被多种有机磷酸酯抑制的神经毒性酯酶的重新激活与老化
Reactivation and aging of neurotoxic esterase inhibited by a variety of organophosphorus esters.
作者信息
Clothier B, Johnson M K
出版信息
Biochem J. 1980 Mar 1;185(3):739-47. doi: 10.1042/bj1850739.
Abstract
- It was proposed [Johnson (1974) J. Neurochem. 23, 785--789] that both inhibition of neurotoxic esterase of nervous tissue and subsequent 'aging' of the inhibited esterase are necessary events in the pathogenesis of organophosphate-induced delayed neuropathy: aging has now been demonstrated with a number of neurotoxic compounds. 2. Reactivation by KF was observed for hen brain neurotoxic esterase inhibited by 14 organophosphates and phosphonates, and time-dependent loss of reactivatibility (aging) occurred in every case. 3. For five other compounds no reactivation occurred and aging could not therefore be established, but independent evidence for two compounds suggests that aging was rapid. 4. Half-lives of aging of neurotoxic esterase inhibited by phosphates ranged from less than 1 min to 10 min, and for phosphonates the range was 3--600 min. 5. The relationship of these findings to the mechanism of toxicity and to the prospects of therapy are considered. 6. Aging occurred rapidly with aryloxy and linear alkoxy groups attached to phosphorus and slowly with a highly branched alkoxy substituent: these effects seem incompatible with an SN1 (dealkylation) mechanism.
摘要
- 有人提出[约翰逊（1974年）《神经化学杂志》23卷，785 - 789页]，神经组织神经毒性酯酶的抑制以及随后被抑制酯酶的“老化”是有机磷酸酯诱导的迟发性神经病发病机制中的必要事件：现已用多种神经毒性化合物证实了老化现象。2. 观察到，被14种有机磷酸酯和膦酸酯抑制的鸡脑神经毒性酯酶可被氟化钾重新激活，并且每种情况下都发生了随时间推移的重新激活能力丧失（老化）。3. 对于其他五种化合物，未发生重新激活，因此无法确定老化情况，但有两种化合物的独立证据表明老化很快。4. 被磷酸盐抑制的神经毒性酯酶的老化半衰期从不到1分钟到10分钟不等，对于膦酸酯，范围是3 - 600分钟。5. 考虑了这些发现与毒性机制以及治疗前景的关系。6. 当磷上连接芳氧基和直链烷氧基时，老化迅速发生，而当有高度支化的烷氧基取代基时，老化缓慢发生：这些效应似乎与SN1（脱烷基化）机制不相符。
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