Avermectin A1a
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| Category | Antibiotics |
| Catalog number | BBF-00229 |
| CAS | 65195-51-9 |
| Molecular Weight | 887.10 |
| Molecular Formula | C49H74O14 |
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Description
Avermectin A1a is produced by the strain of Streptomyces avermitilis. It stimulates nerve cells to release Y-aminobutyric acid (GABA), which blocks the transmission of signals from the central nervous system to the motor nerve. It is not resistant to bacteria and fungi, but has strong activity to nematode parasites such as ancylostoma and Pteria, as well as insects such as flies. Abamectin B1a has the highest activity. Ivermectin obtained by catalytic hydrogenation contains 22 23- dihydroabamectin B1a (above 80%) and 22 23 dioxabamectin B1b (below 20%). Less active than B1a but less toxic. Used as repellent (subcutaneous or oral) for cattle, sheep and pigs, it is also effective against human filariasis.
Specification
| Synonyms | SCHEMBL1681257 |
| IUPAC Name | (1'R,2R,3S,4'S,6S,8'R,10'E,12'S,13'S,14'E,16'E,20'R,21'R,24'S)-2-butan-2-yl-24'-hydroxy-12'-[(2R,4S,5S,6S)-5-[(2S,4S,5S,6S)-5-hydroxy-4-methoxy-6-methyloxan-2-yl]oxy-4-methoxy-6-methyloxan-2-yl]oxy-21'-methoxy-3,11',13',22'-tetramethylspiro[2,3-dihydropyran-6,6'-3,7,19-trioxatetracyclo[15.6.1.14,8.020,24]pentacosa-10,14,16,22-tetraene]-2'-one |
| Canonical SMILES | CCC(C)C1C(C=CC2(O1)CC3CC(O2)CC=C(C(C(C=CC=C4COC5C4(C(C=C(C5OC)C)C(=O)O3)O)C)OC6CC(C(C(O6)C)OC7CC(C(C(O7)C)O)OC)OC)C)C |
| InChI | InChI=1S/C49H74O14/c1-12-26(2)43-29(5)18-19-48(63-43)24-35-21-34(62-48)17-16-28(4)42(60-40-23-38(54-10)45(32(8)58-40)61-39-22-37(53-9)41(50)31(7)57-39)27(3)14-13-15-33-25-56-46-44(55-11)30(6)20-36(47(51)59-35)49(33,46)52/h13-16,18-20,26-27,29,31-32,34-46,50,52H,12,17,21-25H2,1-11H3/b14-13+,28-16+,33-15+/t26?,27-,29-,31-,32-,34+,35-,36-,37-,38-,39-,40-,41-,42-,43+,44+,45-,46+,48+,49+/m0/s1 |
| InChI Key | AFSHKCWTGFDXJR-BWFQMGBFSA-N |
Properties
| Appearance | White Powder |
| Antibiotic Activity Spectrum | parasites |
Reference Reading
1. Intentional avermectin pesticide ingestion: a retrospective multicenter study
Yi-Kan Wu, Chia-Hau Chang, Jiun-Hao Yu, Kai-Ping Lan, Tzung-Hai Yen, Shu-Sen Chang, Chen-June Seak, Hsing-Yuan Chang, Hsien-Yi Chen Clin Toxicol (Phila). 2022 Oct;60(10):1099-1105. doi: 10.1080/15563650.2022.2104729. Epub 2022 Aug 2.
Context: Avermectin pesticides are widely used in agriculture, and are thought to have low toxicity in humans. However, information on their toxicity after accidental or deliberate ingestion is limited. Objective: The aim of this study was to evaluate the clinical manifestations of avermectin pesticide ingestion and identify factors associated with severe outcomes (death, intubation, or sustained hypotension requiring inotrope therapy). Materials and methods: This multicenter retrospective study included patients who visited the emergency departments of six teaching hospitals due to acute avermectin pesticide ingestion between January 2012 and May 2020. Patients who reported ingestion of any other pesticides, drugs, or substances were excluded. Results: In total, 64 patients (median age, 72 years) were included: 60 had ingested emamectin pesticides, and 4 had ingested abamectin. Almost all (98%) were cases of self-harm. The most common presentation was drowsiness (47%), with a median Glasgow Coma Scale (GCS) score of 14, followed by shortness of breath (SOB)/dyspnea (33%) and nausea/vomiting (22%). Concurrent methanol exposure (via the solvent) was confirmed or suspected in five patients. Seventeen patients (27%) were intubated. Three patients who developed respiratory failure were not intubated because of a "do-not-resuscitate" (DNR) order. Four patients developed sustained hypotension requiring inotrope therapy. Fifty patients (78%) were admitted, of whom 27 (42%) required intensive care unit (ICU) admission. Four patients died, three of whom had a DNR order. Based on our definition, 20 patients (31%) had severe outcomes. A multivariate logistic regression model showed that a GCS score < 13 (OR 68.1, 95% CI 3.8-999) and the presence of SOB/dyspnea (OR 50.2, 95% CI 3.0-849.9) were associated with severe outcomes. Conclusions: Most patients who intentionally ingested avermectin pesticides required inpatient treatment. Forty-two percent needed ICU care and 31% had severe outcomes. A GCS score < 13 and SOB/dyspnea were independently associated with severe outcomes.
2. Non-target toxic effects of avermectin on carp spleen involve oxidative stress, inflammation, and apoptosis
Tianmeng Zhang, Zhuhua Dong, Feixue Liu, Enzhuang Pan, Nana He, Fenfen Ma, Xinyu Wu, Yan Wang, Jingquan Dong Pestic Biochem Physiol. 2022 Oct;187:105190. doi: 10.1016/j.pestbp.2022.105190. Epub 2022 Jul 30.
Avermectin is one of the most widely used pesticides, but its toxicity to non-target organisms, especially aquatic organisms, has been ignored. Therefore, an acute spleen injury model of avermectin in carp was established to assess the non-target toxicity of avermectin to carp. In this study, 3.005 μg/L and 12.02 μg/L were set as the low and high dose groups of avermectin, respectively, and a four days acute exposure experiment was conducted. Pathological structure observation showed that avermectin damaged spleen tissue structure and produced inflammatory cell infiltration. Biochemical analysis showed that avermectin significantly reduced the activities of antioxidant enzymes CAT, SOD, and GSH-px, but increased the content of MDA, a marker of oxidative damage. Avermectin exposure also significantly increased the transcription levels of inflammatory cytokines such as IL-1β, IL-6, TNF-α, and INOS, and also significantly enhanced the activity of the inflammatory mediator iNOS, but suppressed the transcription levels of anti-inflammatory factors TGF-β1 and IL-10. In addition, TUNEL detected that the apoptosis rate increased significantly with the increase of avermectin dosage, and the transcription levels of apoptosis-related genes BAX, P53, and Caspase 3/9 also increased in a dose-dependent manner. This study is preliminary evidence that avermectin induces spleen injury in carp through oxidative stress, inflammation, and apoptosis, which has important implications for subsequent studies on the effects of avermectin on non-target organisms.
3. Avermectin induces carp neurotoxicity by mediating blood-brain barrier dysfunction, oxidative stress, inflammation, and apoptosis through PI3K/Akt and NF-κB pathways
Tianmeng Zhang, Zhuhua Dong, Feixue Liu, Enzhuang Pan, Nana He, Fenfen Ma, Guanglu Wang, Yan Wang, Jingquan Dong Ecotoxicol Environ Saf. 2022 Sep 15;243:113961. doi: 10.1016/j.ecoenv.2022.113961. Epub 2022 Aug 12.
Avermectin, a "low toxicity insecticide", has been widely used in recent years, but its non-target toxicity, especially to aquatic organisms, has been neglected. In this study, we evaluated the neurotoxic effects of avermectin on carp by establishing a 96 h avermectin acute toxicity test, and its possible mechanism was discussed. The 96 h LC50 of avermectin in carp was found to be 24.04 μg/L. Therefore, 3.005 μg/L and 12.02 μg/L were used as the low-dose and high-dose groups, respectively, to investigate the neurotoxic effects of avermectin on carp. The results of high-performance liquid chromatography (HPLC) analysis showed that avermectin accumulated in the carp brain. Histopathological observation and immunohistochemical analysis (IHC) of TNF-α and Bax showed that avermectin exposure led to inflammatory cell infiltration and neuronal necrosis. The mRNA levels of tight junction genes and the IHC results of ZO-1 and Occludin showed that the structure of the blood-brain barrier (BBB) was destroyed. Biochemical analysis showed that avermectin induced the accumulation of MDA in the brain and decreased the activity of antioxidant enzymes CAT and SOD, leading to oxidative stress. In addition, avermectin induces brain inflammation by activating NF-κB pathway and releasing inflammatory factors IL-1β, IL-6, TNF-α and iNOS. TEM and TUNEL assays showed that exposure to avermectin induced apoptosis in brain. what is more, the expression of apoptosis-related genes and proteins suggested that avermectin-induced apoptosis may be associated with inhibition of the PI3K/Akt signaling pathway. This study also showed that avermectin-induced NF-κB signaling activation was partially dependent on its upstream PI3K/Akt signaling pathway. Therefore, this study concludes that avermectin can induce neurotoxicity in carp by disrupting the blood-brain barrier structure and generating oxidative stress, inflammation, and apoptosis and that NF-κB and PI3K/Akt signaling pathways are involved in this process.
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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 ╳
