Ammonium chloride and methylamine hydrochloride antagonize clostridial neurotoxins.
Ammonium chloride and methylamine hydrochloride antagonize clostridial neurotoxins.
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发表时间：
1983-06
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通讯作者：
L. Simpson
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作者：
L. Simpson
氯化铵（1- 8mm）和盐酸甲胺（1- 16mm）对A、B和C型肉毒毒素（均为1 × 10(-11) M）和破伤风毒素（3 × 10(-10) M）引起的神经肌肉阻断发作产生浓度依赖性拮抗作用。两种药物均不能拮抗-班加罗毒素（1 × 10(-7) M）或taipoxin （1 × 10(-8) M）引起的麻痹发作。在产生梭状菌神经毒素拮抗的浓度下，氯化铵和盐酸甲胺（8-10 mM）不会使毒素分子失活，也不会对组织功能产生不可逆的变化。在对梭状芽孢杆菌神经毒素作用机制施加部分同步的条件下进行研究时，氯化铵和盐酸甲胺不抑制配体结合，也不逆转神经肌肉封锁。这些药物的作用仅仅是对抗胆碱能神经末梢毒素的内化。由于抑制内化过程，药物将毒素困在抗毒素敏感部位。
Ammonium chloride (1-8 mM) and methylamine hydrochloride (1-16 mM) produce concentration-dependent antagonism of the onset of neuromuscular blockade caused by botulinum toxin types A, B and C (all at 1 X 10(-11) M) and by tetanus toxin (3 X 10(-10) M). Neither drug antagonizes the onset of paralysis caused by beta-bungarotoxin (1 X 10(-7) M) or by taipoxin (1 X 10(-8) M). At concentrations that produce antagonism of clostridial neurotoxins, ammonium chloride and methylamine hydrochloride (8-10 mM) do not inactivate toxin molecules, nor do they produce irreversible changes in tissue function. When studied under conditions that impose partial synchrony on the mechanism of clostridial neurotoxin action, ammonium chloride and methylamine hydrochloride do not inhibit ligand binding and do not reverse neuromuscular blockade. The drugs act solely to antagonize internalization of toxins by cholinergic nerve endings. As a result of inhibiting the process of internalization, the drugs trap the toxins at an antitoxin sensitive site.