Se-Methylselenocysteine (hydrochloride)
(Synonyms: Methylselenocysteine, Se-MeSeCys, Se-methyl-L-Selenocysteine) 目录号 : GC48914Se-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.
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]。
Cell experiment [1]: | |
Cell lines |
SKOV-33 cells |
Preparation Method |
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Reaction Conditions |
100-400 µM; 3 days |
Applications |
Se-Methylselenocysteine(MSC) induces apoptosis in SKOV-33 cells. |
Animal experiment [2]: | |
Animal models |
Sprague-Dawley rats(120 to 150 g) |
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. |
Dosage form |
0.3 /1/3 mg/kg;10weeks; p.o. |
Applications |
MSC treatment alleviated the liver injury. With the increase of MSC concentration, the degree of liver tissue injury was gradually reduced. |
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. |
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 |
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制备储备液 | |||
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 |
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2.
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Quality Control & SDS
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- Purity: >98.00%
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