ORGANOPHOSPHORUS AND OTHER INHIBITORS OF BRAIN NEUROTOXIC-ESTERASE AND DEVELOPMENT OF DELAYED NEUROTOXICITY IN HENS
ORGANOPHOSPHORUS AND OTHER INHIBITORS OF BRAIN NEUROTOXIC-ESTERASE AND DEVELOPMENT OF DELAYED NEUROTOXICITY IN HENS
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DOI：
10.1042/bj1200523
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发表时间：
1970-01-01
影响因子：
4.1
通讯作者：
JOHNSON, MK
中科院分区：
文献类型：
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作者：
JOHNSON, MK
1. 一些有机磷化合物的延迟神经毒性作用与能够水解苯基乙酸苯酯的神经组织酶的活性位点的磷酸化有关。 2. 神经毒性有机磷化合物以及一些氨基甲酸酯和磺酰氟逐渐抑制酶，在活性位点共价连接取代基。 3. N-苄基-N-甲基氨基甲酸苯酯或苯甲磺酰氟对酶的长期抑制不会导致神经毒性作用。 4.预先在体内用氨基甲酸酯或磺酰氟抑制该酶可防止几种有机磷化合物的神经毒性作用。 5.给母鸡施用保护性化合物后，保护持续到大约70%的酶位点再次可用于磷酸化。 6. 所有抑制剂在酶活性位点的反应对苯乙酸苯酯的水解产生相同的抑制作用，但并非在所有情况下都会导致迟发性神经毒性。结论是酶活性位点取代基的性质决定了毒性反应。
1. The delayed neurotoxic effects of some organophosphorus compounds are associated with phosphorylation of the active site of a nervous-tissue enzyme capable of hydrolysing phenyl phenylacetate. 2. Neurotoxic organophosphorus compounds and some carbamates and sulphonyl fluorides progressively inhibit the enzyme, attaching a substituent covalently at the active site. 3. Prolonged inhibition of the enzyme by phenyl N-benzyl-N-methylcarbamate or phenylmethane-sulphonyl fluoride does not lead to neurotoxic effects. 4. Prior inhibition of the enzyme by carbamates or sulphonyl fluorides in vivo prevents the neurotoxic effects of several organophosphorus compounds. 5. After dosage of hens with protective compounds, protection lasts until about 70% of the enzyme site again becomes available for phosphorylation. 6. Reaction of all the inhibitors at the active site of the enzyme leads to the same inhibitory effect with respect to hydrolysis of phenyl phenylacetate but does not in all cases lead to delayed neurotoxicity. It is concluded that the nature of the group substituted at the enzyme active site determines the toxic response.