拟除虫菊酯对大鼠皮层腺苷酸环化酶水平影响

目的研究溴氰菊酯(deltamethrin，DM)和氯菊酯(permethrin，PM)对雄性SD大鼠大脑皮层及纹状体腺苷酸环化酶(adenylyl cyclases，AC)蛋白含量和纹状体环磷酸腺苷(cAMP)水平的影响。方法采用不同剂量的溴氰菊酯、氯菊酯对雄性SD大鼠进行经口灌胃给药后，免疫组化的方法测定大鼠大脑皮层及纹状体AC蛋白含量，及放射免疫方法检测DM和PM对大鼠纹状体cAMP水平的影响。结果连续灌胃10d染毒后，大鼠皮层的AC水平和纹状体的cAMP水平明显被抑制。结论拟除虫菊酯能明显降低大鼠皮层AC含量和纹状体cAMP水平。     

拟除虫菊酯对大鼠脑组织中白介素-1β的影响

目的 探讨细胞因子与拟除虫菊酯中枢神经系统损害机制的关系。方法 用逆转录－聚合酶链式反应（RTPCR)和免疫组织化学方法观察了拟除虫菊酯对大鼠脑组织中白细胞介素1beta(IL－1β)表达的影响。结果 大鼠经氯菊酯一次大剂量和多次小剂量处理后，其皮层和海马的IL－1βmRNA水平有明显的升高，分别是对照组的2．1，1．9和1．9，1．9倍；而一次大剂量氯菊酯处理后其蛋白水平的表达在海马尤其是CA3区显著升高，达到对照的1．5倍，皮层则无明显变化，小剂量反复给药后皮层和海马的蛋白表达均明显上升。溴氰菊酯处理后IL－1β的mRNA也有升高趋势，而蛋白水平没有明显的改善。结论 拟除虫菊酯对IL－1β快速诱导可能是脑组织对损伤的一种保护反应。     

拟除虫菊酯类杀虫剂对大鼠脑突触体ATPase活性的影响

In vitro Effect of several pyrethroids on rat brain synaptosomal ATPase activities was investigated. No significant changes in Na+, K+-ATPase and oligomycin-insensitive Mg2+-ATPase activities were observed under present experimental conditions, but all pyrethroids tested caused significant inhibition of oligomycin-sensitive Mg2+-ATPase activity with certain concentration dependence. The results suggest a possibility that pyrethroids may alter the cellular energy metabolism of the nervous system.     

拟除虫菊酯农药暴露对婴儿生长发育的影响

【目的】 探讨拟除虫菊酯农药暴露对婴儿生长发育的影响,为预防儿童农药中毒提供科学依据。 【方法】 选取江苏某县1岁婴儿449名,收集随机尿样检测拟除虫菊酯代谢物顺式-3-(2,2-二氯乙烯基)-2,2-二甲基环丙烷-1-羧酸(cis-Cl₂CA)、反式-3-(2,2-二氯乙烯基)-2,2-二甲基环丙烷-1-羧酸(trans-Cl₂CA)和3-苯氧基苯甲酸(3-PBA)水平,测量婴儿身长、体重、头围、胸围,用“0~6岁儿童发育筛查测验”(DST)评估婴儿智能发育状况,分析两者之间关系。 【结果】 研究对象尿样拟除虫菊酯代谢物cis-Cl₂CA、trans-Cl₂CA和3-PBA检出率分别为70.4%、97.6%和84.2%。按照总拟除虫菊酯浓度P₂₅、P₇₅分为低中高三组,不同暴露水平组之间婴儿的体重、胸围不完全相同,具有统计学意义(P<0.05),但身长、头围和发育商差异无统计学意义。多重线性回归分析亦提示尿拟除虫菊酯的浓度与体重有相关性(P<0.05)。 【结论】 拟除虫菊酯暴露对婴儿体重有一定的影响。     

拟除虫菊酯对大鼠脑突触体谷氨酸摄取功能的影响

作者观察了拟除虫菊酯对大鼠脑突触体谷氨酸重摄取功能的影响。在一定量的突触体与不同剂量的氯氰菊酯或氯菊酯中加入放射性标记谷氨酸，测定突触体摄取的谷氨酸的放射活性，在１０－ ９ ～１０－ ４ ｍ ｏｌ／ Ｌ的剂量范围内，氯氰菊酯及氯菊酯明显抑制突触体对谷氨酸的重摄取量，并有一定的剂量依赖性。在相同剂量水平，氯氰菊酯作用明显强于氯菊酯。结果表明拟除虫菊酯对大鼠脑突触体谷氨酸高亲和性重摄取功能有抑制作用，提示突触体谷氨酸重摄取系统功能障碍在拟除虫菊酯兴奋性神经毒性中具有重要意义。     

拟除虫菊酯对大鼠脑代谢型谷氨酸受体结合的影响

目的　比较两型拟除虫菊酯 (pyrethroid ,PY)类农药对大鼠脑代谢型谷氨酸受体(mGluR)结合功能的影响。方法　应用放射性配基受体结合试验在体外测定溴氰菊酯 (DM )和氯菊酯 (PM )对大鼠大脑皮层和海马突触膜mGluR结合功能的影响。结果　DM分别在 2× 10 -6、2× 10 -5、2× 10 -4 mol/L和 2× 10 -10 、2× 10 -8、2× 10 -6、2× 10 -4 mol/L剂量范围内直接增加大鼠大脑皮层和海马突触膜氚标记的谷氨酸 (3H Glu)与mGluR的特异结合量 ,分别为 :(10 7.6± 7.7)、(112 .4± 9.6 )、(115 .4± 12 .2 )fmol/mgpro .和 (15 9.8± 16 .9)、(16 6 .9± 2 0 .9)、(183.8± 2 1.2 )、(193.8± 2 5 .8)fmol/mgpro .;PM在 2× 10 -8～ 2× 10 -4 mol/L剂量范围内对大脑皮层突触膜3H Glu与mGluR的特异结合量无明显影响 ,在 2× 10 -6、2× 10 -4 mol/L时直接增加海马突触膜3H Glu与mGluR的特异结合量 ,分别为 :(173.8± 2 0 .1)、(180 .9± 2 4.3 )fmol/mgpro .。 结论　DM和PM均可不同程度地影响海马突触膜mGluR的结合功能 ,带氰基的DM比不带氰基的PM更容易增加大鼠脑mGluR的特异结合量     

急性拟除虫菊酯中毒的临床表现及诊断

国外迄今尚未见有急性拟除虫菊酯中毒的临床报告。国内医学文献自1982年至1988年则已报道急性拟除虫菊酯中毒共573例,其中生产性中毒229例,意外性中毒344例。以急性溴氰菊酯中毒最为多见(325例),其次为戊氰菊酯(196例)及氯氰菊酯(45例)等急性中毒。本文对573例急性拟除虫菊酯中毒的临床表现进行综述与分析,并探讨其诊断分级与鉴别诊断,为制定职业性急性拟除虫菊酯中毒诊断标准提供参考。     

拟除虫菊酯水剂杀虫剂的研制

选择合适的助溶活性剂和拟除虫菊酯配制而成的水剂杀虫剂，经实验室和现场试验，对蚊蝇、蟑螂都有显著杀灭作用，并且有高效、低毒、稳定性好和价格低廉等优点，对卫生害虫的击倒、杀灭作用优于同等含药量的醇制剂，目前已经应用于部队。     

氯菊酯和溴氰菊酯对大鼠血清及脑甲状腺激素水平的影响

目的探讨拟除虫菊酯对大鼠甲状腺激素（TH）水平的影响。方法经口连续１５d给予大鼠氯菊酯（PM）１００、２００、４００mg·kg－１·d－１和溴氰菊酯（DM）６．２５、１２．５０、２５．００mg·kg－１·d－１。用放射免疫分析法检测大鼠血清、脑组织及其亚细胞结构中的TH水平。结果（１）PM：２００、４００mg·kg－１·d－１组大鼠血清三碘甲腺原氨酸（T３）、四碘甲腺原氨酸（T４）、游离T３（fT３）、游离T４（fT４）均下降，而促甲状腺激素（TSH）上升，且现PM呈现剂量依赖关系（T４：r＝０．６７９，fT４：r＝０．５１１，TSH：r＝０．７３８，均P＜０．０１）；１００mg·kg－１·d－１组大鼠T４和fT４下降，T３、fT３、TSH无明显变化。３个处理组大鼠大脑皮层T４分别为（３９．９±５．０）、（３３．４±９．２）、（３２．３±８．２）pg／mgpro，明显低于对照［（４４．２±７．１）g／mgpro］，且有剂量依赖性（r＝０．５２９，P＜０．０１）；而PM染毒４００mg·kg－１·d－１组的T３［（２１．２±５．２）pg／mgpro比对照［（３０．９±１０．０）pg／mgpro］明显降低。２００、４００mg·kg－１·d－１组大鼠海马T４为（１９．１±５．５）、（１９．２±６．５）pg／mgpro，T３为（３     

拟除虫菊酯对神经细胞膜Na^＋,Ca^2＋离子通道的影响

为探讨拟除虫菊酯类（Ｐｙｒｅｔｈｒｏｉｄｓ，Ｐｙｓ）对神经细胞电信号传导系统的作用机制，应用膜片箝（Ｐａｔｃｈｃｌａｍｐ）技术，研究了大鼠神经细胞在Ｐｙｓ农药氰戊菊酯（Ｆｅｎｖａｌｅｒａｔｅ，Ｆｅｎ）和四甲菊酯（Ｔｅ－ｔｒａｍｅｔｈｒｉｎ，Ｔｅｔ）作用下，Ｎａ＋、Ｃａ２＋电流的变化。实验结果表明：Ｆｅｎ和Ｔｅｔ对Ｎａ＋通道的毒作用特点为：低剂量激活、高剂量抑制；对Ｃａ２＋通道的影响亦表现为低剂量激活、高剂量抑制，但激活作用较弱而抑制作用明显。此外，Ｐｙｓ可引起兴奋性突触后电位（ＥＰＳＰ）频率的增高。     

Effects of ethylene glycol on drug metabolizing enzymes in rat liver

We investigated the effects of ethylene glycol (EG) on the hepatic drug metabolizing enzymes. The exposed group was given 1% EG solution and the control group was provided with distilled water for 2 weeks ad libitum. The body weight of the exposed group was the same as that of the control group. The liver and kidney weight per body weight did not change. The daily drinking volume for the exposed group on the average showed an increase of 13.5% over that of the control group. Hematologically and biochemically, anemia, liver and renal dysfunction were not seen. The content of the hepatic microsomal cytochrome P-450 in the exposed group showed an increase of 17% over that of the control group, but the contents of cytochrome b5, protoheme and the activities of NADPH-cytochrome c reductase, NADH-ferricyanide reductase did not change. The activities of the hepatic cytosolic alcohol dehydrogenase and glutathione reductase, glutathione peroxidase, glutathione-S-transferase also did not change. These results indicate that the hepatic microsomal cytochrome P-450 takes part in the metabolism of EG.     

Effect of manganese chloride exposure on liver and brain mitochondria function in rats

Manganese (Mn) is an essential trace element found in many enzymes. As is the case for many essential trace elements, excessive Mn is toxic. Individuals suffering from manganese toxicity exhibit several symptoms, which are similar to those frequently observed in cases of Parkinson's disease. In this investigation, we studied the effect of manganese chloride (7.5, 15.0, and 30.0 mg/kg body weight) on mitochondrial function and attempted to ascertain the mechanism of manganese-induced mitochondrial dysfunction. The production of reactive oxygen species in mitochondria of rat liver and brain was assayed using 2',7'-dichlorofluorescin diacetate, and the activities of respiratory chain enzymes were examined spectrophotometrically. Monoamine oxidase (MAO) activity was assayed by measuring reduction of benzylamine. Manganese and calcium content in mitochondria were determined by atomic absorption spectrophotometry. These results indicate that manganese chloride (MnCl2) can decrease MAO activity and inhibit the respiratory chain. Manganese can accumulate in mitochondria and inhibit efflux of calcium. There is a significant inverse correlation between the amount of superoxide radicals and the specific activities of the mitochondria enzymes. Mitochondrial function was significantly affected in both males and females.     

Effect of ethanol on the microsomal glutathione S-transferase activity in glutathione-depleted rat liver

Depletion of hepatic glutathione in male rats by starvation caused a significant increase in microsomal glutathione S-transferase activity, which was not affected by acute ethanol pretreatment. An additional depletion in fasted rats by diethylmaleate (0.5 g/kg) caused a further increase in the enzyme activity, but this increase was delayed in ethanol intoxicated rats. Although ethanol caused a small increase in hepatic microsomal lipid peroxidation in control animals, this effect of ethanol was not observed in diethylmaleate treated rats and thus was apparently not responsible for the delay in enzyme activation. It is suggested that the activation of microsomal glutathione S-transferase activity towards 1-chloro-2,4-dinitrobenzene in glutathione-depleted rat liver may be produced by changes in thiol/disulfid ratio and/or some reactive oxygen species.     

拟除虫菊酯混配水基杀虫制剂现场杀虫效果观察

本文报道拟除虫菊酯混配水基杀虫制剂现场杀虫试验结果。以1ppm剂量处理污水池,对蚊幼杀灭率为92.1%;5ml/m~3剂量,对淡色库蚊成虫16分钟击倒率为88.5%,24小时死亡率为100%:此剂量对家蝇的杀灭率为98～100%,还可有效地控制德国小蠊的危害。由此可见,它是一种高效广谱卫生杀虫制剂,可广泛用于列车、家庭及公共场所。     

Effects of acute and chronic ethanol administration on thiamine metabolizing enzymes in some brain areas and in other organs of the rat

The effect of ethanol (4.7 g/kg body wt intragastrically as a single dose or once daily for 35 days) on the levels of the thiamine metabolizing enzymes (thiamine pyrophosphokinase, TPKase; thiamine pyrophosphatase, TPPase; and monophosphatase, TMPase) was studied in different organs (liver, kidney, small intestine, heart and skeletal muscle) and nervous regions (cerebral cortex, cerebellum, medulla oblongata, pons, corpus callosum, hypothalamus and sciatic nerve) of the rat. In order to evaluate the non-specific effects of the stress of gastric gavage and of the additional caloric intake, appropriate control groups of animals were treated intragastrically with water or with a saccharose solution isoenergetic with ethanol respectively. All animals were reared on a nutritionally adequate diet supplying amounts of thiamine higher than the recommended daily requirement. Enzymatic activities were determined quantitatively by biochemical methods. Tissue TPKase levels were generally reduced by both acute and chronic ethanol administration. TPPase levels were generally reduced after acute and increased after chronic ethanol treatment. Changes in brain TMPase levels were similar to those observed for TPPase. In visceral organs and skeletal muscle TMPase activity was increased by chronic ethanol treatment as compared to acute ethanol administration. In conclusion, ethanol exerts a marked influence on the tissue levels of the thiamine metabolizing enzymes: the activity of the enzymes dephosphorylating thiamine phosphates is increased whereas the activity of the thiamine pyrophosphate synthesizing enzyme is reduced. These changes may contribute to an important extent to the disturbances in thiamine cellular uptake and metabolism observed in alcoholism.     

拟除虫菊酯对大鼠脑组织γ-氨基丁酸转氨酶活力的影响

目的　研究拟除虫菊酯对大鼠脑组织γ 氨基丁酸转氨酶 (GABAT)活力的影响。方法　应用偶联酶学紫外分光光度法 ,在体外和整体实验中 ,观察溴氰菊酯 (DM)和氯菊酯 (PM)对大鼠大脑皮层、海马、纹状体和小脑GABAT活力的影响。结果　在体外 ,终浓度为 10 -9～ 10 -4mol/L的DM或PM对大鼠大脑皮层、海马、纹状体和小脑的GABAT活力无明显影响 ;一次性经口给予 37.5mg/kg的DM组大鼠大脑皮层、海马和小脑的GABAT活力分别为 (2 .96± 0 .4 3)、(2 .13± 0 .4 4 )、(5 .12± 1.36 )nmol·mgpro-1·min-1,低于对照组 [(3.4 3± 0 .4 1)、(2 .6 8± 0 .4 7)、(6 .74± 1.6 4 )nmol·mgpro-1·min-1],差异有显著性 (P <0 .0 5 ) ,6 0 0mg/kgPM一次性染毒组大鼠大脑皮层和海马的GABAT活力分别为(4.5 7± 0 .30 )、(4.18± 0 .6 3)nmol·mgpro-1·min-1,高于对照组 ,差异有显著性 (P <0 .0 5 ) ;连续 5d每天 1次经口给予 12 .5mg/kg的DM或 2 0 0mg/kg的PM ,均对大鼠大脑皮层、海马、纹状体和小脑的GABAT活力无明显影响。结论　在体外 ,DM和PM均对大鼠脑组织GABAT活力无明显影响 ;在整体实验中 ,DM和PM对大鼠脑组织GABAT活力的影响可能存在差异。     

Early effects of hypervitaminosis A on gluconeogenic activity and amino acid metabolizing enzymes of rat liver.

In an earlier report from this laboratory, one of the early manifestations of hypervitaminosis A was shown to be a marked stimulation of hepatic gluconeogenesis. In the present study, effects of feeding 30,000 IU of retinyl palmitate to young rats (80-100 g), once daily, for 2 days on the incorporation of 14C-labeled precursors into glucose and glycogen by liver slices, levels of amino acids in blood and tissues, and activities of some important amino acid catabolizing enzymes in the liver were investigated. A stimulation of hepatic gluconeogenesis in hypervitaminosis A was indicated by the increased incorporation of 14C-labeled alanine and bicarbonate into glucose and glycogen by liver slices. Excessive intake of retinol caused a marked increase in the activities of hepatic alanine aminotransferase and ornithine aminotransferase and a decrease in that of tryptophan pyrrolase, without affecting those of tyrosine aminotransferase and serine dehydratase. The ratio of NADH:NAD in the livers of rats fed excess retinol was significantly increased. It is suggested that enhancement of glucoeogenesis in hypervitaminosis A is caused by a stimulation of gluconeogenic activity of the liver.