N-Acetyl-DL-penicillamine
(Synonyms: 乙酰青霉胺) 目录号 : GC47736
A chelating agent
Cas No.:59-53-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
N-Acetyl-DL-penicillamine is a chelating agent.1,2,3 It inhibits the binding of methyl mercury to isolated human erythrocytes by 50% and removes 50% of methyl mercury ions from methyl mercury-loaded blood cells when used at a concentration of 1 mM.1,2 N-Acetyl-DL-penicillamine (3 mmol/kg per day, p.o.) reduces the biological half-life of mercury and decreases liver, kidney, brain, and blood mercury levels, as well as increases urinary excretion of mercury in a concentration-dependent manner, in mice when administered following injection of methyl mercuric chloride. It decreases mercuric chloride-induced mortality in mice when administered orally at a dose of 1.6 mmol/kg.3 N-Acetyl-DL-penicillamine is also an analog of SNAP that does not generate nitric oxide and has been used as a negative control in experiments using SNAP.4,5
1.Aaseth, J.Mobilization of methyl mercury in vivo and in vitro using N-acetyl-DL-penicillamine and other complexing agentsActa Pharm. Toxicol. (Copenh.)39(3)289-301(1976) 2.Aaseth, J., Alexander, J., and Deverill, J.Evaluation of methyl mercury chelating agents using red blood cells and isolated hepatocytesChem. Biol. Interact.36(3)287-297(1981) 3.Nielsen, J.B., and Andersen, O.Effect of four thiol-containing chelators on disposition of orally administered mercuric chlorideHum. Exp. Toxicol.10(6)423-430(1991) 4.Ogura, T., DeGeorge, G., Tatemichi, M., et al.Suppression of anti-microtubule agent-induced apoptosis by nitric oxide: Possible mechanism of a new drug resistanceJpn. J. Cancer Res.89(2)199-205(1998) 5.Takhampunya, R., Padmanabhan, R., and Ubol, S.Antiviral action of nitric oxide on dengue virus type 2 replicationJ. Gen. Virol.87(Pt. 10)3003-3011(2006)
| Cas No. | 59-53-0 | SDF | |
| 别名 | 乙酰青霉胺 | ||
| Canonical SMILES | SC(C)(C)C(NC(C)=O)C(O)=O | ||
| 分子式 | C7H13NO3S | 分子量 | 191.2 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,DMSO:PBS (pH 7.2) (1:7): 0.12 mg/ml,Ethanol: 5 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 | 5.2301 mL | 26.1506 mL | 52.3013 mL |
| 5 mM | 1.046 mL | 5.2301 mL | 10.4603 mL |
| 10 mM | 0.523 mL | 2.6151 mL | 5.2301 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。
N-Acetyl-DL-penicillamine and acetaminophen toxicity in mice
J Pharm Sci 1980 Sep;69(9):1005-6.PMID:7411400DOI:10.1002/jps.2600690905.
N-Acetyl-DL-penicillamine (IIIb), a structural analog of N-acetyl-L-cysteine (IIIa), did not protect mice from lethal doses of acetaminophen (I), whereas IIIa offered protection. This lack of efficacy of IIIb probably is due to the decreased nucleophilicity of its sulfhydryl group compared to that of IIIa, the probable involvement of cysteine in and conjugate addition to the reactive intermediates of I, and the absence of metabolic conversion of IIIb to inorganic sulfate.
Decreased hypotensive responsiveness to nitric oxide donor S-nitroso N-Acetyl-DL-penicillamine (SNAP) in spontaneously hypertensive (SHR) rats
J Physiol Pharmacol 1998 Mar;49(1):37-49.PMID:9594409doi
The aim of the study was to compare hemodynamic effects of intravenously (i.v.) applied nitric oxide (NO) donor S-nitroso N-Acetyl-DL-penicillamine (SNAP) in conscious spontaneously hypertensive (SHR) to those observed in normotensive Wistar Kyoto (WKY) rats. The study was performed on 7 SHR and 8 WKY instrumented with polyethylene catheters inserted to the abdominal aorta and vena cava for blood pressure (MAP) and heart rate period (HRp) monitoring, and for i.v. administration of SNAP (0.05, 0.1, 0.2, 0.5, 1.0, 2.0, 5.0, 10.0, 20.0, 40.0 and 75.0 microM/kg of body weight). The following differences were found between SHR and WKY rats: 1) the threshold dose of SNAP, eliciting significant decrease of MAP was markedly higher in SHR (1.0 microM/kg b.w.) than in WKY (0.2 microM/kg b.w.), 2) SHR responded with significantly smaller maximum decreases of MAP to administration of 1.0, 2.0, 5.0 and 10.0 microM/kg b.w. of SNAP and with smaller heart rate acceleration to administration of 10.0, 40.0 and 75.0 microM/kg b.w. of SNAP, 3) in SHR MAP decreased progressively, the greatest decline being observed after administration of the highest dose (75 microM/kg b.w.) of SNAP while in WKY the log dose/delta MAP response curve reached plateau beginning with 2 microM/kg b.w. of SNAP, 4) the slopes and intercepts of the regression lines describing relationship between MAP and HRp after administration of SNAP were significantly different in SHR and WKY rats (P < 0.01). The results indicate that SHR are significantly less sensitive to hypotensive effects of NO generated from moderate doses of SNAP.
Nitric oxide as a potential pathological mechanism in demyelination: its differential effects on primary glial cells in vitro
Neuroscience 1994 Aug;61(3):575-85.PMID:7969931DOI:10.1016/0306-4522(94)90435-9.
Because we believe that macrophage-derived nitric oxide contributes to pathology of demyelinating diseases, we have determined the differential effects of nitric oxide on primary rat glial cells in vitro. Enriched cultures of microglia, astrocytes and oligodendrocytes were treated with S-nitroso,N-Acetyl-DL-penicillamine, a nitric oxide-releasing chemical. There was a significantly decreased function of one of the ferrosulfur-containing mitochondrial enzymes after S-nitroso,N-Acetyl-DL-penicillamine/nitric oxide treatment in oligodendrocytes and astrocytes compared to microglia, which were much less sensitive to S-nitroso,N-Acetyl-DL-penicillamine/nitric oxide at all concentrations. At 0.5 mM S-nitroso,N-Acetyl-DL-penicillamine/nitric oxide, astrocytes and oligodendrocytes suffered a 40% loss in succinate dehydrogenase activity, while microglia were unaffected. A control non-ferrosulfur-containing mitochondrial enzyme, isocitrate dehydrogenase, was not affected in any glial cell type. Although the per cent of mitochondrial damage in oligodendrocytes and astrocytes was the same for all concentrations of S-nitroso,N-Acetyl-DL-penicillamine/nitric oxide, significant cell death occurred in oligodendrocytes at 1.0 mM; at this concentration there was no significant killing of microglia or astrocytes. Furthermore, at a 0.5 mM concentration of S-nitroso,N-Acetyl-DL-penicillamine/nitric oxide, which inhibited mitochondrial respiration but did not kill oligodendrocytes, significant changes in oligodendrocyte morphology (e.g. retraction of processes) occurred. Morphological changes were not seen in microglia and astrocytes at any concentration of S-nitroso,N-Acetyl-DL-penicillamine/nitric oxide. In addition, oligodendrocytes were more sensitive to S-nitroso,N-Acetyl-DL-penicillamine/nitric oxide-induced single stranded DNA breaks than microglia or astrocytes. The mitochondrial damage was attributable to nitric oxide since N-Acetyl-DL-penicillamine had no effect. Oxyhemoglobin, which competitively inhibits toxic effects of nitric oxide, protected these glial cells from mitochondrial damage, single stranded breaks in DNA and cell death in a time- and dose-dependent manner. Once again, oligodendrocytes were less easily rescued from nitric oxide effects by oxyhemoglobin than were astrocytes, suggesting greater vulnerability of the myelin-producing cell to nitric oxide. These findings suggest that there is differential sensitivity of glial cells to nitric oxide. Although oligodendrocytes and astrocytes are equally susceptible to nitric oxide-induced mitochondrial damage, oligodendrocytes are more sensitive to nitric oxide-induced single stranded DNA breaks, morphological changes and cell death. Compared to both oligodendrocytes and astrocytes, microglia, nitric oxide-producing cells, are resistant to nitric oxide-induced damage.