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Se-Methylselenocysteine Sale

(Synonyms: L-硒甲基硒代半胱氨酸,Methylselenocysteine; Se-Methylseleno-L-cysteine) 目录号 : GC38848

A selenium-containing amino acid

Se-Methylselenocysteine Chemical Structure

Cas No.:26046-90-2

规格 价格 库存 购买数量
10mM (in 1mL Water)
¥385.00
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5mg
¥350.00
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10mg
¥595.00
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产品描述

Se-Methylselenocysteine is a selenium-containing amino acid that has been found in Allium and has antioxidative and anticancer augmenting activities.1,2 Se-Methylselenocysteine (0.01-10 ?M) prevents tert-butyl hydroperoxide-induced increases in malondialdehyde (MDA) levels and glutathione reductase and glutathione peroxidase (GPX) activity, as well as decreases in glutathione (GSH) levels, in HepG2 cells.1 It has an additive effect on irinotecan-induced tumor growth reduction in a FaDu mouse xenograft model when administered at a dose of 5 ?g/animal per day.2

1.Cuello, S., Ramos, S., Mateos, R., et al.Selenium methylselenocysteine protects human hepatoma HepG2 cells against oxidative stress induced by tert-butyl hydroperoxideAnal. Bioanal. Chem.389(7-8)2167-2178(2007) 2.Azrak, R.G., Cao, S., Pendyala, L., et al.Efficacy of increasing the therapeutic index of irinotecan, plasma and tissue selenium concentrations is methylselenocysteine dose dependentBiochem. Pharmacol.73(9)1280-1287(2007)

Chemical Properties

Cas No. 26046-90-2 SDF
别名 L-硒甲基硒代半胱氨酸,Methylselenocysteine; Se-Methylseleno-L-cysteine
Canonical SMILES OC([C@@H](N)C[Se]C)=O
分子式 C4H9NO2Se 分子量 182.08
溶解度 Water: 83.33 mg/mL (457.66 mM) 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 5.4921 mL 27.4605 mL 54.9209 mL
5 mM 1.0984 mL 5.4921 mL 10.9842 mL
10 mM 0.5492 mL 2.746 mL 5.4921 mL
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Research Update

Se-Methylselenocysteine: a new compound for chemoprevention of breast cancer

Nutr Cancer 2001;40(1):12-7.PMID:11799917DOI:10.1207/S15327914NC401_5.

Selenium compounds have attracted renewed interest as chemopreventive agents for human cancer on the basis of the pioneering intervention study by Clark and co-workers. The rodent mammary gland has been used extensively as a model for examining the chemopreventive activities of inorganic and organic selenium compounds. This review summarizes the rationale and results for use of a new organic selenium compound, Se-Methylselenocysteine, which exhibits greater efficacy as a chemopreventive agent than several previously used selenium compounds in experimental models of breast cancer and has potential for use in human populations.

Se-Methylselenocysteine (SMC) Improves Cognitive Deficits by Attenuating Synaptic and Metabolic Abnormalities in Alzheimer's Mice Model: A Proteomic Study

ACS Chem Neurosci 2021 Apr 7;12(7):1112-1132.PMID:33689275DOI:10.1021/acschemneuro.0c00549.

Se-Methylselenocysteine (SMC) is a major selenocompound in selenium (Se) enriched plants and has been found to ameliorate neuropathology and cognitive deficits in triple-transgenic mice model of Alzheimer's disease (3 × Tg-AD mice). To explore the underlying molecular mechanisms, the present study is designed to elucidate the protein changes in the cortex of SMC-treated 3 × Tg-AD mice. After SMC supplementation, proteomic analysis revealed that 181, 271, and 41 proteins were identified as differentially expressed proteins (DEPs) between 3 × Tg-AD mice vs wild type (AD/WT group), SMC-treated AD mice vs AD (AD + SMC/AD), and AD + SMC/WT group, respectively. Among these, 138 proteins in the diseased group were reversed by SMC treatment. The DEPs in AD/WT group and AD + SMC/AD group were mainly related to metabolism, synapses, and antioxidant proteins, while their levels were decreased in AD mice but up-regulated after treating with SMC. In addition, we found reduced ATP levels and destroyed synaptic structures in the AD mice brains, which were significantly ameliorated upon SMC treatment. Our study suggests that energy metabolism disorders, abnormal amino acid metabolism, synaptic dysfunction, and oxidative stress may be the key pathogenic phenomena of AD. SMC reversed the expression of proteins associated with them, which might be the main mechanism of its intervention in AD.

Sex-dimorphic distribution and anti-oxidative effects of selenomethionine and Se-Methylselenocysteine supplementation

J Food Sci 2021 Dec;86(12):5424-5438.PMID:34796490DOI:10.1111/1750-3841.15970.

Selenium (Se) is a vital trace element in human beings and is essential for protection against oxidative stress. This study aimed to investigate the accumulation and antioxidant effects of two organic seleniums, L-selenomethionine (SM) and L-Se-methylselenocysteine (SMC), through in vivo and in vitro experiments. L02 cells were pretreated with 10 nM SM or SMC for 24 h, followed by exposure to 100 nM of H₂O₂. Cell viability, apoptosis, and antioxidant capacity were detected to evaluate SM and SMC's protective effect. Organic selenium (SM and SMC) and inorganic selenium (sodium selenite, SS) were compared in terms of their in vivo accumulation and antioxidant capacity when supplemented daily and subsequently deprived in SD rats. Our results show that SM or SMC pre-treatment could significantly prevent elevated apoptosis and declined antioxidant ability. We found that organic Se supplementation resulted in higher Se accumulation than inorganic Se in the liver and kidney. The antioxidant capacity of liver and kidney tissues from rats fed with either organic selenium was significantly improved and was higher than that of SS. In summary, this study suggests that organic selenium supplements are more effective in facilitating Se accumulation in liver and kidney, enhancing antioxidant capacities, thereby protecting cells from oxidative stress. PRACTICAL APPLICATION: This study compared the antioxidant capacity of sodium selenite, L-selenomethionine, and L-Se-methylselenocysteine in vitro and in vivo. The results showed that organic selenium has a stronger antioxidant capacity and that significant differences exist in its absorption and conversion in male and female rats. Our results provide theoretical guidance for dietary supplementation of selenium.

Se-Methylselenocysteine stimulates migration and antioxidant response in HaCaT keratinocytes: Implications for wound healing

J Trace Elem Med Biol 2020 Mar;58:126426.PMID:31743802DOI:10.1016/j.jtemb.2019.126426.

Background: Se-Methylselenocysteine (MSC), a natural organic selenium compound, is known for its anticancer effects. In the present study, we investigated the effects of MSC on cell migration, which is the most limiting step in the reepithelialization process of wound healing and the antioxidant response in HaCaT keratinocytes. Methods: HaCaT cells were treated with various concentrations of MSC. Cell migration and proliferation, the expression of proteins that are involved in the epidermal-mesenchymal transition (EMT) process, the extent of oxidative stress and the antioxidant response, and the associated signaling pathways were analyzed. Results: MSC (100-500 μM) increased HaCaT cell migration. MSC stimulated EMT, which was evidenced by a decrease in E-cadherin in the cells at the wound edge and increases in Snail, Twist, and matrix metalloproteinases. MSC increased the phosphorylation of Akt and glycogen synthase kinase 3β, which led to the stabilization and nuclear accumulation of β-catenin, a transcriptional coactivator involved in EMT. MSC caused a transient increase and then an eventual decrease in cellular reactive oxygen species, which appeared to be associated with the increase in nuclear factor erythroid 2-related factor 2, a key transcription factor for the antioxidant response. Conclusion: Our results suggest that MSC can promote skin wound healing by stimulating keratinocyte migration and, moreover, can protect cells from excessive oxidative stress that often accompanies and impairs the wound healing process, particularly in chronic wounds, by stimulating an antioxidant response.

Combination of Se-Methylselenocysteine, D-α-tocopheryl succinate, β-carotene, and L-lysine can prevent cancer metastases using as an adjuvant therapy

J Zhejiang Univ Sci B 2022 Nov 15;23(11):943-956.PMID:36379613DOI:10.1631/jzus.B2200232.

Objectives: Primary tumor treatment through surgical resection and adjuvant therapy has been extensively studied, but there is a lack of effective strategies and drugs for the treatment of tumor metastases. Here, we describe a functional product based on a combination of compounds, which can be used as an adjuvant therapy and has well-known mechanisms for inhibiting cancer metastases, improving anti-cancer treatment, and enhancing immunity and antioxidant capacity. Our designed combination, named MVBL, consists of four inexpensive compounds: L-selenium-methylselenocysteine (MSC), D-‍α‍-tocopheryl succinic acid (VES), β‍-carotene (β‍-Ca), and L-lysine (Lys). Methods: The effects of MVBL on cell viability, cell cycle, cell apoptosis, cell migration, cell invasion, reactive oxygen species (ROS), and paclitaxel (PTX)-combined treatment were studied in vitro. The inhibition of tumor metastasis, antioxidation, and immune enhancement capacity of MVBL were determined in vivo. Results: MVBL exhibited higher toxicity to tumor cells than to normal cells. It did not significantly affect the cell cycle of cancer cells, but increased their apoptosis. Wound healing, adhesion, and transwell assays showed that MVBL significantly inhibited tumor cell migration, adhesion, and invasion. MVBL sensitized MDA-MB-231 breast cancer cells to PTX, indicating that it can be used as an adjuvant to enhance the therapeutic effect of chemotherapy drugs. In mice, experimental data showed that MVBL inhibited tumor metastasis, prolonged their survival time, and enhanced their antioxidant capacity and immune function. Conclusions: This study revealed the roles of MVBL in improving immunity and antioxidation, preventing tumor growth, and inhibiting metastasis in vitro and in vivo. MVBL may be used as an adjuvant drug in cancer therapy for improving the survival and quality of life of cancer patients.