2-Acetamidofluorene
(Synonyms: 2-AAF, 2-Acetaminofluorene, N-2-Fluorenylacetamide, N-Acetyl-2-aminofluorene) 目录号 : GC250082-Acetamidofluorene (2-AAF, 2-Acetaminofluorene, N-2-Fluorenylacetamide, N-Acetyl-2-aminofluorene) is a carcinogenic and mutagenic compound
Cas No.:53-96-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
2-Acetamidofluorene (2-AAF, 2-Acetaminofluorene, N-2-Fluorenylacetamide, N-Acetyl-2-aminofluorene) is a carcinogenic and mutagenic compound.
[1] M B Sporn, C W Dingman. Nature . 1966 Apr 30;210(5035):531-2.
| Cas No. | 53-96-3 | SDF | Download SDF |
| 别名 | 2-AAF, 2-Acetaminofluorene, N-2-Fluorenylacetamide, N-Acetyl-2-aminofluorene | ||
| 分子式 | C15H13NO | 分子量 | 223.27 |
| 溶解度 | DMSO: 45 mg/mL (201.55 mM);Water: Insoluble;Ethanol: 22.5 mg/mL (100.77 mM) | 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 | 4.4789 mL | 22.3944 mL | 44.7888 mL |
| 5 mM | 0.8958 mL | 4.4789 mL | 8.9578 mL |
| 10 mM | 0.4479 mL | 2.2394 mL | 4.4789 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。
Use of 2-acetamidophenanthrene and 2-Acetamidofluorene in investigations of mechanisms of hepatocarcinogenesis
Environ Health Perspect 1983 Mar;49:81-6.PMID:6832098DOI:10.1289/ehp.834981.
Comparison studies have been undertaken on the hepatocarcinogen 2-Acetamidofluorene (AAF) and its nonhepatocarcinogenic analog 2-acetamidophenanthrene (AAP). Previous studies have shown that amount of compound acutely and persistently bound to rat liver DNA is comparable for the two compounds following single injections into adult Fischer rats, but that AAP fails to initiate tumors in weanling Sprague-Dawley rats. In this work we show that the amount of bound adduct from AAF and AAP is also comparable after three weeks of feeding compound to weanling Sprague-Dawley male rats. Three of the adducts found in RNA of AAP-treated rats cochromatographed on Sephadex LH-20 with two adenosine adducts and one guanosine adduct prepared by reaction of the nucleosides with N-acetoxy-N-trifluoroacetyl-2-aminophenanthrene at neutrality. Because of the lack of initiating ability of AAP in liver, we have also investigated early biochemical alterations in liver after various regimens. Feeding of either AAF or AAP to male weanling rats, followed by three weeks of DDT feeding produced no alteration in either histochemically detected gamma-glutamyltranspeptidase or in ganglioside complement in total liver homogenate. Partial hepatectomy after feeding of either AAF or AAP resulted in the appearance of new fucoganglioside and alteration in the distribution of the major gangliosides. DDT feeding after partial hepatectomy resulted in foci of elevated gamma-glutamyltranspeptidase in AAF-fed rats but not in AAP-fed rats. These results support a previous proposal that AAP may initiate tumorigenesis in rat liver, but that the promoting regimens now in use lack the ability to cause further progression of the initiated cells. The data also suggests that ganglioside synthesis may be a more sensitive marker for early stages in carcinogenesis than are the various histochemical stains now in use.
Activation of benzo(a)pyrene and 2-Acetamidofluorene to mutagens by microsomal preparations from different animal species: role of cytochrome P-450 and P-448
Xenobiotica 1981 Oct;11(10):701-8.PMID:6275616DOI:10.3109/00498258109049090.
1. The metabolic activation of benzo(a)pyrene and 2-Acetamidofluorene to mutagens was studied with liver microsomal preparations from rat, guinea-pig, hamster and mouse, untreated or pretreated with phenobarbitone or 3-methylcholanthrene. 2. Liver microsomal preparations from all animal species activated benzo(a)pyrene, that from mouse being the most efficient. Similarly, microsomal preparations from guinea-pig, hamster and mouse could activate 2-Acetamidofluorene, but that from rat exhibited very weak activity. 3. Activation of benzo(a)pyrene into mutagenic intermediates by liver microsomal preparations was increased for all animals except mouse by pretreatment with 3-methylcholanthrene. In contrast, pretreatment with phenobarbitone decreased the activation by microsomal preparations from all species. 4. Activation of 2-Acetamidofluorene by liver microsomal preparations from rat and guinea-pig, but not mouse and hamster, was increased by pretreatment of the animals with phenobarbitone. Pretreatment with 3-methylcholanthrene decreased the activation of this carcinogen by microsomal preparations from all species. 5. The metabolic activation of benzo(a)pyrene is catalysed by cytochrome P-448 but not cytochrome P-450. 6. The activation of 2-Acetamidofluorene to mutagens may involve, in addition to the mixed-function oxidases, other microsomal enzyme systems.
Inhibitory effect of carbon monoxide on the N- and ring-hydroxylation of 2-Acetamidofluorene by hamster hepatic microsomal preparations
Biochem J 1974 Nov;144(2):427-30.PMID:4462591DOI:10.1042/bj1440427.
The effect of CO on N-, 3-, 5- and 7-hydroxylation of 2-Acetamidofluorene by liver microsomal fractions from control and 3-methylcholanthrene-pretreated hamsters was studied. All hydroxylations were inhibited by CO, but the degree of inhibition was different for each hydroxylation. The ratios of CO to O(2) needed for 50% inhibition of the N-, 3-, 5- and 7-hydroxylations by control preparations were 8.0:1, 8.2:1, 4.2:1 and 7.1:1 respectively and by preparations from treated animals were 4.2:1, 8.9:1, 2.3:1 and 3.2:1 respectively. These results are discussed in terms of the possible presence of more than one type of cytochrome P-450 involved in hydroxylations of 2-Acetamidofluorene by liver microsomal fractions from both control and pretreated hamsters.
The relationship of 2-Acetamidofluorene mutagenicity in plate tests with its in vivo liver cell component distribution and its carcinogenic potential
Mutat Res 1975 Dec;30(3):305-15.PMID:1105163doi
Using a plating technique, the mutagenic potentials of 2-Acetamidofluorene (AAF) and N-hydroxy-AAF were examined after metabolic activation by liver preparations from different animals. Animals used were: male and female rats; male rats treated with 3-methylcholanthrene (MC); male rats treated with AAF; hamsters; guinea pigs; cotton rats and baboons. Irrespective of the animal susceptibility to AAF carcinogenesis, mutation frequency was always increased in the Salmonella typhimurium TA 1538 tester strain. Indeed, the greater response was found in the presence of liver from cotton rats, a species which is resistant to AAF-induced carcinogenesis. Carcinogen binding, with labelled molecules, was also studied in liver cell constituents of rats, guinea pigs and cotton rats. A much better correlation was found between carcinogenicity and carcinogen binding, at least in those species studied, than between carcogenicity and plate test mutagenicity. The difficulty which this new information poses for the interpretation of plate tests is discussed.
In vitro activation of the promutagens 2-Acetamidofluorene, cyclophosphamide and 7,12-dimethylbenzanthracene by constitutive ferret and rat hepatic S-9 fractions
Toxicology 1984 May 1;31(1):73-86.PMID:6427977DOI:10.1016/0300-483x(84)90157-4.
The ability of the ferret to metabolically activate promutagenic compounds was compared with that of the rat, using the Salmonella/microsome assay. Three compounds which require biotransformation to mutagenic metabolites, 2-Acetamidofluorene (2-AAF), cyclophosphamide (CPA), and 7,12-dimethylbenzanthracene (DMBA), were studied. Metabolic activation was provided by ferret or rat hepatic S-9 fractions at 5 levels for each chemical, and optimal S-9 levels as well as dose-response curves were obtained. Interspecies mutagenic activity was quantitated on the basis of mg liver, mg S-9 protein, and nmoles P-450. The slopes of the dose-response curves and the lowest chemical dose required for a significant response were also compared. Although constitutive levels of rat hepatic cytochrome P-450 were shown to be higher than those of the ferret, in vitro mutagenic activation by ferret S-9, at S-9 levels which caused activation in both species, was greater than or equivalent to activation by rat S-9 for these chemicals, based on all parameters studied. The results showed that the equilibrium between activation and detoxification reactions is dependent upon the chemical dose and S-9 level present.