not filopodial bundles after glass contact and reduces the cytochalasin B-sensitive nucleation activity by 60% after thrombin treatment [12].
• Quin-2 loading inhibited insulin-stimulated glucose transport (IC50, 26 microM quin-2 AM) without affecting basal activity [13].
• Use of the fluorescent calcium chelator Quin-2 and consideration of the ATP concentration dependence on the unfolding rate has allowed the intrinsic kinetics to be linked to the accepted reaction scheme for actin denaturation [14].
• Platelet aggregation induced by PdBu plus adrenaline was not inhibited by a high intracellular concentration of the calcium chelator Quin-2 [15].
• The effect of the intracellular calcium chelator Quin-2 on the platelet phosphoinositide metabolism, protein phosphorylation and morphology [16].

Anatomical context of Quin 2

• Total calcium content, determined by atomic absorption spectroscopy, Ca2+ influx, and cytosolic free Ca2+ concentration ( [Ca]i), estimated by a method involving the incorporation of a Ca2+ chelator (Quin 2), were measured in erythrocytes from beta-thalassemic (beta-thal) and hemoglobin C (CC) patients [17].
• Blockage of cytosolic calcium increases induced by thrombin by loading with the cell permeant calcium chelator Quin-2 AM inhibited GPIb-IX centralization by 70%, but did not prevent its association with the activated cytoskeleton [18].
• Studies show that the chlorotetracycline technique is useful for the monitoring of calcium uptake and release by the platelet organelles, and suggests that the Quin 2/chlorotetracycline technique will be useful as a diagnostic of both physiological and pathological activation mechanisms [19].
• If the macrophages were loaded with high doses of Quin 2 or another intracellular chelator, TMB-8, M phi-CF production decreased and cytotoxic activity was impaired [20].
• To better understand the relation between cell calcium and exocytotic secretion, a quantitative dependence of adrenal catecholamine secretion on cytosolic free calcium has been determined for isolated, intact, bovine chromaffin cells, using the fluorescent probe Quin-2 [21].

Associations of Quin 2 with other chemical compounds

• Chelation of extracellular calcium by EGTA prevented the CO2-induced rise in cell calcium measured with the intracellular fluorescent dyes Quin 2 or Fura 2 and also prevented recovery of cell pH [22].
• When the change in cell calcium was buffered by loading the cells with high concentrations of Quin 2, the CO2-induced decrease in pH did not return back to basal levels [22].
• We have studied the changes in membrane-bound and cytoplasmic calcium in PMN and PMN devoid of granules and nucleus by quantifying changes in chlorotetracycline (CTC) and Quin 2 fluorescence and comparing their relation to O(2) release [23].
• Ca2+ release triggered by inositol trisphosphate (Ins(1,4,5)P3) has been measured in saponin-permeabilized hepatocytes with 45Ca2+ or Quin 2 [24].
• However, the initial EGF-stimulated formation of inositol phosphates was substantially diminished in cells loaded with the Ca2+ chelator Quin 2/AM [25].

Gene context of Quin 2

• Inhibition of IL-1 production by interfering with intracellular Ca2+ trafficking in Quin 2/AM-loaded monocytes may be associated with the inhibition of PKC and calmodulin activity [26].
• When monocytes were labelled with Quin 2/AM, IL-1 production by monocytes stimulated with PT and LPS was markedly suppressed [26].
• Intracellular free calcium concentrations were measured by Quin-2 fluorescence assays in Chinese hamster ovary cells stably transfected with the canine C5a receptor [27].
• The concentration of free intracellular Ca2+ ions is also affected by IFN-alpha and IFN-gamma activation, as monitored by the fluorescent probe, Quin 2 [28].
• Using the chromophoric Ca2+ chelators Quin 2 and 5,5'-Br2BAPTA, we have now determined the Ca2+ affinity of recombinant fragments containing EGF modules 1-3, 1-4, 2-3, and 2-4 [29].

Analytical, diagnostic and therapeutic context of Quin 2

• The number of sites and their affinities were determined from Ca2+ titration in the presence of the chromophoric chelator Quin 2 [30].
• After treatment of Quin 2-loaded hepatocytes with cyclosporine, both the amplitude and duration of the vasopressin-induced rise in the cytosolic free Ca2+ are increased [31].
• In this report, we describe the marriage of flow cytometry and Quin 2 technology, which permits discrimination of Ca++ mobilization by subpopulations of cells, as well as in whole populations [32].
• Using stopped-flow fluorometry with three different fluorescence probes [2-[(1-pyrenyl-butyryl)oxy]stearic acid, chlortetracycline and Quin 2], we have studied initial stage of T lymphocyte activation after interleukin 2 (IL-2) binding to a specific cell-surface receptor [33].
• METHODS: PMNs were separated by density centrifugation and [Ca(2+)](i) was determined by spectrofluorimetry using Quin 2/AM fluorescent dye [34].

References