Satratoxin H
目录号 : GC46219A trichothecene mycotoxin
Cas No.:53126-64-0
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
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Satratoxin H is a trichothecene mycotoxin that has been found in Stachybotrys.1 It induces production of reactive oxygen species (ROS), increases in malondialdehyde (MDA) levels, and induces apoptosis in PC12 cells when used at concentrations ranging from 5 to 100 nM. Satratoxin H is cytotoxic to human umbilical vein endothelial cells (HUVECs; IC50 = 6.8 ng/ml), as well as HepG2, A549, A204, U937, and Jurkat cancer cells (IC50s = 1.2-3.4 ng/ml).2 In vivo, satratoxin H induces ulceration of the small intestine in, and is lethal to mice (LD50 = 5.69 mg/kg).3
|1. Nusuetrong, P., Pengsuparp, T., Meksuriyen, D., et al. Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells. Biol. Pharm. Bull. 31(6), 1115-1120 (2008).|2. Nielsen, C., Casteel, M., Didier, A., et al. Trichothecene-induced cytotoxicity on human cell lines. Mycotoxin Res. 25(2), 77-84 (2009).|3. 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).
| Cas No. | 53126-64-0 | SDF | |
| Canonical SMILES | O=C(/C=C\C=C\[C@@](OCC/1)([C@@H](O)C)[C@H](O)C1=C\C2=O)O[C@@H]3C[C@]4([H])[C@@]5(CO5)[C@@]3(C)[C@@]6(CO2)CCC(C)=C[C@@]6([H])O4 | ||
| 分子式 | C29H36O9 | 分子量 | 528.6 |
| 溶解度 | Dichloromethane: soluble,DMSO: soluble,Ethanol: soluble | 储存条件 | Store at -20°C, protect from light |
| 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。 | ||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.8918 mL | 9.4589 mL | 18.9179 mL |
| 5 mM | 0.3784 mL | 1.8918 mL | 3.7836 mL |
| 10 mM | 0.1892 mL | 0.9459 mL | 1.8918 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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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。
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Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells
Biol Pharm Bull 2008 Jun;31(6):1115-20.PMID:18520041DOI:10.1248/bpb.31.1115.
Satratoxin H, a mycotoxin, is thought to induce apoptosis of PC12 cells through the activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) in a glutathione (GSH)-sensitive manner. The present study was undertaken to further elucidate the mechanism by which Satratoxin H induces cell death in PC12 cells. Satratoxin H caused apoptosis of PC12 cells within 24-h, as determined by DNA fragmentation and flow cytometric analysis. Satratoxin H increased reactive oxygen species (ROS) production and lipid peroxidation, as determined by malondialdehyde formation. These effects were attenuated by incubation of cells with GSH, suggesting that satratoxin H-induced increase in apoptosis of serum-deprived PC12 cells may be partially mediated through the generation of ROS.
Apoptotic effects of Satratoxin H is mediated through DNA double-stranded break in PC12 cells
J Toxicol Sci 2012;37(4):803-12.PMID:22863859DOI:10.2131/jts.37.803.
Satratoxin H is an important air- and food-borne mycotoxin, which has been implicated in human health damage. Satratoxin H is known to induce apoptosis as well as genotoxicity in PC12 cells. In the present study, we further investigated the mechanism of apoptotic effects of Satratoxin H with focus on caspase-3 and poly-ADP-ribose polymerase (PARP) pathway. We also examined whether it induces DNA damage in PC12 cells. In the cells treated with Satratoxin H, caspase-3 was cleaved in a time-dependent manner. Furthermore, Satratoxin H induced cleavage of PARP, one of the downstream molecules of caspase-3. The cleavage was inhibited by SB203580, a p38 MAPK inhibitor, or SP600125, a JNK inhibitor. Satratoxin H, however, had no effect on expression levels of Bax and Bcl-2. Furthermore, the micronucleus assay revealed that Satratoxin H induced chromosome break. Also, Satratoxin H increased the level of phosphorylation of histone H2A, indicating that it caused DNA double-stranded breaks in PC12 cells. Meanwhile, no genotoxicity was detected with any of treatments carried out in the alkaline comet assay. These results imply that Satratoxin H induces genotoxicity by DNA double-stranded break. Our results suggest a considerable potential for the genotoxic risk associated with the presence of Satratoxin H.
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.
Involvement of reactive oxygen species and stress-activated MAPKs in satratoxin H-induced apoptosis
Eur J Pharmacol 2005 Jan 10;507(1-3):239-46.PMID:15659314DOI:10.1016/j.ejphar.2004.11.046.
Satratoxins, members of the trichothecene mycotoxin family, have been known to be harmful to health. However, the mechanisms underlying the toxicity still remain unclear. The present study is undertaken to elucidate the mechanisms of the satratoxin H-induced cytotoxicity in PC12 cells. Satratoxin H caused cytotoxicity, which was reflected from apoptosis determined by chromatin staining and flow cytometry. Satratoxin H stimulated the phosphorylation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). Pre-incubation with SB203580, a p38 MAPK inhibitor, or SP600125, a JNK inhibitor, but not PD98059, an ERK inhibitor, reduced satratoxin-induced cytotoxicity. Co-incubation of cells with glutathione, N-acetyl-L-cysteine or glutathione reductase inhibited cytotoxicity and the phosphorylation of p38 MAPK induced by Satratoxin H. Our data suggest that satratoxin H-induced apoptosis in PC12 cells is dependent on the activation of p38 MAPK/JNK and the increase in reactive oxygen species.
Antibodies to molds and satratoxin in individuals exposed in water-damaged buildings
Arch Environ Health 2003 Jul;58(7):421-32.PMID:15143855DOI:10.1080/00039896.2003.11879143.
Immunoglobulin (Ig)A, IgM, and IgG antibodies against Penicillium notatum, Aspergillus niger, Stachybotrys chartarum, and Satratoxin H were determined in the blood of 500 healthy blood donor controls, 500 random patients, and 500 patients with known exposure to molds. The patients were referred to the immunological testing laboratory for health reasons other than mold exposure, or for measurement of mold antibody levels. Levels of IgA, IgM, and IgG antibodies against molds were significantly greater in the patients (p < 0.001 for all measurements) than in the controls. However, in mold-exposed patients, levels of these antibodies against satratoxin differed significantly for IgG only (p < 0.001), but not for IgM or IgA. These differences in the levels of mold antibodies among the 3 groups were confirmed by calculation of z score and by Scheffé's significant difference tests. A general linear model was applied in the majority of cases, and 3 different subsets were formed, meaning that the healthy control groups were different from the random patients and from the mold-exposed patients. These findings indicated that mold exposure was more common in patients who were referred for immunological evaluation than it was in healthy blood donors. The detection of antibodies to molds and Satratoxin H likely resulted from antigenic stimulation of the immune system and the reaction of serum with specially prepared mold antigens. These antigens, which had high protein content, were developed in this laboratory and used in the enzyme-linked immunosorbent assay (ELISA) procedure. The authors concluded that the antibodies studied are specific to mold antigens and mycotoxins, and therefore could be useful in epidemiological and other studies of humans exposed to molds and mycotoxins.