Anguidin
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| Category | Antibiotics |
| Catalog number | BBF-00688 |
| CAS | 2270-40-8 |
| Molecular Weight | 366.40 |
| Molecular Formula | C19H26O7 |
| Purity | ≥97% |
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Description
It is produced by the strain of Fusarium anguioides. It showed weak antifungal activity, and 0.03 μg/mL completely inhibited the mitosis of chicken embryo fibroblasts cultured in vitro. The inhibition rate of 0.51mg/kg/d in vivo for 7 consecutive days was 79%, 70% and 50%, respectively, for Walker cancer, sarcoma 37 and sarcoma 180 in rats.
Specification
| Synonyms | Diacetoxyscirpenol; Anguidine; 4,15-Diacetoxyscirpen-3-ol; CHEBI:4478; 4,15-Di-O-acetylscirpenol; Scirpenetriol 4,15-diacetate; NSC177378; ANG 66; 4,15-Diacetoxyscirp-9-en-3-ol; 4,15-Diacetoxyscirpenol; 12,13-Epoxytrichothec-9-ene-3alpha,4beta,15-triol 4,15-diacetate; 3-alpha-Hydroxy-4-beta,15-diacetoxy-12,13-epoxytrichothec-9-ene |
| Storage | Store in a freezer upon arrival, at -10°C to -25°CUse the original container to store the product.Keep the lid tightly closed.Avoid exposing to strong direct light. |
| IUPAC Name | [(1S,2R,7R,9R,10R,11S,12R)-11-acetyloxy-10-hydroxy-1,5-dimethylspiro[8-oxatricyclo[7.2.1.02,7]dodec-5-ene-12,2'-oxirane]-2-yl]methyl acetate |
| Canonical SMILES | CC1=CC2C(CC1)(C3(C(C(C(C34CO4)O2)O)OC(=O)C)C)COC(=O)C |
| InChI | InChI=1S/C19H26O7/c1-10-5-6-18(8-23-11(2)20)13(7-10)26-16-14(22)15(25-12(3)21)17(18,4)19(16)9-24-19/h7,13-16,22H,5-6,8-9H2,1-4H3/t13-,14-,15-,16-,17-,18-,19-/m1/s1 |
| InChI Key | AUGQEEXBDZWUJY-ZLJUKNTDSA-N |
| Source | Trichothecenes are produced on many different grains like wheat, oats or maize by various Fusarium species such as F. graminearum, F. sporotrichioides, F. poae and F. equiseti. |
Properties
| Antibiotic Activity Spectrum | fungi |
| Boiling Point | 471.2 °C at 760 mmHg |
| Melting Point | 162-164 °C |
| Density | 1.315 g/cm3 |
| Solubility | Soluble in Mthanol, Chloroform |
Toxicity
| Carcinogenicity | No indication of carcinogenicity to humans (not listed by IARC). |
| Mechanism Of Toxicity | Unlike many other mycotoxins, trichothecenes do not require metabolic activation to exert their biological activity, instead directly reacting with cellular components. Trichothecenes are cytotoxic to most eukaryotic cells due to their powerful ability to inhibit protein synthesis. They do this by freely moving across the plasma membrane and binding specifically to ribosomes with high-affinity. Specifically, they interfere with the active site of peptidyl transferase at the 3'-end of large 28S ribosomal RNA and inhibit the initiation, elongation or termination step of protein synthesis, as well as cause polyribosomal disaggregation. Protein synthesis is an essential function in all tissues, but tissues where cells are actively and rapidly growing and dividing are very susceptible to the toxins. Additionally, binding to ribosomes is thought to activate proteins in downstream signalling events related to immune response and apoptosis, such as mitogen-activated protein kinases. This is known as ribotoxic stress response. Trichothecenes may also induce some alterations in membrane structure, leading to increased lipid peroxidation and inhibition of electron transport activity in the mitochondria. They can further induce apoptosis through generation of reactive oxygen species. Further secondary effects of trichothecenes include inhibition of RNA and DNA synthesis, and also inhibition of mitosis. |
| Toxicity | LD50: 1.3 mg/kg (Intravenous, Rat). |
Reference Reading
1. [Carcinogenic and genotoxic effects of mycotoxins]
T Müller Nahrung . 1987;31(2):117-25. doi: 10.1002/food.19870310205.
Aflatoxin B1 is the most potent hepatocarcinogen among the naturally occurring compounds. It's carcinogenic effect was confirmed by longterm-studies in several animal species. There exists detailed knowledge on the molecular mechanism of the carcinogenic effect caused by aflatoxin B1. At present there does not exist a reliable evidence that human primary hepatocellular carcinoma is caused by aflatoxins. Sterigmatocystin is a hepatocarcinogen too. The genotoxicity of sterigmatocystin likewise as of aflatoxin B1 was detected by short-term-tests with microbial systems and mammalian cells in vitro. It is disputable whether ochratoxin A, citrinin and T-2 toxin are carcinogenic or not. Diacetoxyscirpenol, zearalenone and patulin are estimated as not carcinogenic after longterm-studies with oral toxin administration. Patulin and penicillic acid are genotoxic in microbial systems respectively in mammalian cells in vitro. Luteoskyrin is carcinogenic, but there was not detected any genotoxicity.
2. Metabolic pathways of trichothecenes
Kamil Kuca, Qinghua Wu, Vlastimil Dohnal, Zonghui Yuan, Lingli Huang Drug Metab Rev . 2010 May;42(2):250-67. doi: 10.1080/03602530903125807.
Trichothecenes are a group of mycotoxins mainly produced by the fungi of Fusarium genus. Consumers are particularly concerned over the toxicity and food safety of trichothecenes and their metabolites from food-producing animals. The metabolism of T-2 toxin, deoxynivalenol (DON), nivalenol (NIV), fusarenon-X (FX), diacetoxyscirpenol (DAS), 3-acetyldeoxy-nivalenol (3-aDON), and 15-acetyldeoxynivalenol (15-aDON) in rodents, swine, ruminants, poultry, and humans are reviewed in this article. Metabolic pathways of these mycotoxins are very different. The major metabolic pathways of T-2 toxin in animals are hydrolysis, hydroxylation, de-epoxidation, and conjugation. After being transformed to HT-2 toxin, it undergoes further hydroxylation at C-3' to yield 3'-hydroxy-HT-2 toxin, which is considered as an activation pathway, whereas transformation from T-2 to T-2 tetraol is an inactivation pathway in animals. The typical metabolites of T-2 toxin in animals are HT-2 toxin, T-2 triol, T-2 tetraol, neosolaniol (NEO), 3'-hydroxy-HT-2, and 3'-hydroxy-T-2, whereas HT-2 toxin is the main metabolite in humans. De-epoxidation is an important pathway for detoxification in animals. De-epoxy products, DOM-1, and de-epoxy-NIV are the main metabolites of DON and NIV in most animals, respectively. However, the two metabolites are not found in humans. Deacetyl can occur rapidly on the acetyl derivatives, 3-aDON, 15-aDON, and FX. DAS is metabolized in animals to 15-monoacetoxyscirpenol (15-MAS) via C-4 deacetylation and then transformed to scirpentriol (SCP) via C-15 deacetylation. Finally, the epoxy is lost, yielding de-epoxy-SCP. De-epoxy-15-MAS is also the main metabolite of DAS. 15-MAS is the main metabolite in human skin. The review on the metabolism of trichothecenes will help one to well understand the fate of these toxins' future in animals and humans, as well as provide basic information for the risk assessment of them for food safety.
3. Multiple Mycotoxins in Kenyan Rice
Rosemary Murori, Fredrick Ng'ang'a, Joyce Musyoka, J Musembi Mutuku, Vincent Koskei, George N Chemining'wa, James Kamau Gitau, Samuel K Mutiga Toxins (Basel) . 2021 Mar 11;13(3):203. doi: 10.3390/toxins13030203.
Multiple mycotoxins were tested in milled rice samples (n= 200) from traders at different milling points within the Mwea Irrigation Scheme in Kenya. Traders provided the names of the cultivar, village where paddy was cultivated, sampling locality, miller, and month of paddy harvest between 2018 and 2019. Aflatoxin, citrinin, fumonisin, ochratoxin A, diacetoxyscirpenol, T2, HT2, and sterigmatocystin were analyzed using ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). Deoxynivalenol was tested using enzyme-linked immunosorbent assay (ELISA). Mycotoxins occurred in ranges and frequencies in the following order: sterigmatocystin (0-7 ppb; 74.5%), aflatoxin (0-993 ppb; 55.5%), citrinin (0-9 ppb; 55.5%), ochratoxin A (0-110 ppb; 30%), fumonisin (0-76 ppb; 26%), diacetoxyscirpenol (0-24 ppb; 20.5%), and combined HT2 + T2 (0-62 ppb; 14.5%), and deoxynivalenol was detected in only one sample at 510 ppb. Overall, low amounts of toxins were observed in rice with a low frequency of samples above the regulatory limits for aflatoxin, 13.5%; ochratoxin A, 6%; and HT2 + T2, 0.5%. The maximum co-contamination was for 3.5% samples with six toxins in different combinations. The rice cultivar, paddy environment, time of harvest, and millers influenced the occurrence of different mycotoxins. There is a need to establish integrated approaches for the mitigation of mycotoxin accumulation in the Kenyan rice.
Spectrum
Predicted LC-MS/MS Spectrum - 10V, Positive
Experimental Conditions
Ionization Mode: Positive
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
Collision Energy: 10 eV
Instrument Type: QTOF (generic), spectrum predicted by CFM-ID
Mass Resolution: 0.0001 Da
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
