Fluo-3 (potassium salt)
目录号 : GC43682
A fluorescent calcium indicator
Cas No.:853400-67-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >90.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Fluo-3 (potassium salt) is a fluorescent calcium indicator commonly used in flow cytometry and cell-based experiments to detect changes in intracellular calcium levels. Its absorption maximum at 506 nm makes it compatible with excitation at 488 nm by argon-ion laser sources. Fluo-3 provides intense fluorescence upon binding calcium, detected at a maximum emission at 526 nm which can be monitored by FL1 (green, 525 nm band pass) sensors in flow cytometry.
| Cas No. | 853400-67-6 | SDF | |
| Canonical SMILES | O=C1C(Cl)=CC(C(O2)=C1)=C(C3=CC=C(N(CC([O-])=O)CC([O-])=O)C(OCCOC4=C(N(CC([O-])=O)CC([O-])=O)C=CC(C)=C4)=C3)C5=C2C=C([O-])C(Cl)=C5.[K+].[K+].[K+].[K+].[K+] | ||
| 分子式 | C36H25Cl2N2O13•5K | 分子量 | 960 |
| 溶解度 | Water: Soluble | 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 | 1.0417 mL | 5.2083 mL | 10.4167 mL |
| 5 mM | 0.2083 mL | 1.0417 mL | 2.0833 mL |
| 10 mM | 0.1042 mL | 0.5208 mL | 1.0417 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。
Ca2+ sparks and Ca2+ waves in saponin-permeabilized rat ventricular myocytes
J Physiol 1999 Dec 15;521 Pt 3(Pt 3):575-85.PMID:10601490DOI:10.1111/j.1469-7793.1999.00575.x.
1. We carried out confocal Ca2+ imaging in myocytes permeabilized with saponin in 'internal' solutions containing: MgATP, EGTA and Fluo-3 potassium salt. 2. Permeabilized myocytes exhibited spontaneous Ca2+ sparks and waves similar to those observed in intact myocytes loaded with Fluo-3 AM. 3. In the presence of 'low' [EGTA] (0.05 mM), Ca2+ waves arose regularly, even at relatively low [Ca2+] (50-100 nM, free). Increasing [EGTA] resulted in decreased frequency and propagation velocity of Ca2+ waves. Propagating waves were completely abolished at [EGTA] > 0.3 mM. 4. The frequency of sparks increased as a function of [Ca2+] (50-400 nM range) with no sign of a high affinity Ca2+-dependent inactivation process. 5. The rate of occurrence of Ca2+ sparks was increased by calmodulin and cyclic adenosine diphosphate-ribose (cADPR).
Endothelium-independent vasorelaxant effect of sodium ferulate on rat thoracic aorta
Life Sci 2009 Jan 16;84(3-4):81-8.PMID:19038273DOI:10.1016/j.lfs.2008.11.003.
Aims: This study was designed to investigate the effects of sodium ferulate (SF) on rat isolated thoracic aortas and the possible mechanisms. Main methods: Isometric tension was recorded in response to drugs in organ bath. Cytosolic free Ca(2+) concentration ([Ca(2+)](i)) was measured using Fluo-3 in cultured rat aortic smooth muscle cells (RASMC). Key findings: SF (0.1-30 mM) relaxed the isolated aortic rings precontracted with phenylephrine (PE) and high-K(+) in a concentration-dependent manner with respective pD(2) of 2.7+/-0.02 and 2.6+/-0.06. Mechanical removal of endothelium did not significantly modify the SF-induced relaxation. In Ca(2+)-free solution, SF noticeably inhibited extracellular Ca(2+)-induced contraction in high-K(+) and PE pre-challenged rings, and suppressed the transient contraction induced by PE and caffeine. The vasorelaxant effect of SF was unaffected by various K(+) channel blockers such as tetraethylammonium, glibenclamide, 4-aminopyridine, and barium chloride. In addition, SF concentration-dependently reduced the contraction induced by phorbol-12-myristate-13-acetate, an activator of protein kinase C (PKC), in the absence of extracellular Ca(2+), with the pD(2) of 2.9+/-0.03. In RASMC, SF had no effect on PE- or KCl-induced [Ca(2+)](i) increase either in the presence or in the absence of external Ca(2+). Significance: These results indicate that SF acts directly as a non-selective relaxant to vascular smooth muscle. The direct inhibition of the common pathway after [Ca(2+)](i) increase may account for the SF-induced relaxation in Ca(2+)-dependent contraction, while the blockage of the PKC-mediated contractile mechanism is likely responsible for the SF-induced relaxation in Ca(2+)-independent contraction.
Rapid accumulation of phosphatidylinositol 4,5-bisphosphate and inositol 1,4,5-trisphosphate correlates with calcium mobilization in salt-stressed arabidopsis
Plant Physiol 2001 Jun;126(2):759-69.PMID:11402204DOI:10.1104/pp.126.2.759.
The phosphoinositide phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P(2)] is a key signaling molecule in animal cells. It can be hydrolyzed to release 1,2-diacyglycerol and inositol 1,4,5-trisphosphate (IP(3)), which in animal cells lead to protein kinase C activation and cellular calcium mobilization, respectively. In addition to its critical roles in constitutive and regulated secretion of proteins, PtdIns(4,5)P(2) binds to proteins that modify cytoskeletal architecture and phospholipid constituents. Herein, we report that Arabidopsis plants grown in liquid media rapidly increase PtdIns(4,5)P(2) synthesis in response to treatment with sodium chloride, potassium chloride, and sorbitol. These results demonstrate that when challenged with salinity and osmotic stress, terrestrial plants respond differently than algae, yeasts, and animal cells that accumulate different species of phosphoinositides. We also show data demonstrating that whole-plant IP(3) levels increase significantly within 1 min of stress initiation, and that IP(3) levels continue to increase for more than 30 min during stress application. Furthermore, using the calcium indicators Fura-2 and Fluo-3 we show that root intracellular calcium concentrations increase in response to stress treatments. Taken together, these results suggest that in response to salt and osmotic stress, Arabidopsis uses a signaling pathway in which a small but significant portion of PtdIns(4,5)P(2) is hydrolyzed to IP(3). The accumulation of IP(3) occurs during a time frame similar to that observed for stress-induced calcium mobilization. These data also suggest that the majority of the PtdIns(4,5)P(2) synthesized in response to salt and osmotic stress may be utilized for cellular signaling events distinct from the canonical IP(3) signaling pathway.
Anti-oxidant effects of estrogen reduce [Ca2+]i during metabolic inhibition
J Mol Cell Cardiol 2003 Mar;35(3):331-6.PMID:12676548DOI:10.1016/s0022-2828(03)00017-8.
We previously reported that 17beta-estradiol (betaE2) inhibits the rise in [Ca(2+)](i) and [Na(+)](i) during metabolic inhibition (MI) in mouse cardiomyocytes, but the mechanism has not yet been clarified. Estrogen has been reported to have anti-oxidant properties. We, therefore, have investigated whether interaction with the estrogen receptor (ER) is involved, or whether estrogen reduces free-radical-induced impairment of Na(+)-K(+) ATPase in cardiac myocytes, and whether this effect reduces [Ca(2+)](i) rise. Male mouse ventricular myocytes were studied. Flow cytometry was used with Fluo-3 for [Ca(2+)](i) measurement. Dead cells were excluded from analysis by propidium iodide fluorescence. betaE2 reduced the increase in [Ca(2+)](i) during MI even in the presence of the ER blocker tamoxifen. A similar effect on [Ca(2+)](i) was produced by its non-estrogenic isomer, betaE2-estradiol. Other hormones (estrone and estriol) with a phenolic structure also inhibited Ca(2+) overload during MI, but testosterone without the structure did not. The betaE2 effect was attenuated by inhibition of Na(+)-Ca(2+) exchanger (KB-R7943) or Na(+)-K(+) ATPase (low K(+) or ouabain), but not by block of L-type Ca(2+) channel (nifedipine). Tiron (4,5-dihydroxy-1,3-benzenedisulfonic acid), a superoxide scavenger, decreased the rise in [Ca(2+)](i) and abolished the betaE2 effect during MI. We conclude that the acute cardioprotective effect of estrogen during MI may be mediated by an ER-independent anti-oxidant action, which results in improved function of Na(+)-K(+) ATPase.
The restriction of diffusion of cations at the external surface of cardiac myocytes varies between species
Cell Calcium 1997 Dec;22(6):431-8.PMID:9502192DOI:10.1016/s0143-4160(97)90070-1.
In cardiac muscle sarcolemmal structures such as T-tubules, caveolae and negatively charged protein-polysaccharides may affect the rate of cation exchange on the external surface of the cells. To test this hypothesis, we examined the rate of external cation exchange in adult rabbit and rat ventricular myocytes using a rapid solution switcher to change the bulk external solution within 4 ms. To assess the rate of diffusion of monovalent cations, we increased [K+]o from 4.4 to 6.6 or 8.8 mM and measured the time required to achieve a stable membrane depolarization. In rat myocytes, the mean time to 90% depolarization (t90) was significantly longer than that in rabbit myocytes (137 and 64 ms, respectively) and the difference in t90 was not associated with the cell size. To assess the time course of exchange of external Ca2+, we rapidly exposed the myocytes to 0 Ca2+-2 mM EGTA solution at specific time points before action potentials or voltage clamp steps, and measured the rate of alteration of the normalized peak [Ca2+]i transient (Fluo-3) or Ca2+ current. Exposure to 0 Ca2+-2 mM EGTA solution caused a decline in the intracellular calcium transient. In rat myocytes, the rate of decline in the [Ca2+]i transient was much slower (t90 > 1500 ms, the time required for 90% decline) than for the rabbit (t90 = 295 ms). Also, the rate of decline in the Ca2+ current was prolonged in rat myocytes (t90 = 910 ms) compared with rabbit myocytes (t90 = 241 ms). These data indicate that there is a restricted space on the external surface of sarcolemma which limits diffusion of divalent cations more markedly than monovalent cations. The extent of this limitation of cation diffusion varies between species, and may have functional significance.