cis-Parinaric Acid
(Synonyms: α-Parinaric Acid) 目录号 : GC40545A naturally-occurring PUFA
Cas No.:18427-44-6
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >90.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
cis-Parinaric acid is a naturally occurring polyunsaturated fatty acid containing an unusual conjugated (Z,E,E,Z) tetraene. This chromophore provides for a natural fluorescence at 432 nm with an excitation wavelength at 320 nm. cis-Parinaric acid occurs naturally in the seeds of the Makita tree, a tropical rainforest tree indigenous to Fiji. Makita seeds are inedible, and this toxicity may be due at least in part to the unstable conjugated fatty acids, including cis-parinaric acid, contained within the seed. cis-Parinaric acid has been used for the measurement of phospholipase activity, lipase activity, and as an indicator of lipid peroxidation.[1][2][3][4]
Reference:
[1]. Wolf, C., Sagaert, L., and Bereziat, G. A sensitive assay of phospholipase using the fluorescent probe 2-parinaroyllecithin. Biochemical and Biophysical Research Communications 99, 275-283 (1981).
[2]. Beisson, F., Ferté, N., Nari, J., et al. Use of naturally fluorescent triacylglycerols from Parinari glaberrimum to detect low lipase activities from Arabidopsis thaliana seedlings. Journal of Lipid Research 40, 2313-2321 (1999).
[3]. McGuire, S.O., James-Kracke, M.R., Sun, G.Y., et al. An esterification protocol for cis-parinaric acid-determined lipid peroxidation in immune cells. Lipids 32, 219-226 (1997).
[4]. de Hingh, Y.C.M., Meyer, J., Fischer, J.C., et al. Direct measurement of lipid peroxidation in submitochondrial particles. Biochemistry 34, 12755-12760 (1995).
| Cas No. | 18427-44-6 | SDF | |
| 别名 | α-Parinaric Acid | ||
| 化学名 | 9Z,11E,13E,15Z-octadecatetraenoic acid | ||
| Canonical SMILES | CC/C=C\C=C/C=C\C=C\CCCCCCCC(=O)O | ||
| 分子式 | C18H28O2 | 分子量 | 276.4 |
| 溶解度 | 15mg/mL in benzene, or in ether, 10mg/mL in hexane | 储存条件 | Store at -80°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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 3.6179 mL | 18.0897 mL | 36.1795 mL |
| 5 mM | 0.7236 mL | 3.6179 mL | 7.2359 mL |
| 10 mM | 0.3618 mL | 1.809 mL | 3.6179 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。
The partition of cis-Parinaric Acid and trans-parinaric acid among aqueous, fluid lipid, and solid lipid phases
Mol Cell Biochem 1980 Nov 20;32(3):169-77.PMID:7007869DOI:10.1007/BF00227444.
In this article, I review the current information concerning the partition of the fluorescent probes, cis-Parinaric Acid (9, 11, 13, 15-cis, trans, trans, cis-octadecatetraenoic acid) and trans-parinaric acid (9, 11, 13, 15-all trans-octadecatetraenoic acid) among aqueous, solid lipid, and fluid lipid phases. The association of these probes with lipid is described by a mole fraction partition coefficient whose value is trypically in the range of 1-5 x 10(6), a reasonable value in light of partition coefficients for other fatty acids between hydrophobic phases and water. The partition coefficient, in the absence of lipid phase changes, is relatively independent of temperature and only slightly dependent on the total aqueous probe concentration. In lipid samples which contain coexisting fluid and solid phases, trans-parinaric acid preferentially partitions into the solid phase, while cis-Parinaric Acid distributes nearly equally between fluid and solid phases. This partition behavior probably arises from the molecular shape of the cis and trans parinaric acid in mixed lipid systems or membranes it is possible to evaluate the proportion of lipid components involved in phase changes or phase separation. From fluorescence energy transfer between protein typtophan residues and the parinaric acid isomers it is possible to gain information about the organization of lipids and proteins in membranes and model systems. I close the review by considering some of the membrane research areas where these probes and their various lipid derivatives may be particularly useful.
Incorporation of cis-Parinaric Acid, a fluorescent fatty acid, into synaptosomal phospholipids by an acyl-CoA acyltransferase
Biochim Biophys Acta 1983 Dec 7;736(1):79-91.PMID:6580918DOI:10.1016/0005-2736(83)90172-4.
The cis-isomer of parinaric acid, a naturally occurring C-18 polyene fatty acid, was incubated with brain subcellular fractions and the polarization of fluorescence increased in a time dependent manner. Greatest increases occurred in synaptosomal and microsomal membranes. This increase in polarization of fluorescence was found with the cis, but not the trans, isomer of parinaric acid and required Mg2+ or Ca2+ and was stimulated by coenzyme A and ATP. Synaptosomes were incubated with cis-Parinaric Acid and lipids were extracted and examined by high performance liquid chromatography. The highest incorporations of cis-Parinaric Acid were found in phosphatidylcholine (71%) and phosphatidylethanolamine (20%) while only traces were found in phosphatidylserine and phosphatidylinositol. [3H]Oleic acid was also incorporated into membrane phospholipids and unlabeled oleic acid blocked incorporation of cis-Parinaric Acid. It is proposed that cis-Parinaric Acid, like fatty acids normally found in brain, is incorporated into membrane phospholipids by an acyl-CoA acyltransferase. The presence of this enzyme in nervous tissue may make it possible to easily introduce fluorescent fatty acid probes into membrane phospholipids and to thereby facilitate study of membrane-mediated processes.
Cytotoxicity of cis-Parinaric Acid in cultured malignant gliomas
Neurosurgery 1995 Sep;37(3):484-9.PMID:7501114DOI:10.1227/00006123-199509000-00017.
The cytotoxic effects of cis-Parinaric Acid, a plant-derived 18-carbon polyunsaturated fatty acid, were assessed in vitro on normal and neoplastic glia. After being incubated for 24 hours in the presence of 12 mumol/L cis-Parinaric Acid, 36B10 glioma cultures demonstrated nearly 90% toxicity (unpaired Student's t test, P < 0.001). Similar results were obtained after the exposure of C6 rat glioma cultures, A172 human glioma cultures, and U-937 human monocytic leukemia cultures to cis-Parinaric Acid. In contrast, fetal rat astrocytes incubated with 12 mumol/L cis-Parinaric Acid demonstrated no significant toxicity (3% reduction, P = 0.12); fetal rat astrocytes showed only 20% toxicity after exposure to 40 mumol/L cis-Parinaric Acid (P = 0.001). The cytotoxic effects of cis-Parinaric Acid were antagonized with the addition of equimolar concentrations of alpha-tocopherol. Enzyme immunoassay of treated 36B10 glioma supernatant fluid for 8-isoprostane (a known oxidative metabolite) demonstrated a 10-fold increase of 8-isoprostane over 24 hours (123.0 +/- 10.3 versus 10.0 +/- 0.7 pg/ml for control, P < 0.001). These studies indicate that cis-Parinaric Acid may be significantly cytotoxic to malignant glioma cells in concentrations that spare normal astrocytes and that the mechanism of cytotoxicity is related to an oxidative process. The selective cytotoxic effect of cis-Parinaric Acid we describe represents the first step in the development of new chemotherapeutic agents for gliomas; these new agents act by preferentially enhancing lipid peroxidation in neoplastic cells.
cis-Parinaric Acid effects, cytotoxicity, c-Jun N-terminal protein kinase, forkhead transcription factor and Mn-SOD differentially in malignant and normal astrocytes
Neurochem Res 2007 Jan;32(1):115-24.PMID:17160503DOI:10.1007/s11064-006-9236-2.
cis-Parinaric Acid (c-PNA), a natural four conjugated polyunsaturated fatty acid, increases free radical production and it is preferentially cytotoxic to malignant glial cells compared to normal astrocytes in-vitro. In order to explain the increased cytotoxicity of c-PNA in malignant glial cells, we compared the effects of c-PNA on the oxidative stress-dependent signal transducing events in 36B10 cells, a malignant rat astrocytoma cell line, and in fetal rat astrocytes. Our results show that c-PNA treatment in 36B10 cells caused a persistent activation of c-Jun N-terminal protein kinase (JNK) at RNA and protein levels. Specific inhibitors of the kinase significantly reversed the cytotoxicity of c-PNA. Additionally, c-PNA caused the phosphorylated inactivation of forkhead transcription factor-3a (FKHR-L1, FOXO3a) and drastically decreased the activity of mitochondrial superoxide dismutase (Mn-SOD) that protects cells from oxidative stress. On the other hand, identical c-PNA treatments in normal astrocytes increased the dephosphorylated activation of FKHR-L1, maintained activity of Mn-SOD and failed to phosphorylate JNK. Taken together, the results imply that a selective activation of JNK and the opposite regulation of FKHR-L1 and Mn-SOD contribute to the differential cytotoxicity of c-PNA in malignant and normal glial cells.
Cytotoxic effect of cis-Parinaric Acid in cultured malignant cells
Cancer Res 1991 Nov 15;51(22):6025-30.PMID:1933865doi
Parinaric acid, a naturally occurring 18-carbon fatty acid containing 4 conjugated double bonds, is toxic to human monocytic leukemia cells at concentrations of 5 microM or less. Conditioning of the medium reduces the cytotoxic effect, suggesting that parinaric acid and not a metabolite is the active agent. The mechanism of parinaric acid toxicity appears to involve lipid peroxidation because the toxic action can be blocked by the addition of butylated hydroxytoluene. When U-937 cells are differentiated to the monocytic form, they become resistant to as much as 30 microM parinaric acid. This difference in sensitivity may be explained in part by the fact that the undifferentiated cells take up 3 to 4 times more parinaric acid. Concentrations of parinaric acid less than 5 microM are also toxic to human THP-1 monocytic leukemia, HL-60 human promyelocytic leukemia, and Y-79 human retinoblastoma cells. Measurements of protein synthesis indicate that differentiated U-937 cells, confluent cultures of human fibroblasts, bovine aortic endothelial cells, and CaCo-2 colonic mucosal cells are much less sensitive to parinaric acid than the malignant cell lines tested, suggesting that the cytotoxic action may be selective for rapidly growing malignant tumors. Thus, parinaric acid may be the prototype of a new class of lipid chemotherapeutic agents that contain a conjugated system of double bonds and act by sensitizing tumor cells to peroxidation.