8,9-dihydro-8,9-dihydroxy aflatoxin B₁ | 196820-36-7

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 香豆素及其衍生物
• 英文名称: 8,9-dihydro-8,9-dihydroxy aflatoxin B₁
• 英文别名: aflatoxin B1-8,9-dihydrodiol；aflatoxin B1 8,9-dihydrodiol；(3R,7S)-4,5-dihydroxy-11-methoxy-6,8,19-trioxapentacyclo[10.7.0.02,9.03,7.013,17]nonadeca-1,9,11,13(17)-tetraene-16,18-dione
• CAS: 196820-36-7
• 化学式: C₁₇H₁₄O₈
• 分子量: 346.293
• InChiKey: JRZBEIPOZPNWID-MIOCFURKSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -0.2
• 重原子数：
  25
• 可旋转键数：
  1
• 环数：
  5.0
• sp3杂化的碳原子比例：
  0.41
• 拓扑面积：
  112
• 氢给体数：
  2
• 氢受体数：
  8

反应信息

• 作为产物：
  描述：

  aflatoxin B₁ 8,9-epoxide 在 双氧水 作用下， 反应 48.0h， 生成 8,9-dihydro-8,9-dihydroxy aflatoxin B₁
  参考文献：
  名称：

  Biodegradation of aflatoxin B1 with cell-free extracts of Trametes versicolor and Bacillus subtilis

  摘要：

  Aflatoxin B₁ (AFB₁) is one of the most common contaminants of poultry feed and has been linked to adverse effects on animal health and productivity. In this study, the degradation of AFB₁ was studied with cell-free extracts (CFE) of Trametes versicolor and Bacillus subtilis using High-Performance Liquid chromatography (HPLC). CFE from B. subtilis and T. versicolor gave 60% and 34% of AFB₁ degradation respectively, while heat-inactivated extracts showed no degradation. By-products obtained at the end of AFB₁ degradation were analyzed by Liquid Chromatography with tandem mass spectrometry (LC-MS/MS). After 96 h of incubation, by-products with lower m/z values were obtained with CFE from B. subtilis as compared to that from T. versicolor, indicating a higher degradation efficiency of the former. Additionally, the detection of a by-product which could correspond to AFB1-8,9 dihydrodiol - a less toxic derivative of AFB₁ - after 72 and 96 h of incubation with CFE from B. subtilis, could indicate the simultaneous detoxification along with degradation of AFB₁ by B. subtilis CFE.

  DOI：

  10.1016/j.rvsc.2020.09.009

文献信息

• Trp266 determines the binding specificity of a porcine aflatoxin B1 aldehyde reductase for aflatoxin B1-dialdehyde
  作者：Jun Wu、Weiying Xu、Caihui Zhang、Qing Chang、Xianqing Tang、Kangbai Li、Yiqun Deng

  DOI：10.1016/j.bcp.2013.08.014

  日期：2013.11

  Aflatoxin B-1 (AFB(1)) is a severe threat to human and animal health. The aflatoxin B-1 aldehyde reductase (AFAR) family specifically catalyzes AFB(1)-dialdehyde, a toxic metabolic intermediate of AFB(1), producing a nontoxic dialcohol. Although several AFARs have been found and characterized, the binding specificity of the family for AFB(1)-dialdehyde remains unclear. Herein, according to the published sequence, we cloned a porcine AFAR gene. Recombinant porcine AFAR was expressed and purified from Escherichia coli as hexa-histidine tagged fusion protein. Using the cloned porcine AFAR as a model, site-directed mutagenesis combined with high performance liquid chromatography studies revealed that the substitution of Trp266 with Ala resulted in almost complete loss of catalytic activity for AFB(1)-dialdehyde. Interestingly, the substitution of Met86 with Ala exhibited an obviously increased activity to the dialdehyde. Based on these results and by using molecular docking simulations, this work provides a structural explanation for why the AFAR family exhibits high specificity for AFB(1)-dialdehyde. The Trp266 residue in porcine AFAR plays a critical role in stabilizing the binding of AFB(1)-dialdehyde in the active pocket through the hydrophobic interaction of the side-chain indole ring of Trp266 with the fused coumarin rings of the dialdehyde molecule. The enhanced activity of M86A may be attributed to the formed pi-pi stacking interaction between Trp266 and the dialdehyde. In addition, other hydrophobic residues (e.g. Phe and Trp) around the dialdehyde molecule also stabilize the substrate binding. The findings may contribute to understanding the substrate specificity of the AFAR family for AFB(1)-dialdehyde. (C) 2013 Elsevier Inc. All rights reserved.
• Guengerich; Cai; McMahon, Chemical Research in Toxicology, <hi>2001</hi>, vol. 14, # 6, p. 727 - 737
  作者：Guengerich、Cai、McMahon、Hayes、Sutter、Groopman、Deng、Harris

  DOI：——

  日期：——