Se-Methylselenocysteine (hydrochloride)
(Synonyms: Methylselenocysteine, Se-MeSeCys, Se-methyl-L-Selenocysteine) 目录号 : GC48914
Se-methylselenocysteine (MSC)(硒甲基硒基半胱氨酸)是硒基半胱氨酸甲基化的衍生物,是一种天然的单甲基化硒氨基酸。
Cas No.:863394-07-4
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
| Cell experiment [1]: | |
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Cell lines |
SKOV-33 cells |
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Preparation Method |
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Reaction Conditions |
100-400 µM; 3 days |
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Applications |
Se-Methylselenocysteine(MSC) induces apoptosis in SKOV-33 cells. |
| Animal experiment [2]: | |
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Animal models |
Sprague-Dawley rats(120 to 150 g) |
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Preparation Method |
The rats were randomly divided into a Normal control group (n=16), Model group (n=16), and Se-Methylselenocysteine (MSC)-treated groups (n=48). Rats in the Normal control group were fed a normal diet (without MSC). Rats in the Model group were fed a normal diet containing 0.1 mg/kg MSC 5 times per week for 6 consecutive weeks. |
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Dosage form |
0.3 /1/3 mg/kg;10weeks; p.o. |
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Applications |
MSC treatment alleviated the liver injury. With the increase of MSC concentration, the degree of liver tissue injury was gradually reduced. |
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References: [1].Yeo JK, Cha SD,et,al. Se-methylselenocysteine induces apoptosis through caspase activation and Bax cleavage mediated by calpain in SKOV-3 ovarian cancer cells. Cancer Lett. 2002 Aug 8;182(1):83-92. doi: 10.1016/s0304-3835(02)00075-7. PMID: 12175527. | |
Se-methylselenocysteine (hydrochloride) (MSC), a derivative of selenocysteine methylation, is a natural monomethylated selenoamino acid. Se-methylselenocysteine is used primarily for anti-aging, selenium supplementation, treatment of cardiovascular/cerebrovascular diseases, and antioxidation[1]. Se-Methylselenocysteine is orally bioavailable, and induces apoptosis[2,3].
Se-methylselenocysteine(100-400 µM; 3 days) induces apoptosis through caspase activation and Bax cleavage mediated by calpain in SKOV-3 ovarian cancer cells[4]. Se-methylselenocysteine (200 µM; 24 h) can effectively reverse the decrease of cell viability caused by EA (elaidic acid)[5]. Se-methylselenocysteine at an optimum concentration of 1 µM could reverse the alteration in antioxidative capacity, Bcl2/Bax ratio and caspase-8 activity caused by clusterin (Clu) -knockdown, thus inhibiting apoptosis and maintaining cell viability[6].
Se-Methylselenocysteine (0.2 mg/mouse; p.o.; daily for 14 days) potentiates the antitumour activity of Cisplatin (cis-diamminedichloroplatinum (CDDP)) and Cyclophosphamide in nude mice bearing human FaDu and A253 head and neck xenografts[7]. Se-methylselenocysteine (0.3 /1/3 mg/kg;10weeks;p.o.) treatment alleviated the liver injury. With the increase of Se-methylselenocysteine concentration, the degree of liver tissue injury was gradually reduced in mice[8].
References:
[1]. Johnson WD, Morrissey RL, et,al. Subchronic toxicity studies of Se-methylselenocysteine, an organoselenium compound for breast cancer prevention: Food Chem Toxicol, 2008; 46; 1068-78
[2]. El-Bayoumy K, Sinha R, Mechanisms of mammary cancer chemoprevention by organoselenium compounds: Mutat Res, 2004; 551; 181-97
[3]. Medina D, Thompson H, et,al.Se-methylselenocysteine: A new compound for chemoprevention of breast cancer: Nutr Cancer, 2001; 40; 12-17
[4]. Yeo JK, Cha SD, et,al. Se-methylselenocysteine induces apoptosis through caspase activation and Bax cleavage mediated by calpain in SKOV-3 ovarian cancer cells. Cancer Lett. 2002 Aug 8;182(1):83-92. doi: 10.1016/s0304-3835(02)00075-7. PMID: 12175527.
[5]. Xia J, Xia X, et,al. Protective Effect of Se-Methylselenocysteine on Elaidic Acid-Induced Inflammation in Human Arterial Endothelial Cells. J Nutr Sci Vitaminol (Tokyo). 2020;66(6):577-582. doi: 10.3177/jnsv.66.577. PMID: 33390400.
[6]. Wang C, Zeng Z, et,al. Se-methylselenocysteine inhibits apoptosis induced by clusterin knockdown in neuroblastoma N2a and SH-SY5Y cell lines. Int J Mol Sci. 2014 Nov 18;15(11):21331-47. doi: 10.3390/ijms151121331. PMID: 25411798; PMCID: PMC4264228.
[7]. Cao S, Durrani FA, et,al. Se-methylselenocysteine offers selective protection against toxicity and potentiates the antitumour activity of anticancer drugs in preclinical animal models. Br J Cancer. 2014 Apr 2;110(7):1733-43. doi: 10.1038/bjc.2014.85. Epub 2014 Mar 11. PMID: 24619073; PMCID: PMC3974093.
[8]. Ding J, Qi C, et,al. Se-Methylselenocysteine Alleviates Liver Injury in Diethylnitrosamine (DEN)-Induced Hepatocellular Carcinoma Rat Model by Reducing Liver Enzymes, Inhibiting Angiogenesis, and Suppressing Nitric Oxide (NO)/Nitric Oxide Synthase (NOS) Signaling Pathway. Med Sci Monit. 2021 Aug 4;27:e929255. doi: 10.12659/MSM.929255. PMID: 34344856; PMCID: PMC8351367.
Se-methylselenocysteine (MSC)(硒甲基硒基半胱氨酸)是硒基半胱氨酸甲基化的衍生物,是一种天然的单甲基化硒氨基酸。主要用于抗衰老、补充硒、治疗心脑血管疾病和抗氧化[1]。可口服,可诱导细胞凋亡[2,3]。
Se-methylselenocysteine(100 - 400µM;3days)通过calpain介导的caspase激活和Bax切割诱导SKOV-3卵巢癌细胞凋亡[4]。Se-methylselenocysteine (200 µM;24 h)可有效逆转EA(戊酸)引起的细胞活力下降[5]。Se-methylselenocysteine (MSC)在1 µM浓度下可逆转clusterin (Clu) -下调引起的抗氧化能力、Bcl2/Bax比值和caspase-8活性的改变,从而抑制细胞凋亡,维持细胞活力[6]。
Se-Methylselenocysteine (0.2 mg/mouse; p.o.; daily for 14 days) 增强了CDDP和环磷酰胺对异种移植裸鼠(bearing human FaDu and A253 cell)的抗肿瘤活性[7]。Se-methylselenocysteine (0.3 /1/3 mg/kg;10weeks;p.o.) 治疗可减轻肝损伤。随着浓度的增加,小鼠肝组织损伤程度逐渐减轻[8]。
| Cas No. | 863394-07-4 | SDF | |
| 别名 | Methylselenocysteine, Se-MeSeCys, Se-methyl-L-Selenocysteine | ||
| Canonical SMILES | C[Se]C[C@H](N)C(O)=O.Cl | ||
| 分子式 | C4H9NO2Se •HCl | 分子量 | 218.6 |
| 溶解度 | DMF: 1 mg/ml,DMSO: 1 mg/ml,PBS (pH 7.2): 10 mg/ml | 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 | 4.5746 mL | 22.8728 mL | 45.7457 mL |
| 5 mM | 0.9149 mL | 4.5746 mL | 9.1491 mL |
| 10 mM | 0.4575 mL | 2.2873 mL | 4.5746 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。
Selenium supplementation improves antioxidant capacity in vitro and in vivo in patients with coronary artery disease The SElenium Therapy in Coronary Artery disease Patients (SETCAP) Study
Am Heart J 2008 Dec;156(6):1201.e1-11.PMID:19033020DOI:PMC3624729
Background: Selenium is a central determinant of antioxidative glutathione peroxidase 1 (GPx-1) expression and activity. The relevance of selenium supplementation on GPx-1 in coronary artery disease (CAD) needs to be established. We assessed the effect of selenium supplementation on GPx-1 in cell culture and on endothelial function in a prospective clinical trial. Methods: Human coronary artery endothelial cells were incubated with 5.78 to 578 nmol/L sodium selenite, Se-methyl-selenocysteine hydrochloride, or seleno-l-methionine. Glutathione peroxidase 1 mRNA and protein expression and activity were measured. Coronary artery disease patients (n = 465) with impaired endothelial function (flow-mediated dilation [FMD] <8%) were randomly assigned to receive 200 or 500 microg sodium selenite daily or matching placebo during a 12-week period. We tested the effect on red blood cell GPx-1 activity and brachial artery FMD. Furthermore, differences in biomarkers of oxidative stress and inflammation were measured. Results: Sodium selenite and Se-methyl-selenocysteine hydrochloride increased GPx-1 protein and activity in a dose-dependent manner (P < .0001). The intention-to-treat groups comprised 433 CAD patients. Glutathione peroxidase 1 activity increased from 37.0 U/gHb (31.3-41.7) to 41.1 U/gHb (35.2-48.4) (P < .0001) in the 200 microg and from 38.1 U/gHb (33.2-43.8) to 42.6 U/gHb (35.0-49.1) (P < .0001) in the 500 microg sodium selenite group treated for 12-weeks. No relevant changes were observed for FMD or biomarkers of oxidative stress and inflammation. Conclusions: Sodium selenite supplementation increases GPx-1 activity in endothelial cells and in CAD patients. Future studies have to demonstrate whether long-term CAD outcome can be improved.