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Chemical Compound Review

AG-K-10159     1,8-dimethyl-5-phenyl- phenazine-2,7...

Synonyms: SureCN1502460, AC1L1UMB, CTK5D9369, AR-1D5177, AKOS015916442, ...
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Disease relevance of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • Isolated kidney proximal tubules subjected to hypoxia/reoxygenation (H/R) have incomplete recovery of mitochondrial membrane potential (DeltaPsi(m)) that can be improved, but not normalized, by ATP in permeabilized cells as measured by safranin O uptake [1].
  • Evaluation of a safranin-O-stained antigen microagglutination test for francisella tularensis antibodies [2].
  • If the tibial cartilage is separated from the bony collar and cultured alone in serum-free medium, the nonhypertrophic chondrocytes also hypertrophy; the matrix loses Safranin O staining; however, some components of the matrix including type X collagen still remain after 30 days [3].
  • Safranin O-stained antigen microagglutination test for detection of brucella antibodies [4].
  • A microagglutination test with safranin-stained Francisella tularensis antigen was compared with a conventional tube agglutination test for the serodiagnosis of tularemia [5].

High impact information on 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • Although rKL-developed BMMC were safranin+ and produced substantial amounts of 35S-labeled heparin proteoglycans, they contained only minimal amounts of histamine and MC-CPA enzymatic activity relative to serosal MC [6].
  • Mast cells also developed on the glandular stomach mucosa, but these cells stained with alcian blue rather than safranin, and did not stain with berberine sulfate [7].
  • Similar bottlebrush structures were observed in the intercellular matrix of the smooth muscle cell cultures after staining with Safranin 0 [8].
  • We have evaluated this hypothesis by examining the immunofluorescent localization and concentrations of proteoglycan monomer core protein and link protein, and the concentrations of glycosaminoglycans demonstrated by safranin 0 staining, in the different zones of the bovine fetal cartilage growth plate [9].
  • Safranin O staining demonstrated that articular cartilage was well preserved in IL-6 -/- mice, whereas it was destroyed completely in IL-6 +/+ mice [10].

Chemical compound and disease context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine


Biological context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • Wild-type peritoneal mast cells had a mature phenotype characterized by differential histochemical staining with proteoglycan-reactive dyes (cells do not stain with alcian blue but stain with safranin and with berberine) and a high side scatter to forward scatter ratio by flow cytometry and were detergent resistant [16].
  • Absorbance shifts in safranine have been used as a probe to estimate the membrane potential generated under these conditions [17].
  • Histology and immunohistochemistry revealed a dramatic decrease in Safranin O staining and reduced anti-aggrecan staining (primarily in the superficial and middle cartilage layers) with OP-1 antisense treatment [18].
  • Electron microscopy was applied to demonstrate morphologic changes, and Safranin O staining was performed to analyze the relationship between apoptosis and proteoglycan depletion [19].
  • Three weeks after injection, cell death and loss of Safranin O staining had progressed, and surface fibrillation and osteophytes had developed [20].

Anatomical context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • After 12-14 days of coculture, greater than 50% of the BMMC changed histochemically to become safranin+; 30-40% of the 35S-labeled glycosaminoglycans on the proteoglycans synthesized by these cocultured mast cells were heparin, whereas heparin was not detected in the initial BMMC [21].
  • Secretory granules of the rat basophilic leukemia (RBL-1) cell, a chemically generated tumor cell line maintained in tissue culture, were shown to stain with alcian blue but not with safranin counterstain and to have sparse, small, electron-dense granules [22].
  • A phenotypic change from safranin-negative to safranin-positive cells associated with heparin-producing CTMCs was accomplished after coculture of the mast cells with fibroblast cell lines derived from normal mice or from SI/SId mice plus soluble factors [23].
  • Furthermore, expression of these receptors restored the capacity of W/Wv BMMCs to colonize the peritoneal cavity of mast cell-deficient W/Wv mice where they differentiated to safranin-positive cells with similar frequencies as wild-type BMMCs [24].
  • The alcian-blue-safranin technique delineated the maturation of mast cell granules by showing the loss of alcian-blue and increase in safranin-positive organelles presumed to reflect the increase in N-sulfated polysaccharides representing heparin [25].

Associations of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine with other chemical compounds


Gene context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • In culture, all three receptor molecules transduced functional mitogenic signals in infected interleukin-3 (IL-3)-dependent bone marrow-derived mast cells (BMMCs) and enabled their differentiation into safranin-positive mast cells resembling connective tissue-type mast cells (CTMCs) [24].
  • Hyaluronan accumulation was characterized by staining with a hyaluronan-specific binding protein and by fluorophore-assisted carbohydrate electrophoresis, while proteoglycan content was determined by alcian blue and Safranin O staining, CD44 protein expression by immunohistochemistry, and aggrecan biosynthesis by 35S-sulfate incorporation [30].
  • However, Safranin O-stained sections from the Jnk2(-/-) mice exhibited significantly less joint damage [31].
  • Treatment of normal articular cartilage with RANTES increased the release of glycosaminoglycans and profoundly reduced the intensity of Safranin O staining [32].
  • The loss of aggrecan in Safranin O-stained sections was quantified by morphometric methods [33].

Analytical, diagnostic and therapeutic context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • At 24 hr after hepatectomy, absorbance change of safranine O per milligram of mitochondrial protein increased from 15.0 +/- 2.2 X 10(-3) to 37.4 +/- 3.3 X 10(-3) per mg (p less than 0.005) [34].
  • Cartilage damage and activation of BMP signaling were studied by digital image analysis using Safranin O sulfated glycosaminoglycan staining and immunohistochemistry for phosphorylated Smads (Smads 1, 5, and 8), respectively [35].
  • End-point analyses included macroscopic joint examination, immuno- and TUNEL staining, Safranin O staining/microspectrophotometry, and tumor necrosis factor alpha (TNFalpha) convertase enzyme (TACE) inhibition assay [36].
  • In striking contrast, when triamcinolone hexacetonide was injected into the ipsilateral knee 24 hours after the intraarticular injection of iodoacetate, fibrillation was noted in only 1 of 6 samples, osteophytes were much less prominent, pericellular staining with Safranin O persisted, and cell loss was less extensive [37].
  • The preferential binding of NADP+ to reduced enzyme permits prediction of a more positive oxidation-reduction potential of the flavoprotein in the presence of NADP+; a change of about + 0.1 V has been demonstrated by titration with safranine T [38].


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