Disease relevance of Sudan Red III

• The capacity of various Sudan III-related chemicals to prevent DMBA-induced CA paralleled their capacity to prevent DMBA-induced adrenal apoplexy and mammary cancer [1].
• The suppressive effect of Sudan III on DMBA-induced CA paralleled the dose rate of Sudan III when given in the range between 1 and 10 mg Sudan III/kg body weight; higher doses produced no additional suppression [1].
• A single feeding of 1 mg of Sudan III prevented fatal toxicity in all members of large groups of rats injected with massive doses of 7,12-dimethylbenz[a]anthracene, but 50% of the survivors developed leukemia; unprotected rats succumbed in 1--3 days [2].
• Granuloma macrophages from NC rabbits were consistently ORO-negative, contrasting with those from HC rabbits which were strongly ORO-positive, even at 4 and 7 days [3].
• We have determined the effect of beta-naphthoflavone and the azo dye, sudan III, on the level of quinone reductase mRNA in a responsive rat hepatoma cell line [4].

High impact information on Sudan Red III

• Suppression of 7,12-dimethylbenz[a]anthracene-induced chromosome aberrations in rat bone marrow cells after treatment with Sudan III and related azo dyes [1].
• Effects on lipid metabolism were examined by Oil Red O and Sudan III stainings, messenger RNA (mRNA) analysis, and electron microscopy [5].
• Foam-cell formation was demonstrated by accumulation of intracellular, Oil Red O-stained lipid droplets [6].
• Repeated feedings of 1 mg of Sudan III induced cumulative increases in the concentration of menadione reductase (EC 1.6.99.2) in liver, whereas protein concentration was unchanged [2].
• Lipid metabolism was estimated by Oil Red O staining of intracellular lipids, mRNA expression of fatty acid synthase and adipocyte lipid binding protein 2, and insulin activation of lipogenesis [7].

Chemical compound and disease context of Sudan Red III

• Murine macrophage RAW 264.7 cells either infected with C. pneumoniae or treated with the TLR4 ligand E. coli lipopolysaccharide (LPS) or the TLR2 ligand Pam(3)-Cys-Ala-Gly-OH (Pam) became Oil Red O-stained foam cells and showed increased cholesteryl ester (CE) content when cocultured with LDL [8].
• In a 23-year-old man with massive chylous pericardial effusion, oral administration of Sudan III and radio-active 131iodine-labelled triolein revealed an abnormal communication between the lymphatic system and the pericardial sac [9].

Biological context of Sudan Red III

• The effect of treatment of rats with Sudan III on the ability of the liver to transform benzo(a)pyrene (BP) to a mutagen was investigated to elucidate a possible mechanism of the Sudan III-induced prevention of chemical carcinogenesis (Huggins et al., Proc. Natl. Acad. Sci., 75:4524-4527, 1978) using a modified Ames mutagenesis test system [10].
• Hepatocellular lipid levels were profoundly reduced, as determined by Oil Red O staining and transmission electron microscopy, and fewer hepatocytic microvilli were evident, indicating impaired lipoprotein endocytosis [11].
• Intramuscular triacylglycerol (IMTG) content was determined by Oil Red O staining and gene expression was measured by quantitative PCR [12].
• Patients suffering from ACS with Oil Red O-stained macrophages had more extrathoracic concomitant pain than those without (76 vs. 50%, p < 10-8), had more neurologic symptoms (7 vs. 0%, p < 10-8), a lower differential platelet count (-49 +/- 121 vs. +85 +/- 229, p < 0.04), and higher abnormal transaminase values (28 vs. 17%, p < 0.01) [13].
• Heregulin was able to induce cell differentiation as assessed by Oil Red O staining and apoptosis as assessed by sub-G1 peak on flow cytometry and the presence of DNA fragmentation in ApopTag histochemistry staining [14].

Anatomical context of Sudan Red III

• Additionally, frozen sections stained with Oil Red O were analyzed to assess lipid accumulation in the aortic sinus [15].
• We demonstrated the histologic localization of lipid in the articular cartilage, meniscus, and synovium in calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, by staining with Sudan III [16].
• Adipocyte levels were analyzed by light microscopy and flow cytometry (FACS) after staining with Oil red O and Nile red, respectively [17].
• An eight-year-old boy with slowly progressive muscle weakness was found to have Oil red O positive vacuoles in predominanty type i muscle fibers [18].
• Oil red-O staining of the ascending aorta revealed that IL-10 gene transfer resulted in a 31% reduction in plaque surface area [19].

Associations of Sudan Red III with other chemical compounds

• Concomitantly, Asc-P remarkably accelerated the emergence of lipoprotein lipase, glycerophosphate dehydrogenase, and Oil Red O-stainable lipid droplets [20].
• The residuum of bleached substantia nigra neuromelanin and the nonoxidized and oxidized intraneuronal masses of inferior olive lipofuscin gave sudanophilic staining reactions with oil red O, Sudan black B, and a Sudan III and IV combination stain [21].
• In contrast to cells from normal rabbits, Kupffer and endothelial cells from cholesterol-fed rabbits accumulated significant amounts of Oil Red O-positive material (neutral lipids) [22].
• Specimens from the rectum and vermiform appendix showed Sudan black B-, Sudan III-, and PAS-positive granules within the neurons of the myenteric plexus [23].
• The rates of formation of diols of dimethylbenz[a]anthracene (DMBA-3,4-diol, DMBA-5,6-diol and DMBA-8,9-diol) have been determined in hepatic microsomes prepared from untreated rats or from animals treated with phenobarbital (PB) or Sudan III [24].

Gene context of Sudan Red III

• An adipocytic phenotype was observed in BMP-2-treated cells, as shown by upregulation of two adipocytic marker mRNAs, PPAR-gamma and aP2, and by staining of lipid-filled cell vesicles with Oil Red O [25].
• Some of the Sca-1+ cells expressed alkaline phosphatase after osteogenic induction and were stained with Oil-Red O after adipogenic induction [26].
• Treatment in vitro of GO orbital preadipocytes with recombinant sFRP-1 (100 nm) significantly increased adiponectin (2.0-fold; P < 0.05), leptin (7-fold; P < 0.002), and TSH receptor mRNA (13-fold; P < 0.003) levels and enhanced Oil red-O staining in the cultures [27].
• Judging by Oil Red O staining for lipid accumulation and expression of adipocyte markers, we determined that, unlike the full-length Pref-1A and the constructed large soluble form, the artificial membrane form of Pref-1 lacking the processing site proximal to the membrane was not effective in inhibiting adipogenesis [28].
• Histological analysis with Oil Red O staining demonstrated that there was considerable accumulation of lipid in the skin of TNX-deficient (TNX-/-) mice [29].

Analytical, diagnostic and therapeutic context of Sudan Red III

• MEASUREMENTS: Quantitative measurement of fecal fat by the van de Kamer titration, van de Kamer gravimetric, and Jeejeebhoy gravimetric methods and qualitative assessment of fecal fat by Sudan III staining [30].
• This analogue was used in the study of the distribution by low-kVp X-ray examination, Sudan III staining, and autoradiography [31].
• Macrophages and foam cells were isolated by enzymic dispersion with collagenase and cultured for further characterization by scanning electron microscopy, nonspecific esterase (NSE), and oil red O (ORO) staining [3].
• Cells were recovered for Oil Red O (ORO) staining as well as immunocytochemistry for milk proteins: alpha-lactalbumin and beta-lactoglobulin [32].
• We found a correlation between the number of Oil Red O-stained macrophages in sputum and lavage fluid (Spearman's coefficient: rho = 0.657, p < 0.018) [13].

References