L-Cysteine-glutathione disulfide
(Synonyms: L-半胱氨酸) 目录号 : GC44045A mixed disulfide
Cas No.:13081-14-6
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >95.00%
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L-Cysteine-glutathione disulfide, a glutathione derivative endogenous to mammalian cells, is comprised of the oxidized form of free glutathione tripeptide linked via a disulfide bond to L-cysteine. It has been shown to protect mice against acetaminophen-induced hepatotoxicity.
| Cas No. | 13081-14-6 | SDF | |
| 别名 | L-半胱氨酸 | ||
| Canonical SMILES | OC([C@@H](N)CSSC[C@@H](C(NCC(O)=O)=O)NC(CC[C@H](N)C(O)=O)=O)=O | ||
| 分子式 | C13H22N4O8S2 | 分子量 | 426.5 |
| 溶解度 | PBS (pH 7.2): 10 mg/ml,Water: 20 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 | 2.3447 mL | 11.7233 mL | 23.4467 mL |
| 5 mM | 0.4689 mL | 2.3447 mL | 4.6893 mL |
| 10 mM | 0.2345 mL | 1.1723 mL | 2.3447 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。
l-Histidine, arachidonic acid, biliverdin, and L-Cysteine-glutathione disulfide as potential biomarkers for cured pulmonary tuberculosis
Biomed Pharmacother 2019 Aug;116:108980.PMID:31125821DOI:10.1016/j.biopha.2019.108980.
Lack of laboratory standards for cured tuberculosis (TB) can lead to early discharge of untreated TB patients from the hospital, resulting in increased risk of TB spread and of developing drug resistant Mycobacterium tuberculosis (Mtb). We used ultra-high performance liquid chromatography coupled with mass spectrometry (LC-MS) to detect heparin anticoagulant in plasma of untreated TB patients, two-month treated TB patients, cured TB subjects, and healthy controls. Screening of differentially expressed metabolites resulted in identification of four differentially expressed metabolites such as, l-Histidine, Arachidonic acid (AA), Biliverdin, and L-Cysteine-glutathione disulfide after 6 months of TB treatment. Among them, L-Cysteine-glutathione disulfide and AA could be identified after 2 months of TB treatment. We established a cured TB model with an area under the curve (AUC) of 0.909 (95% CI, 0.802-0.970), 86.2% sensitivity, and 85.2% specificity. The diagnostic model fitted from the four differential metabolites in combination (l-Histidine, AA, Biliverdin, and L-Cysteine-glutathione disulfide) can be used as potential biomarkers for cured TB. Our study provided laboratory standards for hospital discharge of TB patients, as well as experimental basis for evaluating the efficacy of anti-TB drugs.
Hepatoprotection by L-cysteine-glutathione mixed disulfide, a sulfhydryl-modified prodrug of glutathione
J Biochem Mol Toxicol 2003;17(2):95-7.PMID:12717742DOI:10.1002/jbt.10069.
L-Cysteine-glutathione disulfide, a ubiquitous substance present in mammalian cells, was shown to be highly effective in protecting mice against acetaminophen-induced hepatotoxicity. Since the corresponding D-cysteine-glutathione disulfide was totally ineffective in this regard, an enzymatic mechanism that provides glutathione directly to cells is postulated.
Biosynthesis of S-(2-hydroxy-2-carboxyethylthio)-L-cysteine (3-mercaptolactate-cysteine disulfide) by the rat heart
Biochem Int 1983 Feb;6(2):291-6.PMID:6679325doi
Incubation of 3-mercaptopyruvate with rat heart homogenate resulted in the formation of S-(2-hydroxy-2-carboxy-ethylthio)-L-cysteine (HCETC, 3-mercaptolactate-cysteine disulfide), L-cysteine and 3-mercaptolactate with the concomitant decrease in glutamate and aspartate. These results indicate that a part of 3-mercaptopyruvate was converted to L-cysteine by transamination, a part was reduced to 3-mercaptolactate, and HCETC was formed from these two products. Another peak which corresponds to L-Cysteine-glutathione disulfide on amino acid analysis was also produced during the incubation.
Metabolism of 3-mercaptopyruvate in rat tissues
Acta Med Okayama 1983 Apr;37(2):85-91.PMID:6869067DOI:10.18926/AMO/32415.
Metabolism of 3-mercaptopyruvate was investigated using homogenates of rat heart, liver and kidney. When 3-mercaptopyruvate was incubated with heart homogenate, L-cysteine, L-alanine, S-(2-hydroxy-2-carboxyethylthio)-L-cysteine and 3-mercaptolactate were produced. At the same time, a decrease in the amounts of L-glutamate and L-aspartate was demonstrated. These results indicate that 3-mercaptopyruvate was converted to L-cysteine by cysteine aminotransferase (EC 2.6.1.3), to 3-mercaptolactate by lactate dehydrogenase (EC 1.1.1.27), and to pyruvate by 3-mercaptopyruvate sulfurtransferase (EC 2.8.1.2), and that HCETC and L-alanine were formed from these products. In the presence of liver homogenate, 3-mercaptopyruvate was mainly metabolized by 3-mercaptopyruvate sulfurtransferase; production of L-cysteine was small and HCETC was not formed. The metabolism of 3-mercaptopyruvate in the presence of kidney homogenate was intermediate between heart and liver: a fair amount of L-cysteine was formed, but HCETC was not produced. A peak which corresponds to L-Cysteine-glutathione disulfide on the chromatogram of amino acid analysis was present when 3-mercaptopyruvate was incubated with heart or liver homogenate, but not with kidney homogenate.