9-Oxo-2-amino-7-nitrofluorene | 88387-73-9

• 分子结构分类: 有机化合物 - 苯类化合物 - 芴
• 英文名称: 9-Oxo-2-amino-7-nitrofluorene
• 英文别名: 2-amino-7-nitro-fluoren-9-one；2-Amino-7-nitro-fluoren-9-on；2-amino-7-nitrofluoren-9-one
• CAS: 88387-73-9
• 化学式: C₁₃H₈N₂O₃
• 分子量: 240.218
• InChiKey: URAFCARZCGLOIL-UHFFFAOYSA-N

物化性质

• 熔点：
  287-288 °C
• 沸点：
  514.3±43.0 °C(Predicted)
• 密度：
  1.511±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.3
• 重原子数：
  18
• 可旋转键数：
  0
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  88.9
• 氢给体数：
  1
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  9-Oxo-2-amino-7-nitrofluorene 在 sodium sulfide 、 sodium hydroxide 作用下， 生成 2,7-二氨基-9-芴酮
  参考文献：
  名称：

  Eckert; Langecker, Journal fur praktische Chemie (Leipzig 1954), 1928, vol. <2> 118, p. 269

  摘要：

  DOI：
• 作为产物：
  描述：

  2,7-二硝基-9-芴酮 在 1,4-dihydronicotinamide adenine dinucleotide 、 次黄嘌呤 、 xanthine oxidase 作用下， 以 二甲基亚砜 为溶剂， 生成 9-Oxo-2-amino-7-nitrofluorene
  参考文献：
  名称：

  在体外硝化硝化的和C-9氧化的芴。

  摘要：

  诱变和致癌的硝基芴对环境造成的广泛污染会危害人类健康。由于硝基还原导致许多硝基化合物的活化，因此研究了单电子和二电子还原剂对硝基芴（NF）衍生物的硝基还原。黄嘌呤氧化酶（XO）/次黄嘌呤催化并通过乙酰化细胞色素c还原的刺激测量的硝基还原速率随硝基数目和C-9处的氧化而增加：9-oxo-2,4,7-triNF> 9-oxo -2,7-diNF> 2,7-diNF> 9-氧代-2-NF = 2,5-diNF> 9-羟基-2-NF> 2-NF。抗坏血酸酯催化单电子还原为硝基阴离子自由基，该自由基与分子O2反应生成超氧化物。9-oxo-2,4,7-triNF和9-oxo-2,7-diNF的O2吸收率分别是它们的63和0.17倍，含等效浓度的呋喃西林（一种经典底物）。加入超氧化物歧化酶和过氧化氢酶后，O2大约再生了75％，表明形成了超氧化物。在XO / NADH存在下，具有典型Michaelis-Menten动力学的9-Oxo-2

  DOI：

  10.1021/tx980152w

文献信息

• Reductions of Nitro and 9-Oxo Groups of Environmental Nitrofluorenes by the Rat Mammary Gland in Vitro
  作者：Clare L. Ritter、Richard W. Decker、Danuta Malejka-Giganti

  DOI：10.1021/tx0000567

  日期：2000.8.1

  mammary gland. Since their metabolism to active carcinogens may involve nitroreduction, this study examined the reduction of 2-nitrofluorene (2-NF) and 2,7-diNF and their 9-oxo- and 9-hydroxy (OH) derivatives by the rat mammary gland. Cytosolic fractions catalyze NADH- and NADPH-dependent reductions of the 2-nitro and 9-oxo to the respective 2-amino and 9-OH compounds at rates 4- and >/=10-fold greater than

  硝基芴和C-9氧化的硝基芴是广泛的环境遗传毒素，根据其对大鼠乳腺的致癌性，特别是对2，7-二硝基芴（2,7-diNF）的致癌性，可能与乳腺癌有关。由于它们代谢为活性致癌物可能涉及硝基还原，因此本研究研究了大鼠乳腺对2-硝基芴（2-NF）和2,7-diNF及其9-氧代和9-羟基（OH）衍生物的还原作用。胞质级分催化NADH和NADPH依赖性的2-硝基和9-氧代还原成各自的2-氨基和9-OH化合物的速率比微粒体的速率高4-和> / = 10倍。由2、7-diNF的胞质溶胶催化的胺形成速率大于2-NF的速率，并且对于C-9氧化的衍生物增加：9-oxo-2-NF> 9-OH-2-NF> 2- NF和9-OH-2，7-diNF >> 9-oxo-2,7-diNF> 2,7-diNF。硝基还原被O（2）或别嘌呤醇（20 microM），双香豆酚（100 microM）和芦丁（50 microM）抑制。芦丁，双香豆酚和消炎痛（100
• DNA Adducts from Nitroreduction of 2,7-Dinitrofluorene, a Mammary Gland Carcinogen, Catalyzed by Rat Liver or Mammary Gland Cytosol
  作者：Clare L. Ritter、Sandra J. Culp、James P. Freeman、M. Matilde Marques、Frederick A. Beland、Danuta Malejka-Giganti

  DOI：10.1021/tx010172p

  日期：2002.4.1

  Nitrofluorenes are mutagenic and carcinogenic environmental pollutants arising chiefly from combustion of fossil fuels. Nitro aromatic compounds undergo nitroreduction to N-hydroxy arylamines that bind to DNA directly or after O-esterification. This study analyzes the DNA binding and adducts from the in vitro nitroreduction of 2,7-dinitrofluorene (2,7-diNF), a potent mammary carcinogen in the rat. Potential adduct(s) of 2,7-diNF was (were) generated by reduction of 2-nitroso-7-NF with ascorbate/H+ in the presence of calf thymus DNA. The major adduct was characterized by HPLC/ESI/MS and H-1 NMR spectrometry as N-(deoxyguanosin-8-yl)-2-amino-7-NF, and a minor one was determined by HPLC/ESI/MS to be a deoxyadenosine adduct of 2-amino-7-NF. Products from enzymatic nitroreduction were monitored by HPLC and DNA adduct formation by P-32-postlabeling. Xanthine oxidase/hypoxanthine-catalyzed nitroreduction of 2.7-diNF, 2-nitrofluorene (2-NF), and 1-nitropyrene (1-NP) yielded the respective amines to similar extents (30-50%). However, the level of the major adducts (similar to0.15/10(6) nucleotides) from 2-NF [N-(deoxyguanosin-8-yl)-2-aminofluorene] and 2,7-diNF [N-(deoxyguanosin-8-yl)-2-amino-7-NF] was less than or equal to2% that from 1-NP. In the presence of acetyl CoA, nitroreduction of 2-NF catalyzed by rat liver cytosol/NADH yielded the same adduct at a level of 2.2/10(6) nucleotides. Liver or mammary gland cytosol with acetyl CoA yielded mainly N-(deoxyguanosin-8-yl)-2-amino-7-NF from 2,7-diNF at >30 adducts/10(6) nucleotides, levels comparable to those from 1,6-dinitropyrene and 4- or 49-fold greater than the respective levels without acetyl CoA. Recovery of 2-nitroso-7-NF and 2-amino-7-NF from cytosol-catalyzed reduction of 2,7-diNF indicated nitroreduction and an N-hydroxy arylamine intermediate. Likewise, the presence of 2-acetylamino-7-NF indicated that reactivity with acyltransferase(s) was not prevented by the nitro group at C7. These data are consistent with activation of 2,7-diNF via nitroreduction to the N-hydroxy arylamine and acetyl CoA-dependent O-acetylation of the latter to bind to DNA. Enzymatic nitroreduction of 2,7-diNF was greatly enhanced by 9-oxidation. The nitroreduction of either 9-oxo-2,7-diNF or 9-hydroxy-2,7-diNF catalyzed by liver cytosol with acetyl CoA yielded two adducts (>2/10(6) nucleotides). Differences in the TLC migration of these adducts, compared to those from 2,7-diNF, and the lack of 2,7-diNF formation in the incubations suggested retention of the C9-oxidized groups. The relative ratios of the amine to amide from nitroreductions of 9-oxo-2,7-diNF and 2,7-diNF catalyzed by liver cytosol suggested that the 9-oxo group decreased reactivity with acyltransferase and, thus, the amount of N-acetoxy arylamine that binds to DNA. The mammary gland tumorigenicity of 2,7-diNF and the extent of its activation by the tumor target tissue shown herein suggest relevance of this environmental pollutant for breast cancer.