乐果等中毒胆碱酯酶的老化和自动重活化

为了研究乐果中毒胆碱酯酶（ＣｈＥ）老化与乐果中毒难治间的关系，以人红细胞乙酰胆碱酯酶（ＡＣｈＥ）作为酶源，用氯磷定（２ＰＡＭ·Ｃｌ）能否重活化作为判断中毒酶老化的标准，测定了乐果、敌敌畏和对硫磷（Ｅ６０５）３种农药中毒酶的体外老化和自动重活化作用。结果发现乐果中毒ＡＣｈＥ体外无明显自动重活化作用；敌敌畏中毒ＡＣｈＥ早期有明显的自动重活化作用，３小时后作用消失；Ｅ６０５中毒ＡＣｈＥ活力随时间的延长明显增加，乐果、敌敌畏和Ｅ６０５抑制人红细胞ＡＣｈＥ的体外半老化时间分别是１１．４小时、４．２小时、１６．９小时，说明乐果中毒ＡＣｈＥ的老化并不快，临床乐果中毒难治与中毒酶老化速度无明显关系。     

二甲基磷酰基对人胆碱酯酶的抑制、重活化和老化动力学

一般认为含有二个甲基的有机磷酸酯如马拉硫磷、甲基对氧磷、乐果和甲氧基内吸磷中毒时,对肟类治疗的拮抗性很大。鉴于肟类的疗效不仅与其本身的重活化能力有关,而且受胆碱酯酶（ＣｈＥ）的抑制程度、老化和自发重活化动力学的影响。本实验对人乙酰胆碱酯酶（ＡＣｈＥ）和丁酰胆碱酯酶（ＢＣｈＥ）的动力学常数进行了研究。实验方法：红细胞ＡＣｈＥ和血浆ＢＣｈＥ活力按照Ｅｌｌｍａｎ等提出的分光光度法测定。首先将甲氧基内吸磷或甲基对氧磷与红细胞ＡＣｈＥ及血浆样品混合后,按照一级速率条件分别计算出ＡＣｈＥ和ＢＣｈＥ的抑制速率…     

特丁硫磷中毒及药物救治的实验研究

特丁硫磷（Ｔｅｒｂｕｆｏｓ）是国产的一种含硫醚基的土壤触杀新型有机磷农药。我们观察了解磷注射液对特丁硫磷中毒大鼠的急救效果及救治过程中全血乙酰胆碱酯酶（ＡＣｈＥ）活力的变化,并通过体外特丁硫磷抑酶、重活化、老化等研究,对其中毒及药物救治的机制进行了初探,为中毒后临床救治提供理论依据。一、材料与方法１．动物：健康Ｗｉｓｔａｒ大鼠,雄性,体重２００～３００ｇ,由军事医学科学院实验动物中心提供。２．药品与试剂：特丁硫磷由天津农药厂提供,纯度９１％;解磷注射液、氯磷定（２ＰＡＭ）、双磷定（ＴＭＢ－４）…     

毒鼠磷中毒解毒试验研究——Ⅳ 绵羊毒鼠磷中毒后血中胆碱酯酶活力测定

毒鼠磷(Gophaclde,Bayer38819,DRC—714)是一种有机磷杀鼠剂,抑制机体的胆碱酶酯而使动物致死。在进行中毒解毒研究的同时,对正常羊、中毒羊、中毒后用胆碱酯酶重活化剂氯磷定和双复磷治疗羊的全血胆碱酯酶活力进行了测定。现将结果报告如下。材料和方法试剂:皂素,上海亭新化工厂生产。Na_2HPO_4·12H_2O,化学纯,天津化学试剂六厂生产。KH_2PO_4,化学纯,北京红星化     

肟类对急性有机磷中毒解毒机制的研究进展

自１９４１年发现有机磷化合物（ＯＰＣ）对乙酰胆碱酯酶（ＡＣｈＥ）具有抑制作用以来，肟类药物（ｏｘｉｍｅｓ）就被作为ＡＣｈＥ重活化剂应用，它们与阿托品联合应用已成为急性有机磷中毒（ＡＯＰＰ）解毒治疗的核心。由于ＯＰＣ可使受抑制的ＡＣｈＥ“老化”（即脱烷...     

有机磷类杀虫剂对脑突触体烟碱型自主受体功能的影响

目的　探讨有机磷杀虫剂 (OPs)对脑突触体烟碱型自主受体功能 (NAF)的影响 ,揭示OPs可能存在的其他作用途径。方法　 (1)体外实验 :以放射性核素氚标记的胆碱与大鼠脑突触体共同温育后用生理缓冲液灌流 ,根据不同有机磷刺激时的放射性胆碱释放量计算NAF值 ,分析氧毒死蜱和对氧磷分别加入灌流系统后NAF的变化 ;(2 )体内实验 :用毒死蜱给大鼠染毒 ,96h后取其大脑皮质制备突触体 ,测定其NAF和乙酰胆碱酯酶 (AChE)活力。结果　对氧磷在体外对NAF影响较小(平均抑制率 <2 3% ) ,但氧毒死蜱却彻底抑制NAF(平均抑制率 >10 0 % )。体内实验亦显示 ,毒死蜱在抑制AChE活力 (抑制率为 91% )的同时 ,对NAF有较强的阻断作用 (抑制率为 6 6 % )。结论　不同的OPs对脑突触体NAF的作用不同 ,毒死蜱可阻断成年大鼠脑突触体的NAF。     

氯解磷定对不同有机磷杀虫剂中毒后乙酰胆碱酯酶活力恢复的影响

目的比较氯解磷定（PAM-Cl）对急性甲胺磷、敌敌畏和氧乐果中毒后乙酰胆碱酯酶（AChE）活力恢复的影响，为临床上合理治疗提供科学依据。方法收集4省1市7家县、市级医院收治的101例急性有机磷杀虫剂中毒患者资料，按接触杀虫剂品种不同分为急性甲胺磷中毒组59例、急性敌敌畏（或敌百虫）中毒组32例、急性氧乐果中毒组10例，比较3组患者红细胞AChE活力抑制程度和PAM-Cl对AChE的复能作用。结果入院时甲胺磷组、敌敌畏组、氧乐果组红细胞AChE活力分别为（9．12±7．99）、（7．32±4．62）和（12．01±9．53）U／gHb，均受抑制，但差异无统计学意义（P〉O．05）。经PAM-Cl治疗后3组患者中毒症状减轻或消失。甲胺磷组红细胞AChE活力在治疗后12、24、48、72h及出院时分别为（11．37±8．67）、（12．51±6．98）、（15．90±7-31）、（18．33±4．78）及（18．91±7．00）U／gHb，均较入院时明显升高并且呈不断回升趋势，差异有统计学意义（P〈O．01或P〈0．05）。敌敌畏组患者AChE活力在治疗后3、12、24、48、72h及出院时均较入院时明显增高，差异有统计学意义（P〈0．05）；12h后各时间点AChE活力则无进一步上升。氧乐果组患者AChE活力只有出院时较入院时明显增高，差异有统计学意义（P〈0．05）；其余各时间点AChE活力较入院时始终无明显恢复，差异均无统计学意义（P〉0.05）。结论PAM-Cl对甲胺磷、敌敌畏、氧乐果中毒均有治疗作用，对甲胺磷抑制的AChE活力有明显的重活化作用，对敌敌畏（敌百虫）抑制的AChE活力有一定重活化作用，而对氧乐果（乐果）抑制的AChE活力无重活化作用。     

几种氨基甲酰化乙酰胆碱酯酶（AChE）的体内代谢过程

目的：观察吡啶斯的明、毒扁豆碱、卡巴呋喃和灭多威四种氨基甲酸酯类化合物其氨基甲酰化乙酰胆碱酯酶（AChE）的体内代谢过程,为氨基甲酸酯类杀虫剂中毒诊断和用药提供理论依据。[f11]方法：[f0]以小鼠为实验对象,其红细胞AChE为酶源,上述四种氨基甲酸酯类化合物为酶抑制剂,改进微量DTNB法测定中毒酶活性,观察不同时间小鼠体内AChE酶抑制率,并对时间进行曲线拟合,同时计算半衰期。[f11]结果：[f0]酶抑制作用于30-45min达到最大,中毒酶体内代谢过程以二甲基氨基甲酰化AChE,即吡啶斯的明中毒酶最慢,半衰期为142.7min;而单甲基氨基甲酰化AChE代谢则相对较快,毒扁豆碱、卡巴呋喃和灭多威中毒酶半衰期分别为102.7min、82.5min、和31.1min,数小时（1.7～7.6小时）后,中毒酶活性可恢复90%以上。[f11]结论：[f0]氨基甲酸酰化AChE的体内代谢过程除与氨基甲酸酯类化合物的结构有关外,还可能有其他的决定因素,且代谢过程较磷酰化AChE快;同时,灭多威作用机理的特殊性也值得临床重视。     

甲胺磷与乙酰甲胺磷对乙酰胆碱酯酶毒效应的比较

目的　探讨高毒有机磷化合物甲胺磷及其替代品乙酰甲胺磷对乙酰胆碱酯酶 (AChE)的抑制作用及机制。方法　提取人红细胞膜及大鼠脑突触体膜后 ,体外实验中用Ellman法测定在不同受试物浓度、不同作用时间下剩余AChE活力 ;整体实验中用Ellman法测定不同脑区AChE活力。结果　乙酰甲胺磷和甲胺磷在体外对人红细胞膜及大鼠大脑皮层突触体膜AChE均有不可逆的抑制作用 ,且有明显的剂量 -效应和时间 -效应关系 ,两者对人红细胞膜及大鼠各脑区突触体膜AChE活力的半数抑制浓度 (IC50 )分别约为 1 0 - 4mol/L、1 0 - 5mol/L ,双分子速率常数 (Ki)分别为 1 0 2mol·L 1 ·min 1 、1 0 3mol·L 1 ·min 1 左右。在整体实验中 ,连续 5d给大鼠腹腔注射乙酰甲胺磷和甲胺磷 ,其全血AChE活力的抑制率逐渐上升 ,第 5天分别达到 68.2 4 %和 54 .80 %。乙酰甲胺磷仅对大鼠脑干AChE活力有抑制作用 (抑制率为 31 .68% ) ,其余脑区均未见明显影响 ;而甲胺磷对各脑区AChE活力均有较强的抑制 ,以小脑和脑干最强 ,分别为 71 .51 %和 61 .85 %。结论　乙酰甲胺磷和甲胺磷在体外对人红细胞膜和大鼠大脑皮层突触体膜AChE活力均有不同程度的抑制作用 ;在整体实验中对大鼠全血AChE活力均有抑制作用。对脑区AChE的抑制存在差异可能是两者毒     

接触对硫磷农药工人监测指标研究

目的 探讨接触有机磷农药（OP）对硫磷工人的监测指标。方法 对某农药厂包装车间进行现场调查,并对56名长期对硫磷接触工人（接触组）和120名无对硫磷接触工人（对照组）进行体格检查及血胆碱酯酶（ChE）、血清对氧磷酶（PON）、β-葡萄糖苷酸酶（-βGD）和羧酸酯酶（CaE）活力测定。结果 （1）对照组红细胞AChE、血清PON、CaE和BChE活力呈正态分布,不同年龄、性别4种酯酶活力差异无统计学意义（P〉0.05）。（2）接触组红细胞AChE、血清PON、CaE和BChE活力明显低于对照组,差异有统计学意义（P〈0.001）;血清-βGD活力两组之间的差异无统计学意义（P〉0.05）。（3）接触组工人红细胞AChE活力低于参考值下限的异常率,为5.4%,而血清CaE、BChE活力异常率分别为37.5%和48.2%,明显高于红细胞AChE活力异常率,差异有统计学意义（P〈0.001）。血清PON活力异常率为5.4%,与红细胞AChE活力异常率之间差异无统计学意义（P〉0.05）。结论 长期职业接触OP工人红细胞AChE、血清BChE、CaE、PON 4种酯酶活力均受到抑制,血清CaE可作为反映OP接触的一个新的生物标志物。     

石杉碱甲对急性水胺硫磷和辛硫磷中毒时AChE活力的影响

目的观察石杉碱甲(哈伯因,HupA)对水胺硫磷和辛硫磷急性染毒小鼠的AChE活力的影响。方法实验小鼠随机分为HupA干预组和未干预组,所有小鼠均经口给予一定剂量水胺硫磷或辛硫磷,干预组小鼠于染毒前2 h经口给予HupA,而后定时测定染毒后全血、红细胞和脑组织的AChE活力值。结果无论是水胺硫磷还是辛硫磷染毒,HupA干预组的全血、红细胞及脑组织AChE活力均高于同时点的未干预组。结论 HupA可以对抗水胺硫磷和辛硫磷对AChE活性的抑制作用,提示HupA可能具有预防和治疗水胺硫磷和辛硫磷中毒的作用。     

Substituted monoquaternary oximes as reactivators of cyclosarin--and chlorpyrifos--inhibited acetylcholinesterase

This paper describes an in vitro study of three potential acetylcholinesterase (AChE; EC 3.1.1.7) reactivators derived from a monoquaternary reactivator pralidoxime. Compounds used were pyridinium-2-aldoxime-4-carbamoyl-N-methyl iodide (TO231), pyridinium-2-aldoxime-4-ethoxycarbonyl-N-methyl iodide (TO237), and pyridinium-2-aldoxime-5-ethoxycarbonyl-N-methyl iodide (TO238). Pralidoxime and obidoxime were used for comparison. Nerve agent cyclosarin and pesticide chlorpyrifos were used as organophosphorus cholinesterase inhibitors. The source of AChE was rat brain homogenate. None of the tested oximes was able to reactivate cyclosarin-inhibited AChE (at 1.0 mmol L(-1) oxime concentration). In case of chlorpyrifos, TO231 was the most potent AChE reactivator with an 82 % reactivation at 1.0 mmol L(-1) oxime concentration. This reactivating potency equals that of pralidoxime and obidoxime. TO238 was less effective, and TO237 did not reactivate chlorpyrifos-inhibited AChE at all. None of the tested AChE reactivators, reference compounds included, could be considered universal for both chlorpyrifos- and cyclosarin-inhibited AChE.     

Pyridinium oximes: rationale for their selection as causal antidotes against organophosphate poisonings and current solutions for auto-injectors

During the last five decades, five pyridinium oximes were found to be worthy of use as antidotes against nerve agents in humans: pralidoxime, in a form of chloride or PAM-2 Cl and mesylate or P2S (against sarin, cyclosarin and VX), trimedoxime or TMB-4 and obidoxime or LüH-6 (both against tabun, sarin and VX), HI-6 (against sarin, soman, cyclosarin and VX) and HL?-7 (against all the five nerve agents). In order to provide the auto-injector with the best and most potent acetylcholinesterase reactivator, the Defence Research and Development Canada (DRDC) received in the 1990s a core funding from the federal government's CBRN research and Technology Initiative (CRTI). Its ultimate result should be three products: (1) 3-in-1 auto-injector (atropine, HI-6 dimethanesulphonate and avizafone, as anticonvulsant), (2) 2-in-1 auto-injector (atropine and HI-6 dimethanesulphonate) and (3) HI-6 dimethanesulphonate in a vial for administration by the medically trained personnel. Previous experimental and clinical experience suggests that, among the oximes mentioned, only trimedoxime and obidoxime can be used for acetylcholinesterase reactivation and antidotal protection against most of the organophosphorus insecticides. The search for an "omnipotent" oxime, effective in reactivation of AChE inhibited with both nerve agents and organophosphorus insecticides, is still ongoing.     

In-vitro regeneration of sarin inhibited electric eel acetylcholinesterase by bis-pyridinium oximes bearing xylene linker

A series of bis-pyridinium oximes connected by xylene linker were synthesized and their in-vitro reactivation potential was evaluated against acetylcholinesterase (AChE) inhibited by nerve agent, sarin. Among the synthesized compounds, alpha,alpha'xylene-bis-[3,3'-(hydroxyiminomethyl) pyridinium] dibromide (3b) was found to be most potent reactivator for AChE inhibited by sarin. The oxime 3b exhibits 34% regeneration of inhibited AChE, in comparison to 20 and 15% regeneration by 2-PAM and obidoxime, respectively, at a concentration of 10(-4) M within 10 min.     

Nonenzymatic functions of acetylcholinesterase splice variants in the developmental neurotoxicity of organophosphates: chlorpyrifos, chlorpyrifos oxon, and diazinon

BACKGROUND: Organophosphate pesticides affect mammalian brain development through mechanisms separable from the inhibition of acetylcholinesterase (AChE) enzymatic activity and resultant cholinergic hyperstimulation. In the brain, AChE has two catalytically similar splice variants with distinct functions in development and repair. The rare, read-through isoform, AChE-R, is preferentially induced by injury and appears to promote repair and protect against neurodegeneration. Overexpression of the more abundant, synaptic isoform, AChE-S, enhances neurotoxicity. OBJECTIVES: We exposed differentiating PC12 cells, a model for developing neurons, to 30 microM chlorpyrifos (CPF) or diazinon (DZN), or CPF oxon, the active metabolite that irreversibly inhibits AChE enzymatic activity, in order to determine whether they differentially induce the formation of AChE-S as a mechanistic predictor of developmental neurotoxicity. We then administered CPF or DZN to neonatal rats on postnatal days 1-4 using daily doses spanning the threshold for AChE inhibition (0-20%); we then evaluated AChE gene expression in forebrain and brainstem on post-natal day 5. RESULTS: In PC12 cells, after 48 hr of exposure, CPF, CPF oxon, and DZN enhanced gene expression for AChE-R by about 20%, whereas CPF and DZN, but not CPF oxon, increased AChE-S expression by 20-40%. Thus, despite the fact that CPF oxon is a much more potent AChE inhibitor, it is the native compound (CPF) that induces expression of the neurotoxic AChE-S isoform. For in vivo exposures, 1 mg/kg CPF had little or no effect, but 0.5 or 2 mg/kg DZN induced both AChE-R and AChE-S, with a greater effect in males. CONCLUSIONS: Our results indicate that nonenzymatic functions of AChE variants may participate in and be predictive of the relative developmental neurotoxicity of organophosphates, and that the various organophosphates differ in the degree to which they activate this mechanism.     

哈伯因对水胺硫磷和辛硫磷染毒小鼠的神经病理改变的影响

目的观察哈伯因(HupA)对水胺硫磷和辛硫磷急性染毒小鼠中枢神经系统的影响。方法染毒组和预防处理组均经口给予一定剂量水胺硫磷或辛硫磷,预防处理组染毒前2h经口给予HupA,对照组经口给予吐温-80或花生油。染毒24h后采用原位整体灌注法固定动物,取脑,做冠状切片,进行HE染色和甲苯胺蓝染色,用Image Pro-Plus720进行神经病理组织学图像分析。结果水胺硫磷和辛硫磷染毒组动物均见到大脑皮质水肿、神经锥体细胞急性水肿、海马锥体细胞急性水肿,尼氏体减少。预防处理组部分动物虽见到大脑皮质水肿、神经锥体细胞急性水肿,而病变程度比染毒组明显减轻。结论HupA对水胺硫磷和辛硫磷染毒小鼠神经病理改变有一定的保护作用。     

美金刚对敌敌畏染毒大鼠脑组织NMDA受体的保护作用

目的　研究美金刚对敌敌畏染毒大鼠脑组织N 甲基 D 天冬氨酸 (NMDA)受体的保护作用及其治疗有机磷农药中毒的机制。方法　雄性SD大鼠用 2 5mg/kg敌敌畏染毒 ,再用美金刚 5、15、45mg/kg治疗 ,观察大鼠中毒症状出现强度与时间 ;染毒后 16h测定大鼠全血和脑组织乙酰胆碱酯酶 (AChE)活力及NMDA受体活性。结果　美金刚 15、45mg/kg治疗组大鼠中毒症状出现时间分别为 (18.40± 1.14 )、(2 1.40±1.52 )min ,较敌敌畏组 [(16.75± 1.62 )min]明显延长 ;肌颤强度分别为 1.60± 1.14、0 .80± 0 .84,较敌敌畏组(2 .85± 0 .3 7)明显减轻 ;症状总评分分别为 8.80± 1.79、9.0 0± 2 .2 4,较敌敌畏组 (14 .60± 1.70 )明显改善。美金刚对敌敌畏染毒大鼠全血和脑组织AChE活力均未见明显影响。敌敌畏染毒大鼠脑组织NMDA受体密度减少、亲和力下降 ,其Bmax和Kd值分别为 (0 .46± 0 .0 6)pmol/mgpro、(75.55± 7.87)nmol/L ,分别较阴性对照组 [(0 .62± 0 .0 4)pmol/mgpro、(3 7.3 7± 4.17)nmol/L]下降和上升。 5、15mg/kg美金刚可拮抗敌敌畏染毒对大鼠脑组织NMDA受体的影响 ,这两组的Bmax值分别为 (0 .55± 0 .0 7)、(0 .64± 0 .0 7)pmol/mgpro ,Kd值分别为 (3 8.68± 4.54)、(3 2 .58± 3 .90 )nmol/L。美金刚 45m     

Effects of Anabaena spiroides (Cyanobacteria) aqueous extracts on the acetylcholinesterase activity of aquatic species

The effects of aqueous extracts from a cyanobacteria species, Anabaena spiroides, on fish (Odontesthes argentinensis), crab (Callinectes sapidus), and purified eel acetylcholinesterase (AChE) activity were studied. In vitro concentrations of A. spiroides aqueous extract that inhibited 50% of enzyme activity (IC50) were 23.0, 17.2, and 45.0 mg/L of lyophilized cyanobacteria for eel, fish, and crab AChE, respectively. Eel AChE inhibition follows pseudo-first-order kinetics, the same expected for organophosphorus pesticides. Inhibition of purified eel AChE using mixtures of bioxidized malathion and aqueous extract of A. spiroides showed a competitive feature (p < 0.05), suggesting that the toxin(s) could be structurally similar to an organophosphorus pesticide and that toxins present in the aqueous extract inhibit the active site of the enzyme. The inhibition recovery assays using 2-PAM (0.3 mM) showed that (1) bioxidized malathion inhibited 27.0 +/- 1.1% of crab and 36.5 +/- 0.1% of eel AChE activities; (2) with bioxidized malathion + 2-PAM the registered inhibition was 13.2 +/- 2.1% and 3.7 +/- 0.5% in crab and eel AChE, respectively; (3) the aqueous extract from A. spiroides inhibited 17.4 +/- 2.2% and 59.9 +/- 0.5% of crab and eel AChE activity, respectively; and (4) aqueous extract + 2-PAM inhibited 22.3 +/- 2.6 and 61.5 +/- 0.2% of crab and eel AChEs. The absence of enzyme activity recovery after 2-PAM exposure could imply that the enzyme aging process was extremely quick.     

Field results using cholinesterase reactivation techniques to diagnose acute anticholinesterase poisoning in birds and fish

The inhibition of brain cholinesterase (ChE) activity in organophosphate (OP)- or carbamate (CB)-poisoned animals is usually determined by comparison with the normal activity in control specimens. Alternatively, the activity of pesticide-inhibited ChE can be restored, ideally up to normal levels, using simple in vitro procedures, thereby providing a reference value against which ChE inhibition can be estimated. The activity of phosphorylated ChE can be increased by the addition of the nucleophilic reagent pyridine 2-aldoxime methiodide (2-PAM), while the spontaneous reactivation of carbamylated ChE can be enhanced by dilution. These procedures can also be used to differentially diagnose OP and CB poisoning. Brain ChE inhibition in birds and fish from field poisoning incidents was determined using reactivation techniques and normal activity data from separate control specimens. In OP-poisoned birds, the mean inhibition relative to 2-PAM-treated samples and controls ranged from 77–82% and 84–87%, respectively. The corresponding values for OP-poisoned fish were 48–82% and 66–86%, respectively. In CB-poisoned birds, the mean inhibition relative to diluted samples and controls ranged from 22–56% and 33–76%, respectively. The reactivation of carbamylated ChE was further enhanced by increasing the dilution ratio and lengthening the incubation period. Although ChE activity was not fully restored to normal levels in many individuals, diagnostically significant inhibition was demonstrated in most cases. In OP-poisoned fish held 24 h postmortem at 20°C, 2-PAM restored brain ChE activity to that of similarly handled, unexposed controls. After postmortem storage for 48 h, ChE activities in reactivated and inhibited samples were statistically indistinguishable due to the aging of the phosphorylated ChE. Despite the limitations imposed by aging, ChE reactivation is a potentially useful diagnostic technique, particularly when control data are unavailable or difficult to obtain.     

溴氰菊酯和辛硫磷亚致死剂量对德国小蠊酶活性的影响

目的研究溴氰菊酯和辛硫磷亚致死剂量处理后德国小蠊羧酸酯酶、谷胱甘肽S-转移酶、乙酰胆碱酯酶的活性变化规律。方法采用分光光度计离体测定酶的活性,应用DPS软件进行统计分析。结果辛硫磷亚致死剂量处理德国小蠊后24h,羧酸酯酶活性降到最低,与处理前相比降低了79．33％,24h后其活性逐渐恢复,168h达到处理前的37．10％;溴氰菊酯亚致死剂量处理后,羧酸酯酶活性略有下降;经溴氰菊酯和辛硫磷亚致死剂量处理后,谷胱甘肽S-转移酶的活性略有下降,72h后其活性分别为处理前的74．97％和79．77％;经溴氰菊酯亚致死剂量处理后,乙酰胆碱酯酶活性24h略有升高,随后逐渐下降,经辛硫磷处理后其活性略有降低。结论经溴氰菊酯和辛硫磷亚致死剂量处理后德国小蠊体内酶活性在不同的时间与处理前存在差异。