Satratoxin G
目录号 : GC46218
A macrocyclic trichothecene mycotoxin
Cas No.:53126-63-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Satratoxin G is a macrocyclic trichothecene mycotoxin that has been found in S. chartarum.1,2 It induces cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP) in HL-60 cells when used at a concentration of 40 nM and is cytotoxic to HepG2, Hep-2, Caco-2, A204, U937, and Jurkat cells (IC50s = 2.2-9.7 ng/ml).3,4 Intranasal administration of satratoxin G (500 μg/kg) induces apoptosis of olfactory sensory neurons in olfactory epithelium and ethmoid turbinate expression of the genes encoding IL-1α, IL-1β, IL-6, TNF-α, and MIP-2 in mice.2 Satratoxin G induces lethality in 4 week-old male mice (LD50 = 1.23 mg/kg, i.p.).1
|1. Yoshizawa, T., Ohtsubo, K., Sasaki, T., et al. Acute toxicities of satratoxins G and H in mice--a histopathological observation with special reference to the liver injury caused by satratoxin G. Proc. Jpn. Assoc. Mycotoxicol. 23, 53-57 (1986).|2. Islam, Z., Harkema, J.R., and Pestka, J.J. Satratoxin G from the black mold Stachybotrys chartarum evokes olfactory sensory neuron loss and inflammation in the murine nose and brain. Environ. Health Perspect. 114(7), 1099-1107 (2006).|3. Nagase, M., Shiota, T., Tsushima, A., et al. Molecular mechanism of satratoxin-induced apoptosis in HL-60 cells: Activation of caspase-8 and caspase-9 is involved in activation of caspase-3. Immunol. Lett. 84(1), 23-27 (2002).|4. Nielsen, C., Casteel, M., Didier, A., et al. Trichothecene-induced cytotoxicity on human cell lines. Mycotoxin Res. 25(2), 77-84 (2009).
| Cas No. | 53126-63-9 | SDF | |
| Canonical SMILES | O=C(/C=C\C=C\C1(C(O)C)C(O)C2(C3O2)CCO1)OC4CC(C56OC6)OC(C=C(C)CC7)C7(COC3=O)C45C | ||
| 分子式 | C29H36O10 | 分子量 | 544.6 |
| 溶解度 | Dichloromethane: soluble,DMSO: soluble,Ethanol: soluble | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.8362 mL | 9.1811 mL | 18.3621 mL |
| 5 mM | 0.3672 mL | 1.8362 mL | 3.6724 mL |
| 10 mM | 0.1836 mL | 0.9181 mL | 1.8362 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Production of Satratoxin G and H Is Tightly Linked to Sporulation in Stachybotrys chartarum
Toxins (Basel) 2022 Jul 28;14(8):515.PMID:36006177DOI:10.3390/toxins14080515.
Stachybotrys chartarum is a toxigenic fungus that is frequently isolated from damp building materials or improperly stored forage. Macrocyclic trichothecenes and in particular satratoxins are the most potent mycotoxins known to be produced by this fungus. Exposure of humans or animals to these secondary metabolites can be associated with severe health problems. To assess the pathogenic potential of S. chartarum isolates, it is essential to cultivate them under conditions that reliably promote toxin production. Potato dextrose agar (PDA) was reported to be the optimal nutrition medium for satratoxin production. In this study, the growth of S. chartarum genotype S strains on PDA from two manufacturers led to divergent results, namely, well-grown and sporulating cultures with high satratoxin concentrations (20.8 ± 0.4 µg/cm2) versus cultures with sparse sporulation and low satratoxin production (0.3 ± 0.1 µg/cm2). This finding is important for any attempt to identify toxigenic S. chartarum isolates. Further experiments performed with the two media provided strong evidence for a link between satratoxin production and sporulation. A comparison of three-point and one-point cultures grown on the two types of PDA, furthermore, demonstrated an inter-colony communication that influences both sporulation and mycotoxin production of S. chartarum genotype S strains.
Detection of Satratoxin G and h in indoor air from a water-damaged building
Mycopathologia 2008 Aug;166(2):103-7.PMID:18443920DOI:10.1007/s11046-008-9126-z.
The occurrence of Stachybotrys chartarum in indoor environments has been linked to adverse health effects as well as few cases of pulmonary haemorrhages in humans. Although the highly toxic secondary metabolites of this fungus, like Satratoxin G and H, were frequently claimed with outbreaks of such diseases, these toxins have hardly been identified in the air of naturally contaminated indoor environments. Herein, a case of a LC-MS/MS-confirmed occurrence of airborne S. chartarum-toxins in a water-damaged dwelling is reported. Satratoxin G (0.25 ng/m(3)) and satratoxin H (0.43 ng/m(3)) were detected. This provides further evidence that Stachybotrys-toxins can be transferred from mouldy indoor materials into air, which could be a factor in the aetiology of health symptoms related to the sick building syndrome.
Satratoxin G-induced apoptosis in PC-12 neuronal cells is mediated by PKR and caspase independent
Toxicol Sci 2008 Sep;105(1):142-52.PMID:18535002DOI:10.1093/toxsci/kfn110.
Satratoxin G (SG) is a macrocyclic trichothecene mycotoxin produced by Stachybotrys chartarum, a mold suggested to play an etiologic role in damp building-related illnesses. Acute intranasal exposure of mice to SG specifically induces apoptosis in olfactory sensory neurons of the nose. The PC-12 rat pheochromocytoma cell model was used to elucidate potential mechanisms of SG-induced neuronal cell death. Agarose gel electrophoresis revealed that exposure to SG at 10 ng/ml or higher for 48-h induced DNA fragmentation characteristic of apoptosis in PC-12 cells. SG-induced apoptosis was confirmed by microscopic morphology, hypodiploid fluorescence and annexin V-fluorescein isothiocyanate (FITC) uptake. Messenger RNA expression of the proapoptotic genes p53, double-stranded RNA-activated protein kinase (PKR), BAX, and caspase-activated DNAse was significantly elevated from 6 to 48 h after SG treatment. SG also induced apoptosis and proapoptotic gene expression in neural growth factor-differentiated PC-12 cells. Although SG-induced caspase-3 activation, caspase inhibition did not impair apoptosis. Moreover, SG induced nuclear translocation of apoptosis-inducing factor (AIF), a known contributor to caspase-independent neuronal cell death. SG-induced apoptosis was not affected by inhibitors of oxidative stress or mitogen-activated protein kinases but was suppressed by the PKR inhibitor C16 and by PKR siRNA transfection. PKR inhibition also blocked SG-induced apoptotic gene expression and AIF translocation but not caspase-3 activation. Taken together, SG-induced apoptosis in PC-12 neuronal cells is mediated by PKR via a caspase-independent pathway possibly involving AIF translocation.
Satratoxin G interaction with 40S and 60S ribosomal subunits precedes apoptosis in the macrophage
Toxicol Appl Pharmacol 2009 Jun 1;237(2):137-45.PMID:19306889DOI:10.1016/j.taap.2009.03.006.
Satratoxin G (SG) and other macrocyclic trichothecene mycotoxins are potent inhibitors of eukaryotic translation that are potentially immunosuppressive. The purpose of this research was to test the hypothesis that SG-induced apoptosis in the macrophage correlates with binding of this toxin to the ribosome. Exposure of RAW 264.7 murine macrophages to SG at concentrations of 10 to 80 ng/ml induced DNA fragmentation within 4 h that was indicative of apoptosis. To relate these findings to ribosome binding of SG, RAW cells were exposed to different toxin concentrations for various time intervals, ribosomal fractions isolated by sucrose density gradient ultracentrifugation and resultant fractions analyzed for SG by competitive ELISA. SG was found to specifically interact with 40S and 60S ribosomal subunits as early as 5 min and that, at high concentrations or extended incubation times, the toxin induced polysome disaggregation. While co-incubation with the simple Type B trichothecene DON had no effect on SG uptake into cell cytoplasm, it inhibited SG binding to the ribosome, suggesting that the two toxins bound to identical sites and that SG binding was reversible. Although both SG and DON induced mobilization of p38 and JNK 1/2 to the ribosome, phosphorylation of ribosomal bound MAPKs occurred only after DON treatment. SG association with the 40S and 60S subunits was also observed in the PC-12 neuronal cell model which is similarly susceptible to apoptosis. To summarize, SG rapidly binds small and large ribosomal subunits in a concentration- and time-dependent manner that was consistent with induction of apoptosis.
Kinetics of Satratoxin G tissue distribution and excretion following intranasal exposure in the mouse
Toxicol Sci 2010 Aug;116(2):433-40.PMID:20466779DOI:10.1093/toxsci/kfq142.
Intranasal exposure of mice to Satratoxin G (SG), a macrocyclic trichothecene produced by the indoor air mold Stachybotrys chartarum, selectively induces apoptosis in olfactory sensory neurons (OSNs) of the nose and brain. The purpose of this study was to measure the kinetics of distribution and clearance of SG in the mouse. Following intranasal instillation of female C57B16 mice with SG (500 microg/kg bw), the toxin was detectable from 5 to 60 min in blood and plasma, with the highest concentrations, 30 and 19 ng/ml, respectively, being observed at 5 min. SG clearance from plasma was rapid and followed single-compartment kinetics (t(1/2) = 20 min) and differed markedly from that of other tissues. SG concentrations were maximal at 15-30 min in nasal turbinates (480 ng/g), kidney (280 ng/g), lung (250 ng/g), spleen (200 ng/g), liver (140 ng/g), thymus (90 ng/g), heart (70 ng/g), olfactory bulb (14 ng/g), and brain (3 ng/g). The half-lives of SG in the nasal turbinate and thymus were 7.6 and 10.1 h, respectively, whereas in other organs, these ranged from 2.3 to 4.4 h. SG was detectable in feces and urine, but cumulative excretion over 5 days via these routes accounted for less than 0.3% of the total dose administered. Taken together, SG was rapidly taken up from the nose, distributed to tissues involved in respiratory, immune, and neuronal function, and subsequently cleared. However, a significant amount of the toxin was retained in the nasal turbinate, which might contribute to SG's capacity to evoke OSN death.