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T3D3698 - 4-Acetoxyscirpendiol
| Record Information | |
|---|---|
| Version | 1.0 |
| Creation Date | 2010-04-28 14:49:46 UTC |
| Update Date | 2013-04-25 08:48:38 UTC |
| Accession Number | T3D3698 |
| Identification | |
| Common Name | 4-Acetoxyscirpendiol |
| Description | 4-Acetoxyscirpendiol is a trichothecene. Trichothecenes are a very large family of chemically related mycotoxins produced by various species of Fusarium, Myrothecium, Trichoderma, Trichothecium, Cephalosporium, Verticimonosporium, and Stachybotrys. The most important structural features causing the biological activities of trichothecenes are: the 12,13-epoxy ring, the presence of hydroxyl or acetyl groups at appropriate positions on the trichothecene nucleus and the structure and position of the side-chain. They 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. Some molds that produce trichothecene mycotoxins, such as Stachybotrys chartarum, can grow in damp indoor environments and may contribute to health problems among building occupants. (W801) |
| Compound Type |
|
| Chemical Structure |
|
| Synonyms |
|
| Chemical Formula | C17H24O6 |
| Average Molecular Weight | 324.3689 |
| Monoisotopic Molecular Weight | 324.1572885 |
| Chemical IUPAC Name | 11'-hydroxy-2'-(hydroxymethyl)-1',5'-dimethyl-8'-oxaspiro[oxirane-2,12'-tricyclo[7.2.1.0^{2,7}]dodecan]-5'-en-10'-yl acetate |
| CAS Registry Number | 70402-13-0 |
| SMILES | CC(=O)OC1C(O)C2(C)C3(CO3)C1OC1C=C(C)CCC21CO |
| InChI Identifier | InChI=1S/C17H24O6/c1-9-4-5-16(7-18)11(6-9)23-14-12(22-10(2)19)13(20)15(16,3)17(14)8-21-17/h6,11-14,18,20H,4-5,7-8H2,1-3H3 |
| InChI Key | InChIKey=NFFRTZSZVQIMDJ-UHFFFAOYSA-N |
| Chemical Taxonomy | |
| Kingdom | Organic Compounds |
| Super Class | Lipids |
| Class | Prenol Lipids |
| Sub Class | Sesquiterpenes |
| Direct Parent | Trichothecenes |
| Alternative Parents |
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| Molecular Framework | Aliphatic Heteropolycyclic Compounds |
| Substituents |
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| External Descriptors | Not Available |
| External Links | |
| DrugBank ID | Not Available |
| PubChem Compound ID | 155564  |
| KEGG ID | Not Available |
| UniProt ID | Not Available |
| OMIM ID | Not Available |
| ChEBI ID | Not Available |
| BioCyc ID | Not Available |
| CTD ID | Not Available |
| Stitch ID | Not Available |
| PDB ID | Not Available |
| ACToR ID | Not Available |
| Wikipedia Link | Not Available |
| Physical Properties | |
| Appearance | Not Available |
| Melting Point | Not Available |
| Solubility | Not Available |
| Predicted LogP | -0.06412580500000042 |
| Toxicity Profile | |
| Route of Exposure | Oral, dermal, inhalation, and parenteral (contaminated drugs). (W967) |
| Mechanism of Action | 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. (W801, W802, W803, W804, W806, W830) |
| Metabolism | Trichothecenes are lipophilic and thus easily absorbed through the skin, gut, and pulmonary mucosa. They are metabolized mainly by cytochrome P-450 and trichothecene-specific carboxylesterase activity in the liver, although other tissues such as the kidney, spleen, and intestine also show some metabolic activity. Trichothecenes are metabolically transformed to less toxic metabolites by such reactions as hydrolysis, hydroxylation, de-epoxidation, and glucuronidation. Metabolites are excreted in the urine and feces. (W680, W802) |
| Toxicity Values | Not Available |
| Lethal Dose | Not Available |
| Carcinogenicity (IARC Classification) | Not Available |
| Uses/Sources | Trichothecenes are a very large family of chemically related mycotoxins produced by various species of Fusarium, Myrothecium, Trichoderma, Trichothecium, Cephalosporium, Verticimonosporium, and Stachybotrys. They 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. Some molds that produce trichothecene mycotoxins, such as Stachybotrys chartarum, can grow in damp indoor environments and may contribute to health problems among building occupants. (W801) |
| Minimum Risk Level | Not Available |
| Health Effects | Trichothecenes have multiorgan effects including anoerxia and weight loss, growth retardation, nervous disorders, cardiovascular alterations, immunodepression, hemostatic derangements, skin toxicity, decreased reproductive capacity, bone marrow damage, and alimentary toxic aleukia. (W801, W802, W806) |
| Symptoms | After direct dermal application or oral ingestion, the trichothecene mycotoxins can cause rapid irritation to the skin or intestinal mucosa, including skin irritation, burning and itching, rash or blisters, and bleeding. Eye contact can cause tearing, eye pain, conjunctivitis, burning sensations about the eyes, and blurred vision for up to 1 week. Symptoms also include nausea, vomiting, fatigue, dyspnea, and acute vascular effects leading to hypotension and shock. (W801, W802) |
| Treatment | There are no known antidotes to trichothecene mycotoxins. Treatments are directed at supporting hemopoietic abnormalities, gastrointestinal damage, and skin damage. Administer charcoal as a slurry in case of acute oral exposure. In case of inhalation: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. In case of dermal exposure, Remove contaminated clothing and wash exposed area thoroughly with soap and water. (W574) |
| References | |
| General References |
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Targets
1. 28S ribosomal protein S5, mitochondrial
Trichothecenes move freely across the plasma membrane and bind 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. Trichothecenes are cytotoxic because protein synthesis is an essential function in all tissues. 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. (W802, W803, W830)UniProt ID: P82675
Gene: MRPS5
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report
References:
- W802 — Wannemacher, R.W. JR., and Wiener, S.L. (1997). Chapter 34: Trichothecene Mycotoxins. In R. Zajtchuk (Ed.), Medical Aspects of Chemical and Biological Warfare. Maryland: Office of The Surgeon General. [Link]
- W803 — Pestka JJ. Mechanisms of deoxynivalenol-induced gene expression and apoptosis. Food Addit Contam. 2008 Jun 24:1-13. [Epub ahead of print]
[18608486 ]
- W830 — Bae HK, Pestka JJ. Deoxynivalenol induces p38 interaction with the ribosome in monocytes and macrophages. Toxicol Sci. 2008 Sep;105(1):59-66. Epub 2008 May 22.
[18502741 ]