Anthraflavic acid
(Synonyms: 2,6-二羟基蒽醌) 目录号 : GC35359
2,6-Dihydroxyanthraquinone (Anthraflavic acid, Anthraflavin) is a potent and specific inhibitor of cytochrome P-448 activity.
Cas No.:84-60-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
2,6-Dihydroxyanthraquinone (Anthraflavic acid, Anthraflavin) is a potent and specific inhibitor of cytochrome P-448 activity.
[1] Ayrton AD, et al. Biochim Biophys Acta. 1987, 916(3):328-31.
| Cas No. | 84-60-6 | SDF | |
| 别名 | 2,6-二羟基蒽醌 | ||
| Canonical SMILES | O=C1C2=C(C=C(O)C=C2)C(C3=CC=C(O)C=C13)=O | ||
| 分子式 | C14H8O4 | 分子量 | 240.21 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.163 mL | 20.8151 mL | 41.6302 mL |
| 5 mM | 0.8326 mL | 4.163 mL | 8.326 mL |
| 10 mM | 0.4163 mL | 2.0815 mL | 4.163 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Anthraflavic acid inhibits the mutagenicity of the food mutagen IQ: mechanism of action
Mutat Res 1988 Mar-Apr;207(3-4):121-5.PMID:3282161DOI:10.1016/0165-7992(88)90075-9.
The ability of Anthraflavic acid to inhibit the mutagenicity of IQ was investigated using the Ames test and employing hepatic activation systems from Aroclor 1254-pretreated rats. Incorporation of Anthraflavic acid into the S9 mix caused a concentration-dependent decrease in the mutagenicity of IQ. A similar effect was seen when microsomes only were employed as activation systems. Cytosol, as we have previously demonstrated, potentiated the microsome-mediated mutagenicity of IQ and this potentiation was also inhibited by Anthraflavic acid. In contrast, Anthraflavic acid had no effect on the mutagenicity of the direct-acting microsome-generated metabolites of IQ. It is concluded that Anthraflavic acid is a potent inhibitor of IQ mutagenicity by virtue of its ability to inhibit both its microsomal and cytosolic activation pathways.
Anthraflavic acid is a potent and specific inhibitor of cytochrome P-448 activity
Biochim Biophys Acta 1987 Dec 18;916(3):328-31.PMID:3689794DOI:10.1016/0167-4838(87)90177-4.
Consideration of the computer-optimised dimensions of Anthraflavic acid indicates that it is essentially a planar molecule with a large area/depth ratio, that would preferentially interact with the polycyclic aromatic hydrocarbon-induced family of cytochrome P-450 proteins (cytochromes P-448). Anthraflavic acid was a potent inhibitor of the O-deethylations of ethoxycoumarin and ethoxyresorufin, both catalysed primarily by cytochromes P-448, in Arochlor-1254-induced hepatic microsomes. Similarly Anthraflavic acid markedly inhibited the mutagenicity of 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-I) in the Ames test. In contrast, it has no effect on the dealkylation of pentoxyresorufin, a reaction catalysed primarily by the phenobarbital-induced cytochromes P-450, and NADPH-dependent reduction of cytochrome c. It is concluded that Anthraflavic acid is a potent and specific inhibitor of cytochrome P-448 activity.
Induction of rat hepatic cytochrome P-450 I proteins by the antimutagen Anthraflavic acid
Food Chem Toxicol 1988 Nov-Dec;26(11-12):909-15.PMID:3209131DOI:10.1016/0278-6915(88)90088-9.
Administration of the antimutagen Anthraflavic acid to rats gave rise to significant increases in the hepatic microsomal O-deethylations of ethoxyresorufin and ethoxycoumarin, but not in the O-dealkylation of pentoxyresorufin nor in cytosolic glutathione S-transferase activity. Immunoblot studies of solubilized microsomes from anthraflavic acid-treated rats revealed that Anthraflavic acid induced the apoproteins P-450 I A1 and A2 but not P-450 B1 and B2. Pretreatment with Anthraflavic acid resulted in a marked increase in the in vitro bioactivation of 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole and 2-amino-3,2-amino-3-methylimidazomethylimidazo[4,5-f]-quinoline (IQ) to mutagenic intermediate(s); IQ is a carcinogen against which Anthraflavic acid has displayed strong antimutagenic effect in the Ames test when incorporated into the metabolic activation system. The increase in mutagenicity of IQ was the result of enhancement of both the microsomal and cytosolic activation steps. It is concluded that Anthraflavic acid is a specific inducer of P-450 I proteins in the rat and this compound is not only unlikely to exhibit any anticarcinogenic effect in vivo but may act as a co-carcinogen.
Inhibition of the mutagenicity of bay-region diol-epoxides of polycyclic aromatic hydrocarbons by tannic acid, hydroxylated anthraquinones and hydroxylated cinnamic acid derivatives
Carcinogenesis 1985 Feb;6(2):237-42.PMID:3918802DOI:10.1093/carcin/6.2.237.
Tannic acid and several hydroxylated anthraquinone and cinnamic acid derivatives inhibited the mutagenic activity of (+/-)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo [a]pyrene (B[a]P 7,8-diol-9,10-epoxide-2), an ultimate mutagenic and carcinogenic metabolite of benzo [a]pyrene. The mutagenic activity of 0.05 nmol of B[a]P 7,8-diol-9,10-epoxide-2 towards strain TA 100 of Salmonella typhimurium was inhibited 50% by incubation of the bacteria and the diol-epoxide with tannic acid (0.5 nmol), Anthraflavic acid (7 nmol), rufigallol (7 nmol), quinalizarin (10 nmol), alizarin (30 nmol), purpurin (60 nmol), and danthron (88 nmol). Dose-dependent, but weaker antimutagenic activity was observed for quinizarin, and a number of hydroxylated cinamic acid derivatives. Gallic acid and m-digallic acid, major components of tannic acid, possessed less than 1% of the anti-mutagenic activity of tannic acid, although m-digallic acid was over 3 times more active than gallic acid. The anti-mutagenic activity of tannic acid was a result of its interaction with B[a]P 7,8-diol-9,10-epoxide-2 since the rate of disappearance of the diol-epoxide from cell-free solutions in 1:9dioxane:water was markedly stimulated by the polyphenol. Tannic acid was a highly potent inhibitor of the mutagenic activity of the bay-region diol-epoxides of benzo[a]pyrene, dibenzo[a,h]pyrene and dibenzo[a,i]pyrene, but higher concentrations of tannic acid were needed to inhibit the mutagenicity of the chemically less reactive benzo[a]-pyrene 4,5-oxide and the bay-region diol-epoxides of benz[a]-anthracene, chrysene and benz[c]phenanthrene.
Inhibition of epidermal xenobiotic metabolism in SENCAR mice by naturally occurring plant phenols
Cancer Res 1987 Feb 1;47(3):760-6.PMID:3492267doi
Naturally occurring plant phenols such as tannic acid, quercetin, myricetin, and Anthraflavic acid have been shown to inhibit the mutagenicity of several bay-region diol-epoxides of polycyclic aromatic hydrocarbons including benzo(a)pyrene (BP). The present study was designed to determine whether these plant phenols can alter epidermal cytochrome P-450-dependent monooxygenases in SENCAR mice. In vitro addition of these plant phenols to epidermal microsomal preparations inhibited aryl hydrocarbon hydroxylase (AHH) activity in a concentration-dependent manner. The 50% inhibitory concentrations for tannic acid, myricetin, quercetin, and Anthraflavic acid ranged from 4.4 X 10(-5) M to 12.4 X 10(-5) M in microsomes prepared from control and 3-methylcholanthrene-pretreated animals. Of the plant phenols studied tannic acid was found to be the most potent inhibitor of epidermal AHH activity. Tannic acid, quercetin, myricetin, and Anthraflavic acid exhibited a mixed type of inhibitory effect with Ki values of 81, 63, 135, and 165 microM, respectively. In vitro addition of these plant phenols (240 microM) to the incubation mixture prepared from control and 3-methylcholanthrene-treated animals resulted in varying degrees of inhibition of epidermal microsomal AHH (57-92%), ethoxycoumarin O-deethylase (19-58%), and ethoxyresorufin O-deethylase (33-85%) activities. High pressure liquid chromatographic analysis of the organic solvent-soluble metabolites of BP produced by epidermal microsomes indicated a substantial decrease in the formation of BP-diols (23-67%) and BP-phenols (29-57%) by each of the plant phenols. The formation of BP-7,8-diol was substantially inhibited (29-52%) by each of the plant phenols. Further in vivo studies showed that a single topical application of tannic acid, quercetin, and myricetin greatly diminished epidermal AHH (53-65%), ethoxycoumarin O-deethylase (30-68%), and ethoxyresorufin O-deethylase (66-97%) activities whereas Anthraflavic acid was ineffective in this regard even when repeatedly applied. Our results indicate that plant phenols have substantial though variable inhibitory effects on epidermal monooxygenase activities and BP metabolism suggesting that these compounds may be capable of inhibiting the carcinogenic effects of polycyclic aromatic hydrocarbons in the skin.