α-Bungarotoxin - CAS 11032-79-4
Category: Inhibitor
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Molecular Formula:
C338H529N97O105S11
Molecular Weight:
7984.14
COA:
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Targets:
nAChR
Description:
α-Bungarotoxin, a kind of neurotoxin, has been found to be a nAChRs inhibitor.
Purity:
≥95% by HPLC
Appearance:
White Solid
MSDS:
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InChIKey:
LYTCVQQGCSNFJU-UHFFFAOYSA-N
InChI:
InChI=1S/C50H70O14/c1-25(24-51)14-28-17-37(52)50(8)41(54-28)19-33-34(61-50)18-32-29(55-33)10-9-12-46(4)42(58-32)23-49(7)40(62-46)21-39-47(5,64-49)13-11-30-44(60-39)26(2)15-31-36(56-30)22-48(6)38(57-31)20-35-45(63-48)27(3)16-43(53)59-35/h9-10,16,24,26,28-42,44-45,52H,1,11-15,17-23H2,2-8H3
Canonical SMILES:
CC1CC2C(CC3(C(O2)CC4C(O3)C(=CC(=O)O4)C)C)OC5C1OC6CC7C(CC8C(O7)(CC=CC9C(O8)CC1C(O9)CC2C(O1)(C(CC(O2)CC(=C)C=O)O)C)C)(OC6(CC5)C)C
1.Exposure of phosphatidylcholine and phosphatidylinositol in plasma membranes from rat brain synaptosomes treated with phospholipase A2 toxins (beta-bungarotoxin, notexin) and enzymes (Naja nigricollis, Naja naja atra).
Shina R;Crain RC;Rosenberg P;Condrea E Toxicon. 1994 Jun;32(6):675-85.
Phospholipase A2 (PLA2) toxins act presynaptically to block acetylcholine release and are much more potent and specific in their actions than PLA2 enzymes even though they have lower enzymatic activity. Since their mechanism of action is not completely understood, it was of interest to examine the toxins' effects on phospholipid asymmetry as changes in asymmetry are associated with changes in membrane functioning. Rat brain synaptosomes were treated with the PLA2 toxins beta-bungarotoxin (beta-BuTx) and notexin and with the PLA2 enzymes Naja nigricollis and Naja naja atra under relatively non-disruptive conditions as judged by leakage of lactate dehydrogenase (LDH) and levels of phospholipid hydrolysis. The exposure of phosphatidylcholine (PC) and phosphatidylinositol (PI) on the synaptosomal surface was investigated by means of a specific PC-exchange protein (PCEP) and a PI-specific phospholipase C (PI-PLC), respectively. Treatment of the synaptosomes with N. nigricollis PLA2, beta-BuTx and notexin did not affect the availability of PC to exchange by PCEP, but significantly increased the exposure of PI to hydrolysis by PI-PLC. In contrast, N. n. atra PLA2 slightly decreased the exposure of PC and did not affect that of PI.
2.Snakebite in Taiwan.
Mao YC;Liu PY;Chiang LC;Liao SC;Su HY;Hsieh SY;Yang CC Am J Trop Med Hyg. 2017 Jun;96(6):1497-1504. doi: 10.4269/ajtmh.17-0005.
AbstractAlthough specific antivenom is available in Taiwan, respiratory failure and general pain frequently accompany ;Bungarus multicinctus; envenomation and there have been few reports on the management of ;B. multicinctus; envenomation. We retrospectively analyzed 44 cases of ;B. multicinctus; bite admitted to Taichung Veterans General Hospital (VGH) or to Taipei VGH. Demographic data, treatment, and outcome of patients with and without respiratory failure were compared. In this study, 20.5% patients had bites without noticeable signs or symptoms of significant envenoming, 27.3% developed respiratory failure, and 27.3% experienced general pain. Bivalent specific antivenom for ;B. multicinctus; and ;N. atra; was administered in all envenomed cases. Respiratory failure occurred 1.5-6.5 hours post-bite and general pain occurred 1-12 hours post-bite. Specific antivenom for ;B. multicinctus; and ;N. atra; at the recommended dose (i.e., 2-4 vials) might not effectively prevent respiratory failure and pain. Respiratory failure, general pain, and autonomic effects after ;B. multicinctus; bite were probably caused, at least partly, by β-bungarotoxin. Although general weakness, ptosis, dysarthria, and dilated pupils were significantly associated with respiratory failure, their predictive value could not be accurately determined in such a retrospective study.
3.The facilitatory actions of snake venom phospholipase A(2) neurotoxins at the neuromuscular junction are not mediated through voltage-gated K(+) channels.
Fathi H B;Rowan EG;Harvey AL Toxicon. 2001 Dec;39(12):1871-82.
Electrophysiological investigations have previously suggested that phospholipase A(2) (PLA(2)) neurotoxins from snake venoms increase the release of acetylcholine (Ach) at the neuromuscular junction by blocking voltage-gated K(+) channels in motor nerve terminals. We have tested some of the most potent presynaptically-acting neurotoxins from snake venoms, namely beta-bungarotoxin (BuTx), taipoxin, notexin, crotoxin, ammodytoxin C and A (Amotx C & A), for effects on several types of cloned voltage-gated K(+) channels (mKv1.1, rKv1.2, mKv1.3, hKv1.5 and mKv3.1) stably expressed in mammalian cell lines. By use of the whole-cell configuration of the patch clamp recording technique and concentrations of toxins greater than those required to affect acetylcholine release, these neurotoxins have been shown not to block any of these voltage-gated K(+) channels. In addition, internal perfusion of the neurotoxins (100 microg/ml) into mouse B82 fibroblast cells that expressed rKv1.2 channels also did not substantially depress K(+) currents. The results of this study suggest that the mechanism by which these neurotoxins increase the release of acetylcholine at the neuromuscular junction is not related to the direct blockage of voltage-activated Kv1.
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CAS 11032-79-4 α-Bungarotoxin

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