Disease relevance of Zinquin

• Zn2+ was shown to accumulate in CA1 pyramidal neurons expressing ZnT-1 mRNA after the ischemia by using zinquin, a zinc-specific fluorescent dye [1].
• Reactive changes in free intracellular zinc cation concentration ([Zn(2+)](i)) were monitored, using the fluorescent probe Zinquin, in human lymphoma cells exposed to the DNA-damaging agent VP-16 [2].
• Administration of the NO donor S-nitrosocysteine (SNOC) caused a rapid drop in the fluorescence of the zinc-specific fluorescence of the zinc probe zinquin in C6 glioma cells [3].

High impact information on Zinquin

• ZnT3 gene expression was analyzed by using real-time PCR, free zinc in brain tissue was determined by zinquin staining, and total zinc concentrations in plasma and cerebrospinal fluid were determined by atomic absorption spectrophotometry [4].
• We present that 4 has advantages in detection of apoptosis over annexin V-Cy3 and Zinquin 1 [5].
• The granules of a variety of mast cell types fluoresced intensely with the Zn-specific fluorophore Zinquin, and fluorescence was quenched by functional depletion of Zn using a membrane-permeable Zn chelator N, N, N', N'-tetrakis (2-pyridyl-methyl)ethylenediamine (TPEN) [6].
• Zinquin staining also revealed that msc2 had a marked increase in fluorescence compared with the wild type, again reflecting an increase in intracellular Zn2+ [7].
• Double labelling indicated that there was no obvious overlap between Zinquin and the hZnT4 protein, suggesting that hZnT4 was not directly involved in the transport of zinc into vesicles [8].

Biological context of Zinquin

• Cytoplasmic zinc (zinquin) was coincident, in time and location, with cell degeneration, thus implicating zinc in cell death [9].
• It is concluded that great caution should be employed when using S-nitroso compounds together with zinquin in investigations of intracellular zinc homeostasis [3].

Anatomical context of Zinquin

• Further experiments were undertaken on unilamellar liposomes to study the interaction of Zinquin and its metal complexes in membranes [10].
• Measurement of zinc in hepatocytes by using a fluorescent probe, zinquin: relationship to metallothionein and intracellular zinc [11].
• Zinquin fluorescence, confirmed by autometallography in rat kidney, indicated that consistent with its physiological role, the central glomerulus was weakly stained, whereas the epithelium that lines convoluted tubules was strongly labeled [12].
• Experiments on rat hippocampal and neocortical slices gave indications that Zinquin in its free acid form was able to diffuse across the plasma and synaptic vesicle membranes [10].
• Confocal microscopy with Zinquin, a fluorogenic Zn(2+)-specific indicator, was used for spatially and temporally resolved measurement of Zn2+ efflux from single pancreatic beta-cells [13].

Associations of Zinquin with other chemical compounds

• CONCLUSIONS: The phenomenon of Zn(II) mobilization, revealed by Zinquin, presents a new element in the process of apoptosis for investigation and may permit rapid and sensitive identification of apoptotic cells, particularly in those tissues where their frequency is low [14].
• Microspectrofluorometry with Zinquin revealed that the exposure of cultured sheep pulmonary artery endothelial cells to S-nitrosocysteine resulted in the release of N, N,N',N'-tetrakis(2. pyridylmethyl)ethylendiamine (TPEN) chelatable zinc [15].
• Zinquin fluorescence was unaffected by carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP) treatment [16].
• Sodium nitrite or an NO donor devoid of sulfhydryl groups (diethylamine NONOate) exerted no degrading effect on the Zn/zinquin fluorescence, but cysteine alone evoked a similar decline as SNOC [3].
• Employing the zinc-specific fluorescence probe Zinquin, we observed that the very low concentration of 1.9 nM A23187 significantly and rapidly raised the intracellular mobile Zn2+ content [17].

Gene context of Zinquin

• Double staining of rat kidney with Zinquin and anti-ZnT4 antibodies confirmed the in vitro observations, as Zinquin fluorescence appeared to be distinct from ZnT4 immunofluorescence [12].
• Zinc stimulation of PBMC resulted in an increase of intracellular free zinc, measured by a zinc-specific fluorescence probe, zinquin, the amount of which could be raised by substitution of neither transferrin nor insulin [18].
• Second, ZN and ZL OVA-treated mice had significant decreases in airway epithelial Zinquin fluorescence, indicating a lowered availability of Zn compared with their SAL-treated counterparts [19].
• L-Homocysteine induced a dose-dependent increase in intracellular free zinc in zinquin-loaded human aortic endothelial cells within 30 minutes, followed by the appearance of early growth response protein-1 within 60 minutes [20].

References