Ethylene dimethanesulfonate
(Synonyms: 乙二磺酸乙烯酯) 目录号 : GC60824
Ethylenedimethanesulfonate是一种温和的烷基化乙二醇非挥发性甲烷磺酸二酯。Ethylenedimethanesulfonate对LC具有选择性的促凋亡作用。
Cas No.:4672-49-5
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
Ethylene dimethane sulfonate is a mild alkylating, non-volatile methanesulfonic diester of ethylene glycol. Ethylene dimethanesulfonate has selective pro-apoptotic effects on LCs[1].
Ethylene dimethanesulfonate (subcutaneous injection; 75 mg/kg; 7 days) disrupts epididymal function and leads to sperm granuloma formation in rat[1].
[1]. Dutta D, et al. Ethylene dimethane sulfonate (EDS) ablation of Leydig cells in adult rat depletes testosterone resulting in epididymal sperm granuloma: Testosterone replacement prevents granuloma formation. Reprod Biol. 2019 Mar;19(1):89-99.
| Cas No. | 4672-49-5 | SDF | |
| 别名 | 乙二磺酸乙烯酯 | ||
| Canonical SMILES | CS(=O)(OCCOS(C)(=O)=O)=O | ||
| 分子式 | C4H10O6S2 | 分子量 | 218.25 |
| 溶解度 | DMSO: 100 mg/mL (458.19 mM) | 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 | 4.5819 mL | 22.9095 mL | 45.819 mL |
| 5 mM | 0.9164 mL | 4.5819 mL | 9.1638 mL |
| 10 mM | 0.4582 mL | 2.291 mL | 4.5819 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。
Ethylene dimethanesulfonate inhibits the function of Sertoli cells in culture at sublethal doses
Endocrinology 1990 Mar;126(3):1618-22.PMID:2155105DOI:10.1210/endo-126-3-1618.
The dose-dependent effects of Ethylene dimethanesulfonate (EDS) on transferrin production and viability of Sertoli cells in culture have been investigated. Sertoli cells, isolated from the testes of 20-day-old rats, exhibited decreased transferrin production in response to EDS at a dose of 0.3 mM. The suppression of transferrin synthesis by EDS reached a maximum (15% of control) with a dose of 1.1 mM, without significant cell mortality. An EDS dose of 2.7 mM proved lethal to Sertoli cells, reducing the number of viable cells per well by 85%. Sertoli cells preincubated with a sublethal dose of EDS (0.3-0.5 mM) appeared to recover upon removal of EDS from the culture medium, as evidenced by an increase in transferrin mRNA levels. Sertoli cells given 2.7 mM EDS did not recover. These data demonstrate a direct cytotoxic effect of EDS on Sertoli cell function at relatively low doses and a lethal effect of the alkylating agent at high doses. These results also indicate that EDS may affect Sertoli cells in vivo and, consequently, directly affect the function of the seminiferous epithelium.
Ethylene dimethanesulfonate destroys Leydig cells in the rat testis
Endocrinology 1986 Feb;118(2):709-19.PMID:3002764DOI:10.1210/endo-118-2-709.
Ultrastructural changes in the interstitial cells of the adult rat testis were studied up to 45 days after administration of a single dose (100 mg/kg) of the antifertility compound Ethylene dimethanesulfonate (EDS). Most Leydig cells showed degenerative changes 12 h after treatment. Twenty-four and 48 h after injection, all Leydig cells observed showed gross degenerative changes. At 4 and 14 days, intact Leydig cells could not be identified in the interstitial spaces. Twenty-one days after treatment with EDS, small Leydig cells were visible, and at 45 days, Leydig cells appeared normal. The seminiferous epithelium appeared morphologically normal until 4 days after injection of EDS, when slight abnormalities were observed. At 14 and 21 days, the seminiferous epithelium was grossly abnormal, but at 48 days, spermatogenesis appeared normal. Twelve, 24, and 48 h after treatment, large quantities of material, presumably from dead Leydig cells, were observed within the macrophage cytoplasm. The predominant cell in the interstitial space 4 and 14 days after EDS was the macrophage. Inclusions from the dead Leydig cells within the cytoplasm of the macrophages had almost disappeared. LH receptors (hCG binding) in testicular homogenates were consistent with the cytological changes in Leydig cells. Receptor concentration was low at 24 h and was almost zero at 4 days. This change was accompanied by a decrease in serum testosterone to castrate levels by 2 days. The responses of the endocrine system to destruction of the Leydig cell by EDS, as monitored by serum FSH, LH, and testosterone, were slower than those after castration, indicating that the response to EDS reflects the time required to kill the Leydig cell rather than direct impairment of the steroidogenic pathway. These experiments demonstrate that Leydig cells can be specifically destroyed by a cytotoxic drug. The availability of a specific cytotoxic agent for Leydig cells offers further opportunities to study the interrelationships between the Leydig cell and the seminiferous tubule.
Differentiation of human adipose derived stem cells into Leydig-like cells with molecular compounds
J Cell Mol Med 2019 Sep;23(9):5956-5969.PMID:31293077DOI:10.1111/jcmm.14427.
Leydig cells (LCs) are the primary source of testosterone in the testis, and testosterone deficiency caused by LC functional degeneration can lead to male reproductive dysfunction. LC replacement transplantation is a very promising approach for this disease therapy. Here, we report that human adipose derived stem cells (ADSCs) can be differentiated into Leydig-like cells using a novel differentiation method based on molecular compounds. The isolated human ADSCs expressed positive CD29, CD44, CD59 and CD105, negative CD34, CD45 and HLA-DR using flow cytometry, and had the capacity of adipogenic and osteogenic differentiation. ADSCs derived Leydig-like cells (ADSC-LCs) acquired testosterone synthesis capabilities, and positively expressed LC lineage-specific markers LHCGR, STAR, SCARB1, SF-1, CYP11A1, CYP17A1, HSD3B1 and HSD17B3 as well as negatively expressed ADSC specific markers CD29, CD44, CD59 and CD105. When ADSC-LCs labelled with lipophilic red dye (PKH26) were injected into rat testes which were selectively eliminated endogenous LCs using Ethylene dimethanesulfonate (EDS, 75 mg/kg), the transplanted ADSC-LCs could survive and function in the interstitium of testes, and accelerate the recovery of blood testosterone levels and testis weights. These results demonstrated that ADSCs could be differentiated into Leydig-like cells by few defined molecular compounds, which might lay the foundation for further clinical application of ADSC-LC transplantation therapy.