|Source:||The roots of Atractylodes lancea (Thunb.) DC.|
|Biological Activity or Inhibitors:||1. Carboxyatractyloside induces the inhibitory effect of tamoxifen on nonspecific membrane permeability.
2. Carboxyatractyloside can induce permeability transition, and that ageing induced mitochondrial DNA disruption and release of cytochrome c.
3. Carboxyatractyloside poisoning causes multiple organ dysfunction and can be fatal, the signs of a poor prognosis including coagulation abnormalities, hyponatraemia, marked hypoglycaemia, icterus and hepatic and renal failure, without antidote.
|Solvent:||Pyridine, Methanol, Ethanol, DMSO, etc|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||1.1298 mL||5.6491 mL||11.2982 mL||22.5963 mL||28.2454 mL|
|5 mM||0.226 mL||1.1298 mL||2.2596 mL||4.5193 mL||5.6491 mL|
|10 mM||0.113 mL||0.5649 mL||1.1298 mL||2.2596 mL||2.8245 mL|
|50 mM||0.0226 mL||0.113 mL||0.226 mL||0.4519 mL||0.5649 mL|
|100 mM||0.0113 mL||0.0565 mL||0.113 mL||0.226 mL||0.2825 mL|
Life Sci. 2011 Apr 11;88(15-16):681-7.
|Protective action of tamoxifen on carboxyatractyloside-induced mitochondrial permeability transition.[Pubmed: 21324322]|
|Permeability transition was induced after the addition of Carboxyatractyloside, which is a specific reagent that interacts with the adenine nucleotide translocase. MAIN METHODS: Permeability transition was assessed by analyzing matrix Ca(2+) release, transmembrane electric gradient, and mitochondrial swelling in aged, as well as in freshly prepared mitochondria. Also, cytochrome c content was analyzed in membrane mitochondria as well as in the supernatant. KEY FINDINGS: In freshly prepared mitochondria, tamoxifen, at the concentration of 10 μM, totally inhibited nonspecific membrane permeability induced by 1 μM Carboxyatractyloside. In addition, tamoxifen inhibited non-specific permeability in aged mitochondria and diminished membrane fluidity. SIGNIFICANCE: Plausibly, the inhibitory effect of tamoxifen on nonspecific membrane permeability, as induced by Carboxyatractyloside, should be ascribed to a diminution, of membrane fluidity by this drug.|
Radiat Res. 2009 Nov;172(5):575-83.
|Cyclosporin A inhibits UV-radiation-induced membrane damage but is unable to inhibit carboxyatractyloside-induced permeability transition.[Pubmed: 19883225]|
|These modifications, taken together with findings indicating that cyclosporin resulted unable to inhibit Carboxyatractyloside-induced permeability transition, prompted us to conclude that the translocase could constitute the nonspecific pore or at least be an important modulator of it.|
Comp Biochem Physiol C Toxicol Pharmacol. 2009 Apr;149(3):374-81.
|Cyclosporin A is unable to inhibit carboxyatractyloside-induced permeability transition in aged mitochondria.[Pubmed: 18835371]|
|Two important findings in this work were the fact that despite of the presence of cyclosporin A, Carboxyatractyloside was still able to induce permeability transition, and that ageing induced mitochondrial DNA disruption and release of cytochrome c. It is likely that the membrane's increased permeability is due to the effect of fatty acids, since bovine serum albumin makes mitochondria able to retain Ca2+. However, the possibility that the damage might be the result of oxidative stress cannot be discarded.|
Ann Trop Paediatr. 2005 Jun;25(2):125-34.
|Carboxyatractyloside poisoning in humans.[Pubmed: 15949201]|
|OBJECTIVE: Cocklebur (Xanthium strumarium) is an herbaceous annual plant with worldwide distribution. The seeds contain the glycoside Carboxyatractyloside, which is highly toxic to animals. We describe nine cases of Carboxyatractyloside poisoning in humans which, to our knowledge, has not previously been reported. The clinical, laboratory and histopathological findings and our therapeutic approach are also discussed. SUBJECTS AND METHODS: The patients presented with acute onset abdominal pain, nausea and vomiting, drowsiness, palpitations, sweating and dyspnoea. Three of them developed convulsions followed by loss of consciousness and death. RESULTS: Laboratory findings showed raised liver enzymes, indicating severe hepatocellular damage. BUN and creatinine levels were raised, especially in the fatal cases who also displayed findings of consumption coagulopathy. CPK-MB values indicative of myocardial injury were also raised, especially in the fatal cases. Three of the patients died within 48 hours of ingesting Carboxyatractyloside. Post-mortem histopathology of the liver confirmed centrilobular hepatic necrosis and renal proximal tubular necrosis, secondary changes owing to increased permeability and microvascular haemorrhage in the cerebrum and cerebellum, and leucocytic infiltrates in the muscles and various organs including pancreas, lungs and myocardium. CONCLUSIONS: Carboxyatractyloside poisoning causes multiple organ dysfunction and can be fatal. Coagulation abnormalities, hyponatraemia, marked hypoglycaemia, icterus and hepatic and renal failure are signs of a poor prognosis. No antidote is available and supportive therapy is the mainstay of treatment.|