Indo-1 (potassium salt)
(Synonyms: 荧光钙探针INDO-1FF五钾盐) 目录号 : GC43899A ratiometric fluorescent calcium indicator
Cas No.:132319-56-3
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
Indo-1 is a ratiometric fluorescent calcium indicator. It is ideal for analyses using flow cytometry, as it uses a single excitation source, typically 349-364 nm light from an argon-ion laser. The emission maximum shifts from 475-485 nm without calcium to 400-410 nm when indo-1 binds calcium. Indo-1 is prone to photobleaching, which limits its usefulness in methods involving microscopy.
| Cas No. | 132319-56-3 | SDF | |
| 别名 | 荧光钙探针INDO-1FF五钾盐 | ||
| Canonical SMILES | [O-]C(CN(CC([O-])=O)C1=CC=C(C2=CC3=C(C=C(C([O-])=O)C=C3)N2)C=C1OCCOC4=C(N(CC([O-])=O)CC([O-])=O)C=CC(C)=C4)=O.[K+].[K+].[K+].[K+].[K+] | ||
| 分子式 | C32H26N3O12•5K | 分子量 | 840.1 |
| 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 | 1.1903 mL | 5.9517 mL | 11.9033 mL |
| 5 mM | 0.2381 mL | 1.1903 mL | 2.3807 mL |
| 10 mM | 0.119 mL | 0.5952 mL | 1.1903 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。
Nitric oxide stimulates Ca(2+)-independent synaptic vesicle release
Neuron 1994 Jun;12(6):1235-44.PMID:7912090DOI:10.1016/0896-6273(94)90440-5.
A new fluorescence method using the dye FM1-43 was used to examine exocytotic release from hippocampal synaptosomes. Nitric oxide caused a marked transient stimulation of vesicle release. Several structurally unrelated nitric oxide donors, sodium nitroprusside, S-nitroso-N-acetylpenicillamine, 3-morpholino-sydnonimine, and acidified sodium nitrite, were effective. Release stimulated by nitric oxide and KCl were comparable in time course, using both the fluorescence assay and [3H]L-glutamate to monitor neurotransmitter release. Activation of guanylyl cyclase was not responsible for nitric oxide-stimulated release. Unlike release stimulated by KCl or A23187, nitric oxide-stimulated release was found to be independent of a rise in intrasynaptosomal Ca2+. Indo-1/AM measurements indicated that nitric oxide actually decreased intracellular Ca2+, and the Ca2+ channel blocker Cd2+ did not affect nitric oxide-stimulated vesicle release. Nitric oxide does, however, appear to act on the Ca(2+)-sensitive pool of vesicles. Nitric oxide may be the first physiological mediator that induces vesicle exocytosis without raising Ca2+ and may provide an interesting new tool for the study of molecules involved in vesicle exocytosis.
A monounsaturated fatty acid (oleic acid) modulates electrical activity in atrial myocytes with calcium and sodium dysregulation
Int J Cardiol 2014 Sep;176(1):191-8.PMID:25064200DOI:10.1016/j.ijcard.2014.07.004.
Background: Obesity and metabolic syndrome are important risk factors for atrial fibrillation. High plasma concentrations of monounsaturated fatty acids, including oleic acid (OLA), are frequently noted in obese individuals and patients with metabolic syndrome. However, it is not clear whether monounsaturated fatty acids (MUFAs) can directly modulate the electrophysiological characteristics of atrial myocytes. Methods: Whole-cell patch clamp, Indo-1 fluorescence, and Western blot analyses were used to record the action potentials (APs), ionic currents, and protein expressions of HL-1 myocytes incubated with and without (control) OLA (0.5mM) for 24h. Results: Compared to control myocytes (n=14), OLA-treated myocytes (n=16) had shorter APD90 (65 ± 6 vs. 85 ± 6 ms, p<0.05) and APD50 (24 ± 6 vs. 38 ± 4 ms, p<0.05) with a higher incidence of delayed afterdepolarizations (35.7% vs. 7%, p<0.05), which were suppressed by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, a blocker of the calcium-activated chloride current). In addition, OLA-treated myocytes (n=19) exhibited larger calcium transients (0.54 ± 0.06 vs. 0.38 ± 0.05 R410/485, p<0.05), and sarcoplasmic reticular calcium contents (0.91 ± 0.05 vs. 0.64 ± 0.08 R410/485, p<0.05) than control myocytes (n=15). OLA-treated myocytes had larger late sodium currents, smaller sodium-calcium exchanger currents, and smaller sodium-potassium pump currents. Moreover OLA-treated myocytes had higher expressions of sarcoplasmic reticular Ca(2+)-ATPase and calmodulin kinase II, but lower expression of the sodium-potassium ATPase protein than control myocytes. Conclusions: MUFAs can regulate atrial electrophysiological characteristics with calcium and sodium dysregulation, which may contribute to atrial arrhythmogenesis.
Cytosolic calcium accumulation and delayed repolarization associated with ventricular arrhythmias in a guinea pig model of Andersen-Tawil syndrome
Heart Rhythm 2010 Oct;7(10):1428-1435.e1.PMID:20380896DOI:10.1016/j.hrthm.2010.03.044.
Background: Andersen-Tawil syndrome (ATS1)-associated ventricular arrhythmias are initiated by frequent, hypokalemia-exacerbated, triggered activity. Previous ex vivo studies in drug-induced Andersen-Tawil syndrome (DI-ATS1) models have proposed that arrhythmia propensity in DI-ATS1 derives from cytosolic Ca(2+) ([Ca(2+)](i)) accumulation leading to increased triggered activity. Objective: The purpose of this study was to test the hypothesis that elevated [Ca(2+)](i) with concomitant APD prolongation, rather than APD dispersion, underlies arrhythmia propensity during DI-ATS1. Methods: DI-ATS1 was induced in isolated guinea pig ventricles by perfusion of 2 mM KCl Tyrode solution containing 10 μM BaCl(2). APD and [Ca(2+)](i) from the anterior epicardium were quantified by ratiometric optical voltage (di-4-ANEPPS) or Ca(2+) (Indo-1) mapping during right ventricular pacing with or without the ATP-sensitive potassium channel opener pinacidil (15 μM). Results: APD gradients under all conditions were insufficient for arrhythmia induction by programmed stimulation. However, 38% of DI-ATS1 preparations experienced ventricular tachycardias (VTs), and all preparations experienced a high incidence of premature ventricular complexes (PVCs). Pinacidil decreased APD and APD dispersion and reduced VTs (to 6%), and PVC frequency (by 79.5%). However, PVC frequency remained significantly greater relative to control (0.5% ± 0.3% of DI-ATS1). Importantly, increased arrhythmia propensity during DI-ATS1 was associated with diastolic [Ca(2+)](i) accumulation and increased [Ca(2+)](i) transient amplitudes. Pinacidil partially attenuated the former but did not alter the latter. Conclusion: The study data suggest that arrhythmias during DI-ATS1 may be a result of triggered activity secondary to prolonged APD and altered [Ca(2+)](i) cycling and less likely dependent on large epicardial APD gradients forming the substrate for reentry. Therefore, therapies aimed at reducing [Ca(2+)](i) rather than APD gradients may prove effective in treatment of ATS1.
The importance of calcium in the appearance of p32, a boar sperm tyrosine phosphoprotein, during in vitro capacitation
J Androl 2003 Sep-Oct;24(5):727-33.PMID:12954665DOI:10.1002/j.1939-4640.2003.tb02734.x.
After ejaculation, mammalian sperm must undergo a preparation period known as "capacitation" to become capable of fertilizing the oocyte. Although physiological capacitation occurs in the female genital tract, the process can be reproduced in vitro by incubation in appropriate media. However, the signaling events regulating capacitation are poorly understood, especially in boar sperm. Calcium is thought to be of fundamental importance in capacitation. Our laboratory recently identified a tyrosine-phosphorylated protein of M(r) 32,000 ("p32") from boar sperm, and its appearance is closely related to capacitation. The objective of this study was to understand the mechanism regulating the appearance of our p32 tyrosine phosphoprotein. Since calcium has been linked to sperm capacitation and protein tyrosine phosphorylation in other species, we hypothesized that extracellular calcium is involved in the appearance of the p32. Sperm were incubated in either noncapacitating medium (NCM) or capacitating medium (CM) for various times. Proteins were extracted with sodium dodecyl sulfate (SDS), separated by SDS-polyacrylamide gel electrophoresis (PAGE), and then immunoblotted with an antiphosphotyrosine antibody. To assess intracellular calcium levels, fresh sperm were loaded with the fluorescent calcium indicator Indo-1, and relative fluorescence was measured by flow cytometry. Analysis demonstrated that relative intracellular calcium levels increased during incubation in capacitating conditions but not in NCM, which coincides with the appearance of the p32. The p32 tyrosinephosphorylated protein appeared only in the presence of calcium, and the calcium ionophore Br-A23187 accelerated its appearance. Consistent with our hypothesis, the appearance of the p32 was inhibited by extracellular calcium chelators (ethylene glycol-bis(2-aminoethylether)-N,N,N',N',-tetraacetic acid [EGTA], EDTA, and 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid potassium salt [BAPTA-K(+)]), showing the importance of calcium in protein tyrosine phosphorylation related to capacitation in boar sperm.
Dependence of hypoxic cellular calcium loading on Na(+)-Ca2+ exchange
Circ Res 1992 Sep;71(3):547-57.PMID:1323432DOI:10.1161/01.res.71.3.547.
Na(+)-Ca2+ exchange has been shown to contribute to reperfusion- and reoxygenation-induced cellular Ca2+ loading and damage in the heart. Despite the fact that both [Na+]i and [Ca2+]i have been documented to rise during ischemia and hypoxia, it remains unclear whether the rise in [Ca2+]i occurring during hypoxia is linked to the rise in [Na+]i via Na(+)-Ca2+ exchange before reoxygenation and how this relates to cellular injury. Single electrically stimulated (0.2 Hz) adult rat cardiac myocytes loaded with Na(+)-sensitive benzofuran isophthalate (SBFI), the new fluorescent probe, were exposed to glucose-free hypoxia (PO2 less than 0.02 mm Hg), and SBFI fluorescence was monitored to index changes in [Na+]i. Parallel experiments were performed with indo-1-loaded cells to index [Ca2+]i. The SBFI fluorescence ratio (excitation, 350/380 nm) rose significantly during hypoxia after the onset of ATP-depletion contracture, consistent with a rise in [Na+]i. At reoxygenation, the ratio fell rapidly toward baseline levels. The Indo-1 fluorescence ratio (emission, 410/490 nm) also rose only after the onset of rigor contracture and then often showed a secondary rise early after reoxygenation at a time when [Na+]i fell. The increase in both [Na+]i and [Ca2+]i, seen during hypoxia, could be markedly reduced by performing experiments in Na(+)-free buffer. These experiments suggested that hypoxic Ca2+ loading is linked to a rise in Na+i via Na(+)-Ca2+ exchange. To show that Na(+)-Ca2+ exchange activity was not fully inhibited by profound intracellular ATP depletion, cells were exposed to cyanide, and then buffer Na+ was abruptly removed after contracture occurred. The sudden removal of buffer Na+ would be expected to stimulate cell Ca2+ entry via Na(+)-Ca2+ exchange. A large rapid rise in the Indo-1 fluorescence ratio ensued, which was consistent with abrupt cell Ca2+ loading via the exchanger. The effect of reducing hypoxic buffer [Na+] on cell morphology after reoxygenation was examined. Ninety-five percent of cells studied in a normal Na(+)-containing buffer (144 mM NaCl, n = 38) and reoxygenated 30 minutes after the onset of hypoxic rigor underwent hypercontracture. Only 12% of cells studied in Na(+)-free buffer (144 mM choline chloride, n = 17) hypercontracted at reoxygenation (p less than 0.05). Myocytes were also exposed to hypoxia in the presence of R 56865, a compound that blocks noninactivating components of the Na+ current. R 56865 blunted the rise in [Na+]i typically seen after the onset of rigor, suggesting that Na+ entry may occur, in part, through voltage-gated Na+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)