新型脂环驱避剂的合成及驱蚊活性

本文介绍了将不饱阳环烷甲酰氯与二乙胺缩合制得一种新型脂环驱避剂——环烯酰胺驱避剂,实验代号R_(202),并报道其合成路线。所得样品通过元素分折、红外光谱证实了其结构,其驱蚊活性经测定,10％R_(202)酊剂对埃及伊蚊绝对驱避时间为9h,同样条件下10％Deet酊剂其绝对驱避时间为7.5h。     

驱避剂新剂型的研究

目的：研究驱避剂新剂型（驱蚊肤宁）的驱蚊效果和动物毒性。方法：实验室和现场驱蚊试验，分别在试者手背和小臂涂驱避剂，观察被蚊虫刺叮时间；动物毒性试验，按ＧＢ１５６７０－１９９５进行。结果：实验室对白纹伊蚊和埃及伊蚊的完全有效时间为６．４６±２．２２和７．６０±２．１９小时。现场试验，在以凶小库蚊为主，且刺叮频率很高的情况下，２小时有效率６０％～７３．７％；在以淡色库蚊为主，刺叮率低的情况下，６小时有效率为５２．４％～９３．７％。驱蚊肤宁对大鼠经口ＬＤ５０＞５０００ｍｇ／ｋｇ，大鼠经皮ＬＤ５０＞８０００ｍｇ／ｋｇ，对家兔皮肤和眼睛无刺激性。结论：驱蚊肤宁效果良好，对温动物毒性低，使用安全。     

R-301驱避剂化学合成及生物活性的研究

目的:阐述新型R-301驱避剂的合成及其驱避效果;方法:驱蚊活性按GB/T 17322.10-1998规定进行试验,驱蠊活性用选室法进行试验,驱螨活性采用计算驱避率法进行试验;结果:7％浓度R-301对白纹伊蚊有效保护时间平均为3.80±0.86 h,100％保护率的时间为3 h,0.1％和0.3％浓度对德国小蠊1～10 d具有杀灭作用,11-46 d有驱避作用,驱避率均为100％。对尘螨的驱避率,其浓度为0.1％、0.3％和0.5％均为100％,R-301对大肠杆菌、金黄色葡萄球菌和糠秕孢子菌的最小抑菌浓度(MTC)分别为0.125、0.25和0.01;结论:R-301驱避剂合成线路简便合理,对蚊、蠊、螨和菌具有生物活性,为一新型广谱的驱避剂,有开发推广应用前景。     

一种长效涂抹驱避剂驱蚊效果的研究

目的观察一种长效涂抹驱蚊剂的驱蚊效果。方法将标准驱避剂避蚊胺与伊默宁、高分子聚合物缓释剂相结合,研制成一种长效液相驱避剂,与市售驱蚊花露水进行现场驱蚊效果比较。结果人体按1．5μl／cm^2或1．5mg／cm^2处理,复配制剂对白纹伊蚊的平均有效驱避时间达9—11h,使用10h后的有效保护率为92．3％,优于其他2种驱避剂,现场驱蚊效果达8h以上。结论长效涂抹驱避剂使用方便,无油腻感,效果较好。     

新型脂环驱避剂的合成及驱蚊活性

介绍了用不饱和环烷甲酰氯与二乙胺缩合制得的一种新型脂环驱避剂—环烯酰胺驱避剂（实验代号Ｒ２０２）的合成路线。所得样品通过元素分析、红外光谱证实了其结构。其驱蚊活性为１０％Ｒ２０２酊剂对埃及伊蚊绝对驱避时间为９ｈ，同样条件下１０％避蚊胺（Ｄｅｔ）酊剂的绝对驱避时间为７．５ｈ。     

驱蚊露和驱蚊霜的驱蚊效果研究

本文报告了增效复方驱避剂两种剂型的实验室和现场驱蚊效果。以当时国内生产的最佳驱避剂蚊怕水为对照,效果均优于蚊怕水。实验室对白纹伊蚊、中华按蚊和淡色库蚊的有效时间,驱蚊露分别是10.4、10.0和13.1小时,驱蚊霜分别是10.8、12.8和14.1小时。在吉林草原驱蚊露对凶小库蚊和背点伊蚊的有效时间平均5.8小时。在津郊农场驱蚊露和驱蚊霜对凶小库蚊和刺扰伊蚊的平均有效时间为7.4和7.6小时,蚊怕水为4.7～5.7小时。在苏北农村对三带喙库蚊和淡色库蚊平均有效时间6.2小时,蚊怕水为4.7小时。在广西对白纹伊蚊的有效时间大于9.6小时。本文还讨论了影响驱避效果的一些因素。     

几种驱避剂对埃及伊蚊驱避效果的研究

目的观察9种市售驱避剂对埃及伊蚊的驱避效果。方法选择不同浓度及剂型的驱避剂9种,在实验室对埃及伊蚊进行驱避剂效果试验。结果驱避剂的驱避效果随着驱避剂浓度的升高而增加。5%、10%、15%避蚊胺的驱蚊效果持续时间分别为4、5. 3、7. 5 h; 5%、10%、15%驱蚊酯的驱蚊效果持续时间分别为4. 3、4. 5、5 h。15%、20%、30%羟哌酯的驱蚊效果持续时间分别为7. 3、8、10 h。结论不同品种与浓度的驱避剂对埃及伊蚊表现出不同的驱避效果,有效保护时间总体上随使用浓度提高而提升,可根据需要选择使用相应的驱避剂。     

4种植物精油驱蚊贴驱避效果的初步研究

目的研究4种植物精油驱蚊贴对白纹伊蚊的驱避效果,并评估其持效性和实际使用效果。方法采用蚊笼叮咬法和Y型圆筒法进行室内生物测定,模拟房现场法观察现场驱避效果,问卷调查评估推广应用前景。结果在蚊笼叮咬法1中,香茅油驱蚊贴的驱避效果最好,达到78.2%,其次为复方精油驱蚊贴的驱避率为56.0%。Y型圆筒法测试结果显示,5%驱蚊酯驱蚊贴驱赶90%蚊虫到达无药端的时间最短,为10 min;香茅油驱蚊贴次之,为14 min。所有测试的驱蚊贴在24 h后驱蚊效果明显减弱。模拟房驱避效果观察显示,5%驱蚊酯的驱避率最高,达到72.4%;香茅油驱蚊贴次之,为68.4%。推广应用调查反映大多数使用者对香茅油驱蚊效果感到满意。结论香茅油驱蚊贴具有良好的驱蚊效果,值得进一步推广应用。     

板栗花精油的化学组成及对白纹伊蚊驱避作用研究

目的研究板栗花精油及精油4种单一有效组分、板栗花蒸馏液对蚊虫的驱避活性。方法采用气质联用法(GC-MS)对板栗花精油进行成分分析;以白纹伊蚊为试虫,并以有效保护时间及驱避率测定精油及其4种单一有效组分和板栗花蒸馏液的驱避活性。结果板栗花精油主要有醛、酮、醇、酯类化合物11种,精油及其单一有效组分薄荷醇、香叶醇、芳樟醇和松油醇的有效驱避时间分别为3.00、4.25、6.00、3.75、5.00 h,而板栗花蒸馏液仅为0.08 h,市售花露水为2.25 h,显示出板栗花精油具有显著的驱避活性。同时,以有效单一组分为强化剂,以100 ml板栗花蒸馏液为基础,通过正交实验,优化板栗花蒸馏液的驱蚊活性,得到板栗花花露水配方,其驱蚊有效时间为2.50 h。结论板栗花精油具有驱避作用,可以开发以其为有效驱蚊组分的无醇花露水。     

萜类化合物对蚊虫驱避活性的研究

目的用小白鼠筛选对白纹伊蚊有驱避活性的8个化合物进行人体保护试验,以筛选出符合国家标准的驱避剂。方法人体保护试验。结果10%和20%的23号化合物对白纹伊蚊有2.5～3h和4.5～5h的驱避活性,10%和20%的31号化合物对中华按蚊则有4～5h和5～6h的驱避活性。结论23号化合物和31号化合物可分别用于家居和野外的驱蚊保护剂。     

酒精灌胃大鼠血浆中乙醇浓度变化

目的通过实验了解大鼠酒精灌胃后体内乙醇代谢的特点,为建立大鼠乙醇中毒所致慢性酒精性肝病模型提供依据。方法雄性Wistar大鼠30只,随机分成三个剂量组。实验大鼠以50%的酒精按各组剂量给予灌胃,灌胃后分别于第0.5、1、1.5、2、2.5、3、5、10h经眼眶静脉丛采集大鼠血标本,以乙醇脱氢酶法测定血浆中乙醇浓度。结果对各时段点乙醇浓度测定分析,大鼠摄入酒精后乙醇浓度的高峰均出现在灌胃后1~1.5h处,随后开始缓慢下降,代谢曲线与醉酒表现一致。结论酒精灌胃剂量小于8g/kg是比较安全的,灌胃后1~1.5h达到代谢吸收高峰期,10h后醉酒状态基本恢复,这为制备大鼠酒精性肝病模型提供理论依据。     

Acute ethanol ingestion by humans and subacute treatment of rats increase urinary folate excretion

Previous studies with rats showed that acute treatment with ethanol (4 g/kg) produce a marked increase in urinary folate levels, followed by a decrease in plasma folate levels. Analogous studies with human volunteer subjects using a lower dose of ethanol showed that there were small, but statistically significant increases in urinary folate levels after four hours. The initial ethanol dose was 1.0 g/kg with a single supplement of 0.1-0.2 g/kg to maintain ethanol blood levels at about 100 mg/dl for six hours. Further studies with rats were designed to test the cumulative effects of repeated daily doses of ethanol. Male Sprague-Dawley rats were treated for 1, 2, 3, or 4 days either with ethanol orally in 4 doses of 1 g/kg each at 0, 1, 2, and 3 hours or with glucose orally in 4 isocaloric doses. Urine was collected at timed intervals up to 12 hours after each daily dose. The pattern of the increase in urinary folate levels was similar in all groups, whether treated for 1, 2, 3 or 4 days. These results suggest that repeated ethanol treatment can lead to a marked cumulative folate loss via increased urinary excretion and that increased urinary folate excretion may contribute to the development of folate deficiency in humans.     

Monoamine uptake inhibitors attenuate ethanol intake in alcohol-preferring (P) rats

The P line of alcohol-preferring rats drink pharmacologically significant amounts of ethanol when given free choice between a 10 percent ethanol solution and water. Serotonin (5-HT) uptake inhibitors and desipramine, a norepinephrine (NE) uptake inhibitor, were found to significantly reduce their ethanol consumption for up to 24 hours after intraperitoneal injection. To determine if this effect of 5-HT uptake inhibitors could be altered by receptor antagonists, some of which are short acting, P rats were trained to drink ethanol by free choice during scheduled availability, with ethanol being presented one hour every four hours during the light cycle. The majority of the ethanol was consumed during the first hour of availability, and the ethanol intake was significantly reduced by the 5-HT uptake inhibitors, fluoxetine and fluvoxamine. Pretreatment with antagonists for 5-HT1, 5-HT2 and alpha- and beta-NE receptor systems failed to alter the fluvoxamine attenuation of ethanol intake. The mechanism by which 5-HT uptake inhibitors alter ethanol preference remains unclear.     

Chronic tolerance to the locomotor stimulating effect of ethanol in preweanling rats as a function of social stress

During early stages of development rats are highly sensitive to the locomotor stimulating effect of relatively high ethanol doses, an effect strongly modulated by social stress. This ethanol effect can be modulated by pharmacological treatments that also can attenuate the development of ethanol-induced locomotor sensitization in mice. By the end of the preweanling period the mechanisms underlying sensitization induced by psychostimulants are functional. The aim of the present study was to analyze the locomotor response to ethanol in preweanling rats as a function of repeated exposure to the drug under two different social conditions. Subjects were treated with ethanol between postnatal days 15 and 18 after being isolated for four hours (Experiment 1a) or simply residing in their home-cage (Experiment 1b). After two days of withdrawal locomotor response to ethanol was assessed in both social conditions. In Experiment 2 naïve rats were tested in terms of ethanol-induced activation of the locomotor response in both social conditions. Results from the present study showed no evidence of locomotor sensitization in preweanling rats in any of the social conditions. Instead we observed behavioral tolerance to the stimulating effect of ethanol in animals trained in the home-cage condition, in which subjects trained with ethanol showed sedation in response to ethanol at testing. Overall these results contribute to the understanding of the sensitivity of rats to the acute and chronic locomotor response to ethanol in an ontogenetic period characterized by high sensitivity to ethanol.     

口腔脱落细胞乙醇现场固定法微核试验的研究

目的建立乙醇现场固定口腔脱落细胞进行微核试验的方法。方法利用无水乙醇现场固定口腔脱落细胞,保存0～30h后进行微核试验与常规口腔脱落细胞微核试验、外周血淋巴细胞微核试验进行比较。结果乙醇现场固定法的口腔脱落细胞在4、8、24h后的微核率与常规口腔脱落细胞微核率和外周淋巴细胞法微核率（Oh）差异无统计学意义（P〉0．05）,而常规法口腔脱落细胞在保存4h后则出现微核率下降,与外周血培养法的微核率差异有统计学意义（P〈0．05）。结论无水乙醇现场固定口腔脱落细胞能够有效延长保存时间,微核试验结果稳定,适合用于现场采样。     

Harman (1-methyl-beta-carboline) in blood plasma and erythrocytes of nonalcoholics following ethanol loading

Eleven subjects having no history of substance abuse or dependence who agreed to abstain from alcohol for one week prior to the investigation were selected to participate in the present study. On two occasions, separated by four to six weeks, blood was drawn over an 8-hour period (0, 0.5, 1, 2, 4 and 8 hours). On the first occasion, subjects were given an oral dose of ethanol (1 g/kg) after the first blood sample was drawn (ethanol-loading condition). On the second occasion no ethanol was administered (control condition). On both occasions no detectable harman was found in the plasma of subjects. In the control condition harman was detected in the erythrocytes of 7 subjects which remained relatively stable over time. In the ethanol-loading condition, however, a time-dependent increase of harman in the erythrocytes was observed. The concentration of ethanol, acetaldehyde, and erythrocyte-harman showed a parallel trend over time. These findings demonstrate an increased level of harman following ethanol loading in humans.     

Chronic intermittent exposure to ethanol during adolescence produces tolerance to the hypnotic effects of ethanol in male rats: a dose-dependent analysis

Adolescence is a time period when distinct behavioral and neurophysiological changes occur. Novelty seeking is common during this developmental period, and binge alcohol consumption by adolescents is prevalent. Adolescents, as compared to adults, have been shown to display decreased sensitivity to many effects of ethanol, including effects that may serve as cues to moderate consumption. Consequently, reduction of these factors could facilitate drinking behaviors in adolescents, which may disrupt normal developmental processes. Chronic intermittent ethanol exposure (CIEE) to high doses of ethanol in rats has been shown to prevent normal developmental increases in sensitivity to ethanol-induced loss of righting reflex (LORR). However, it is unknown whether the same disruptions would occur following CIEE to more moderate and low alcohol doses. The present study was designed to evaluate the effects of CIEE in rats to several different doses during adolescence on ethanol-induced LORR in adulthood. Male rats were weighed and treated intraperitoneal with 1.0, 2.0, 3.0, or 4.0 g/kg ethanol or equivolume saline (equivalent to 4.0 g/kg dosings) every 48 hours for 20 days beginning on postnatal day (PN) 30. LORR was measured following each ethanol exposure. Finally, LORR was measured in both ethanol and saline-exposed animals following 4.0 g/kg ethanol challenge on PN 50 and following a 12-day withdrawal period (PN62). Duration of LORR remained unchanged throughout the adolescent exposure period. However, when LORR was measured on PN50 and PN62, 4.0 and 3.0 g/kg treatment groups displayed significantly less LORR compared to the free feeding and 1.0 g/kg ethanol treated groups. Animals displayed no tolerance development to LORR throughout the chronic exposure period even though moderate and high doses of ethanol were used. CIEE to high (3.0 or 4.0 g/kg) doses of ethanol disrupted the expected developmental increase in sensitivity to ethanol-induced LORR. These results may have implications for human adolescent drinkers. Specifically due to adolescents' relative resistance to the hypnotic effects of alcohol and their tendency to intake alcohol in an intermittent, or binge-like, manner such tolerance might lead to increases in alcohol abuse in this population of drinkers.     

Plasma testosterone in rats exposed to ethanol during vitamin E deficiency

The effects of short and long-term ethanol administration on plasma testosterone level were studied in rats with vitamin E deficiency. The animals underwent a vitamin E depletion period of 5 weeks followed by an acute dose of ethanol (1 g/kg body wt i.p.). Two hours after the ethanol dose, the plasma testosterone level had decreased both in a control group (-32%, nonsignificant) and in the vitamin E deficient group (-45%, P less than 0.05) as compared with saline-treated rats. The rats which had received an ethanol dose were then exposed to ethanol in the drinking water (10% w/v) for two weeks, after which the acute ethanol dose was repeated. One hour after this second acute dose of ethanol, the plasma testosterone showed a decrease of 24% (nonsignificant) in the control group and 50% (P less than 0.05) in the vitamin E deficient group compared with saline-treated rats. Two hours after the second acute dose of ethanol, the plasma testosterone level was significantly (P less than 0.05) down both in the control group and in the vitamin E deficient group (-41 and -54%, respectively). Thus, vitamin E deficiency strengthened the effect of acute ethanol treatment on plasma testosterone in rats. Long-term exposure to ethanol appeared to sensitize rats to acute doses of ethanol, as judged by the fall in plasma testosterone levels. The present results are in agreement with previous findings in vitro thus supporting the notion that free radicals arising during ethanol oxidation have an inhibitory effect on testosterone synthesis.