Direct Black 38
(Synonyms: 直接黑38,Chlorazol Black E; Ferristatin II disodium; C.I. 30235) 目录号 : GC38068An iron uptake inhibitor,dye content ≥45%(based on Nitrogen)
Cas No.:1937-37-7
Sample solution is provided at 25 µL, 10mM.
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Ferristatin II is an inhibitor of iron uptake.1 It inhibits iron uptake (IC50 = ~12 ?M), as well as induces degradation of transferrin receptor protein 1 (TfR1), an effect that can be reversed by the lipid membrane disruptor nystatin, in HeLa cells. In vivo ferristatin II (0.2, 10, and 40 mg/kg) reduces serum iron levels and transferrin saturation in rats. It also suppresses traumatic brain injury-induced lipid peroxidation, neuronal apoptosis, and the number of cortical iron deposits in rats.2
1.Byrne, S.L., Buckett, P.D., Kim, J., et al.Ferristatin II promotes degradation of transferrin receptor-1 in vitro and in vivoPLoS One8(7)e70199(2013) 2.Cheng, Y., Qu, W., Li, J., et al.Ferristatin II, an iron uptake inhibitor, exerts neuroprotection against traumatic brain injury via suppressing ferroptosisACS Chem. Neurosci.13(5)664-675(2022)
Cas No. | 1937-37-7 | SDF | |
别名 | 直接黑38,Chlorazol Black E; Ferristatin II disodium; C.I. 30235 | ||
Canonical SMILES | O=S(C1=C(/N=N/C2=CC=C(C3=CC=C(/N=N/C4=CC=C(N)C=C4N)C=C3)C=C2)C(N)=C5C(O)=C(/N=N/C6=CC=CC=C6)C(S(=O)(O[Na])=O)=CC5=C1)(O[Na])=O | ||
分子式 | C34H25N9Na2O7S2 | 分子量 | 781.73 |
溶解度 | Water: 5 mg/mL (6.40 mM) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 1.2792 mL | 6.3961 mL | 12.7921 mL |
5 mM | 0.2558 mL | 1.2792 mL | 2.5584 mL |
10 mM | 0.1279 mL | 0.6396 mL | 1.2792 mL |
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给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
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2.
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13-week subchronic toxicity studies of direct blue 6, Direct Black 38, and direct brown 95 dyes
Natl Cancer Inst Carcinog Tech Rep Ser 1978;108:1-117.PMID:12799683doi
Thirteen-week subchronic toxicity studies of direct blue 6, Direct Black 38, and direct brown 95 dyes were conducted by administering the test chemicals in feed to Fischer 344 rats and B6C3F1 mice. Groups of 10 rats and 10 mice of each sex were administered one of the three dyes at one of five concentrations for 13 weeks and then necropsied, beginning the second day after the end of the dosing period. The concentrations used for the rats were 190, 375, 750, 1,500, and 3,000 ppm. The concentrations used for the mice were 750, 1,500, 3,000, 6,000, and 12,500 ppm, except for the female mice administered direct brown 95 dye, which were given concentrations of 375, 750, 1,500, 3,000, and 6,000 ppm. Matched controls consisted of groups of 10 untreated rats and 10 untreated mice of each sex. Mean body weights of the male and female rats administered the two or three highest doses of any one of the test dyes were lower than mean body weights of the corresponding controls, and the depressions in mean body weight were dose related. Mean body weights of the male and female mice administered the highest dose of any one of the test dyes were slightly lower than mean body weights of the corresponding controls; mean body weights of mice administered lower doses were generally unaffected. All male and female rats administered 3,000 ppm of any one of the dyes or 1,500 ppm of direct brown 95 dye died before the end of the studies. One male administered 1,500 ppm direct blue 6 dye, six males administered 1,500 ppm Direct Black 38 dye, and two males administered 750 ppm direct brown 95 dye also died by the end of the studies. No deaths occurred in any other dosed group or in any control group of rats. All male and female mice administered the test dyes survived to the end of the studies, except for one male whose death was attributed to bacterial infection. Benzidine and monoacetyl benzidine were detected in the urine of male and female rats and mice administered the test dyes, but neither compound was detected in the urine of control rats and mice. Determinations of methemoglobin in control and dosed rats showed no differences. In rats, neoplastic lesions occurred only in dosed groups and consisted of hepatocellular carcinomas and neoplastic nodules of the liver. The incidences of hepatocellular carcinomas in female rats administered 3,000 ppm direct blue 6 dye (4/9) and male rats administered 1,500 ppm Direct Black 38 dye (4/9) were significant (P=0.033) when related to the incidences of the tumors in the corresponding controls (0/10); hepatocellular carcinomas were also observed in two male rats administered 1,500 ppm direct blue 6 dye and in one female rat administered 1,500 ppm direct brown 95 dye. No control rats from any of the three studies developed hepatocellular carcinomas. When incidences of neoplastic nodules were combined with those of hepatocellular carcinomas, the significance increased to P<0.001 for male rats administered 1,500 ppm direct blue 6 dye, P=0.001 for females administered 3,000 ppm direct blue 6 dye, P<0. 001 for males administered 1, 500 ppm Direct Black 38 dye, and P=0.007 for females administered 1,500 ppm direct brown 95 dye. No controls developed neoplastic nodules. Female rats administered Direct Black 38 dye developed no hepatocellular carcinomas, but had an incidence of neoplastic nodules of 5/10, with a significance of P=0.016. Male rats administered direct brown 95 dye developed neither hepatocellular carcinomas nor neoplastic nodules, but as indicated below, had significant incidences of preneoplastic lesions. The failure of groups of rats administered 3,000 ppm dye to develop tumors when other groups administered 1,500 ppm did develop tumors may be due to earlier deaths at the higher dose. Preneoplastic hepatic lesions (basophilic foci) occurred only in dosed rats and did not occur in the controls. The incidences of the basophilic foci were significant (P<0.033) in male (4/9) and female (7/9) rats administered 3,000 ppm direct blue 6 dye and in male rats (7/8) administered 1, 500 ppm direct brown 95 dye. Basophilic foci also occurred, at lower incidences, in males (1/10) administered 1,500 ppm direct blue 6 dye, in males (3/9) administered 1,500 ppm Direct Black 38 dye, in females (1/8) administered 3,000 ppm Direct Black 38 dye, in males administered 750 ppm (3/10) or 3,000 ppm (2/9) direct brown 95 dye, and in females administered 1,500 ppm (3/8) or 3,000 ppm (3/8) direct brown 95 dye. When incidences of foci of cellular alteration, a possible preneoplastic lesion, were added to those of basophilic foci, significance occurred in additional dosed groups. In mice, no neoplastic lesions occurred in the liver or other tissues of groups administered the different dyes. However, three mice administered 12,500 ppm Direct Black 38 dye and one mouse administered 12,500 ppm direct brown 95 dye had foci of cellular alteration, in which the cells were basophilic when compared with surrounding normal cells. It is concluded that under the conditions of these 13-week subchronic toxicity studies, direct blue 6 and Direct Black 38 dyes were carcinogenic in male and female Fischer 344 rats and direct brown 95 was carcinogenic in female rats; all three dyes induced hepatocellular carcinomas and neoplastic nodules in the liver. The test dyes were not carcinogenic for B6C3F1 mice in the 13-week subchronic toxicity studies.
Ames testing of Direct Black 38 parallels carcinogenicity testing
J Appl Toxicol 1981 Dec;1(6):308-13.PMID:6764474DOI:10.1002/jat.2550010608.
Studies have established that Direct Black 38 and two other benzidine-based dyes are carcinogenic. The carcinogenic effect has been generally considered attributable to the metabolic release of benzidine from Direct Black 38 and similar dyes. However, Ames tests indicated that when Direct Black 38 is reduced with sodium dithionate it is more mutagenic than can be accounted for by complete release of all the benzidine present in the dye molecule. While most dyes are not mutagenic when tested with S-9, a series of benzidine congener dyes were all found to be mutagenic with either TA 98 or TA 100 strains, if the dyes were first reduced with sodium dithionate. Unreduced dyes were not mutagenic. Neither anaerobic conditions nor addition of riboflavin induced mutagenicity of these dyes under the condition of our experiments.
Chemical and enzymatic interactions of Direct Black 38 and Direct Brown 1 on release of carcinogenic amines
Chemosphere 2004 Sep;56(9):833-41.PMID:15261529DOI:10.1016/j.chemosphere.2004.04.042.
Release of amine products from azo compounds is of considerable interest, since most of the metabolized amine products have toxic and carcinogenic characters. Moreover, most of the azo dyes are extensively used as coloring agents in inks, textiles, leathers, food and pharmaceutical industries. The present study emphasis on the quantification and comparison of amines released from water soluble dyes by (i) extra cellular protein (ECP) of Streptomyces sp. SS07 and by (ii) chemical methods. It has been observed that both the methods release considerable quantities of similar type of amine products. Release of amine compounds by ECP and chemical reduction in acid and alkaline sweat medium from a leather garment sample was also assessed. ECP (0.7852 mg protein/mg of ECP) releases benzidine and 4-amino biphenyl from Direct Black 38 and Direct Brown 1 as stable products at pH 9.2 and at 37 degrees C for a contact period of 24 h. On comparison with chemical reduction, it was observed that about 5-20% increase in the release of amine products by ECP was observed. However, more than 60% of amine products were released by chemical method from leather garment samples than direct treatment with ECP.
Biological decolourization of C.I. Direct Black 38 by E. gallinarum
J Hazard Mater 2008 Aug 30;157(1):187-93.PMID:18280646DOI:10.1016/j.jhazmat.2007.12.085.
In the present study, an Enterococcus gallinarum strain was isolated from effluent treatment plant of a textile industry based on its ability to decolourize C.I. Direct Black 38 (DB38), a benzidine-based azo dye. Effects of dye concentration and medium composition on dye decolourization were studied. The strain was found to decolourize DB38 even under aerobic conditions. Kinetics of DB38 decolourization was also examined, and V(max) and K(s) of decolourization were found to be higher in Luria broth (12.8 mg l(-1)h(-1) and 490.6 mg l(-1)) than in minimal medium (4.09 mg l(-1)h(-1) and 161.84 mg l(-1)). However, decolourization rate/biomass was found to be higher in minimal medium than in Luria broth, indicating greater decolourization efficiency of biomass in the former. The study also revealed biodegradation of DB38 to benzidine and its further deamination to 4-aminobiphenyl (4-ABP) by the culture. Ammonia released during this process was used as nitrogen source for growth of the culture.
Degradation of Direct Black 38 dye under visible light and sunlight irradiation by N-doped anatase TIO₂ as photocatalyst
J Environ Manage 2012 May 15;98:107-11.PMID:22257572DOI:10.1016/j.jenvman.2011.12.029.
The N-doped TiO(2) photocatalyst was prepared by calcination of a hydrolysis product composed of titanium (IV) isopropoxide with ammonia as the precipitator. X-ray diffraction, surface area, XPS and UV-vis spectra analyses showed a nanosized anatase structure and the appearance of a new absorption band in the visible region caused by nitrogen doping. The degradation of Direct Black 38 dye on the nitrogen-doped TiO(2) photocatalyst was investigated under visible light and sunlight irradiation. The N-doped anatase TiO(2) demonstrated excellent photocatalytic activity under visible light. Under sunlight irradiation, the N-doped sample showed slightly higher activity than that of the non-doped sample.