啶虫脒对淡色库蚊幼虫的致死和亚致死影响

啶虫脒是日本曹达公司新开发的一种氯代烟碱类杀虫剂,为了探讨其用于蚊虫幼虫控制的可能性,我们在室内用浸渍法测定了啶虫脒对淡色库蚊幼虫的致死和亚致死影响,结果表明,淡色库蚊幼虫对啶虫脒较敏感,幼虫的死亡高峰出现在处理后第3天,幼虫的四个龄期中,一龄最敏感,四龄耐药力最强,二在处理后72h时的LC50值分别为0.020mg/L/升和0.296mg/L。幼虫在亚致死浓度的啶虫脒溶液作用下,发育期延长,蛹重下降。说明啶虫脒可用于蚊虫幼虫的控制。     

应用微核试验和单细胞凝胶电泳技术来检测农药对青蛙蝌蚪及成体的遗传毒性

应用青蛙红细胞微核试验和单细胞凝胶电泳试验研究了两种新型杀虫剂 -吡虫啉和抑食肼对青蛙蝌蚪和成体的遗传毒性 ,结果表明 :当吡虫啉为 2mg/L时 ,蝌蚪红细胞微核率与对照组相比 ,无显著性差异 (p >0 .0 5) ;浓度升高到 8mg/L时 ,微核率与对照组相比 ,有显著性差异 (p <0 .0 5) ;当浓度为 3 2mg/L时 ,微核率与对照组相比 ,有极显著性差异 (p <0 .0 1) ;并有明显的剂量 -效应关系 (r =0 .9843 )。而抑食肼在浓度为 2 .5mg/L和 10mg/L时 ,微核率与对照组相比 ,无显著性差异 (p >0 .0 5) ;当浓度增至 40mg/L时 ,微核与对照组相比 ,有极显著性差异 (p <0 .0 1) ;吡虫啉与抑食肼各浓度组对青蛙红细胞的DNA损伤与阴性对照组相比 ,都有极显著性差异 (p <0 .0 1) ,且具有明显的剂量 -效应关系 (r =0 .960 ,r=0 .990 )。     

棉蚜啶虫脒抗性种群交互抗性和增效剂增效作用的研究

【目的】明确棉蚜Aphis gossypii Glover啶虫脒抗性品系与其它杀虫剂的交互抗性现状以及增效剂的增效作用,为延缓和治理棉蚜对啶虫脒的抗性提供依据。【方法】采用单头反选育和群体汰选的方式,获得了棉蚜啶虫脒敏感和抗性品系;采用叶片药膜法测定了13种杀虫剂对啶虫脒的交互抗性以及增效剂对啶虫脒的增效作用。【结果】经过室内棉蚜敏感和抗性品系的筛选,获得了相对抗性倍数为82.33倍的棉蚜啶虫脒抗性品系。棉蚜啶虫脒抗性品系的交互抗性谱的研究表明,交互抗性倍数小于5的药剂为:吡蚜酮,甲基阿维菌素;交互抗性倍数在5~10倍的药剂为:噻虫嗪,联苯菊酯,毒死蜱,马拉硫磷,丙溴磷,辛硫磷;交互抗性倍数在10~15倍的药剂为:硫丹,阿维菌素,高效氯氰菊酯,三唑磷,氧化乐果;交互抗性倍数大于1 5倍的药剂为:吡虫啉。增效剂实验表明,TPP和PBO在啶虫脒敏感品系中增效作用不明显,但在抗性品系中增效作用显著。在啶虫脒抗性品系中的增效比为1.77、1.61,在啶虫脒敏感品系中的增效比为1.02、1.03。DEM在啶虫脒抗性、敏感品系中的增效作用均不明显,增效比为1.04、1.02。TPP和PBO对啶虫脒有很好的增效作用。以室内棉蚜敏感品系(LC_(50)为0.180 mg/L)为基础,对新疆各主要棉区的棉蚜种群进行了啶虫脒药剂的抗性调查,结果表明新疆各主要棉区棉蚜对啶虫脒的相对抗性倍数为6.1~22.0倍。【结论】由此说明新疆主要棉区棉蚜对啶虫脒具有一定的抗性风险,生产中可以利用无交互抗性的吡蚜酮和甲基阿维菌素来治理抗性棉蚜种群。     

联苯菊酯和啶虫脒对苹果黄蚜的区分剂量研究

【目的】为了快速简便地明确苹果黄蚜Aphis citricola对常用药剂的敏感性,研究了联苯菊酯和啶虫脒对苹果黄蚜的区分剂量。【方法】在诊断剂量法的基础上进行了改进,采用玻璃管药膜法进行了研究,并进行了重现性和田间试验验证。【结果】联苯菊酯和啶虫脒的区分剂量分别为0.021μg/cm2和0.003μg/cm2,联苯菊酯和啶虫脒玻璃管药膜在4℃下,最长均可保存20 d,其毒力效果不变。【结论】研究得出的区分剂量具有较好的重现性,可用于快速检测苹果黄蚜对联苯菊酯和啶虫脒的敏感性。     

高效氯氰菊酯和啶虫脒对螟黄赤眼蜂繁殖的亚致死效应

螟黄赤眼蜂 Trichogramma chilonis是害虫生物防治中一种重要的卵寄生蜂,其在防治害虫的同时,也会受到田间杀虫剂的影响。本研究选择高效氯氰菊酯和啶虫脒亚致死剂量,以两性生命表法计算种群参数,揭示了这两种药剂亚致死剂量对该种群生长、繁殖的影响。试验测定了高效氯氰菊酯和啶虫脒对螟黄赤眼蜂的亚致死剂量LC20值分别为0.119和1.091 mg/L。研究结果显示,经亚致死浓度LC20的啶虫脒处理后,螟黄赤眼蜂的寄生卵量显著低于对照（P<0.05）,寿命(1.17 d)显著缩短,种群参数（内禀增长率 rm、周限增长率λ、净生殖力R0和世代平均历期T）均低于对照,其中净生殖力R0（27.573）显著低于对照（P<0.05）。经亚致死剂量LC20的高效氯氰菊酯处理后,螟黄赤眼蜂的单雌产卵量显著高于对照(P<0.05)。试验结果表明高效氯氰菊酯的亚致死剂量对螟黄赤眼蜂的增殖有一定的刺激作用,而亚致死剂量的啶虫脒则会影响螟黄赤眼蜂的寄生能力,在螟黄赤眼蜂盛发期,田间施用啶虫脒时,应注意其残留量对螟黄赤眼蜂的影响。     

啶虫脒对西方蜜蜂蜂王培育质量的影响

【目的】本实验旨在研究王台中残留啶虫脒对西方蜜蜂Apis mellifera蜂王培育质量的影响。【方法】通过融化蜂蜡并添加啶虫脒药液制作王台,使各王台中分别含4个不同剂量的啶虫脒(0, 10, 100和1 000 μg/kg蜂蜡)。同时,控制蜂王产卵6 h, 3 d后,将孵化为1日龄的幼虫分别移入各组王台中,并放入蜂群哺育。移虫后第3和6天分别统计各组王台中幼虫的接受率和封盖率,待蜂王出房时,计算其出房率,测定蜂王个体初生重、胸重和胸宽指标;采用实时荧光定量PCR(qPCR)技术测定蜂王卵巢中卵黄原蛋白基因(Vg)、储存蛋白基因(hex110和hex70b)的相对表达量。【结果】100 μg/kg蜂蜡和1 000μg/kg蜂蜡这两个啶虫脒剂量组西方蜜蜂蜂王的出房率都显著低于0 μg/kg蜂蜡和10 μg/kg蜂蜡剂量组,而0 μg/kg蜂蜡与10 μg/kg蜂蜡剂量组之间及100 μg/kg蜂蜡与1 000 μg/kg蜂蜡剂量组之间出房率 均差异不显著;这4个剂量组的王台幼虫接受率和封盖率以及蜂王的初生重、胸重和胸宽均无显著差异。qPCR结果显示,Vg基因的相对表达量随啶虫脒浓度的增加而下降,其中,1 000 μg/kg蜂蜡剂量组Vg基因的相对表达量显著低于10 μg/kg蜂蜡剂量组和0 μg/kg蜂蜡剂量组,其余各剂量组之间差异不显著;这4个剂量组之间hex110和hex70b基因的表达量差异不显著。【结论】西方蜜蜂王台中啶虫脒残留超过100 μg/kg蜂蜡剂量时,会对蜂王培育产生不利影响。     

苯酚和对苯二酚对鲫血细胞DNA损伤的研究

酚类可通过水产动物皮肤、鳃吸入或摄入肠道引起肌肉异味;挥发酚对鱼类有一定的急性毒性1 ,这必然会引起人们对食品安全的担忧。       

高温和啶虫脒处理西花蓟马对其F1 代生命表参数的联合作用

【目的】西花蓟马 Frankliniella occidentalis (Pergande) (缨翅目: 蓟马科）是一种危险的入侵害虫,其生长发育受温度影响显著。我们的前期研究表明,高温热激对西花蓟马的杀灭效果并不理想,但高温热激可以改变西花蓟马的药剂敏感性。为了探究高温热激后再进行杀虫剂减量处理能否提高高温对西花蓟马的防治效果,本实验测定了45℃高温热激 2 h后恢复不同时间（8 h 和24 h）啶虫脒对西花蓟马F₁代生命表参数的影响,从控制种群发展的角度探究高温和啶虫脒防治西花蓟马最佳结合方式。【方法】应用特定年龄 龄期及两性生命表的方法,研究45℃高温热激和啶虫脒处理西花蓟马后其F₁代种群的生命表参数。【结果】45℃热激2 h后恢复不同时间用啶虫脒处理西花蓟马亲代,其F₁代卵、1龄幼虫和蛹的平均发育历期均显著长于对照（仅45℃热激2 h）的西花蓟马F₁代（P<0.01）;而且其F₁代雌成虫的寿命和产卵量均显著少于对照（P<0.01）。热激恢复8 h后啶虫脒处理西花蓟马亲代,其F₁代发育历期和雌成虫的寿命虽然与热激恢复24 h的F₁代不存在显著性差异,但是其F₁代的平均产卵前期（adult pre-oviposition period, APOP）和平均总产卵前期（total pre-oviposition period, TPOP）显著长于恢复24 h的F₁代（P<0.01）,单雌平均产卵量显著小于恢复24 h的F₁代（P<0.01）。【结论】相比单一高温防治,高温和杀虫剂综合使用对西花蓟马有更好的防控效果。相比热激后恢复24 h,热激后恢复8 h再进行杀虫剂处理对西花蓟马有更好的防控效果。     

喷雾方式及喷液量对吡蚜酮和啶虫脒在棉田的沉积分布及棉蚜防治效果的影响

为探明防治棉田棉蚜Aphis gossypii (Glover)的最佳喷雾方式及喷液量, 提高棉田的农药利用率, 作者于2011-2012年在山东省棉花苗期和成株期分别使用背负式手动喷雾器和背负式机动弥雾机以常规大容量和低容量喷雾, 比较杀虫剂25%吡蚜酮可湿性粉剂和3%啶虫脒乳油的喷雾雾滴在棉花田的沉积分布及棉蚜防治效果。结果表明： 在棉花苗期, 3%啶虫脒乳油用量450 mL/ha时, 使用机动弥雾机以75, 150和225 L/ha喷液量喷雾, 药剂在地面的流失率分别为24.4%, 28.9%和26.7%; 使用手动喷雾器以300, 450和600 L/ha喷液量喷雾, 杀虫剂在地面的流失率分别为35.6%, 37.8%和46.7%; 啶虫脒不同喷雾处理对棉蚜的防效无显著性差异（P>0.05）。在棉花成株期, 25%吡蚜酮可湿性粉剂用量为300 g/ha时, 使用手动喷雾器以600 L/ha喷液量喷雾, 药剂地面流失率为13.3%; 使用机动弥雾机以喷液量150 L/ha喷雾时, 药剂地面流失率为3.3%; 25%吡蚜酮可湿性粉剂用量减少至225 g/ha, 使用机动弥雾机以喷液量150和300 L/ha喷雾, 对棉蚜的防效与吡蚜酮用量300 g/ha、 使用手动喷雾器在喷液量600 L/ha条件下喷雾相比没有显著差异（P>0.05）。使用机动弥雾机喷雾可以减少田间用药量和喷液量, 降低药液的流失率, 减轻对环境的污染。     

贺氏菱头蛛和食虫沟瘤蛛对稻纵卷叶螟和稻褐飞虱的捕食作用研究

应用二次正交旋转组合设计方法建立贺氏菱头蛛Bianor hotingchiehi和食虫沟瘤蛛Ummeliata insecticeps对稻纵卷叶螟Cnaphalocrocis medinalis和稻褐飞虱Nilaparvata lugens捕食作用的数学模型分别为:Y'cm=3.9984-0.2083 x1 0.7917 x2 2.1250 x3 0.2917 x4 0.5625 x1x2-0.1875 x1x3 0.1875 x1x4 0.8125 x2x3 0.1875 x2x4 0.1875 x3x4-0.4703 x21 0.0305 x22 0.0305 x23-0.0940 x24;Y'nl=6.2832 0.2917 x1 0.5417 x2-0.1250 x3 3.625 x4-0.0625 x1x2 0.5625 x1x3 0.4375 x1x4-0.4375 x2x3 0.4375 x2x4-0.4375 x3x4-0.2299 x21-0.1047 x22 0.0250 x23 0.2709 x24 .结果表明,食虫沟瘤蛛是稻纵卷叶螟和稻褐飞虱的更为重要的捕食性天敌.贺氏菱头蛛对各种干扰作用表现更为敏感.     

DNA damage and nitric oxide synthesis in experimentally infected Balb/c mice with Trypanosoma cruzi

This study aimed to evaluate whether experimental Chagas disease in acute phase under benznidazole therapy can cause DNA damage in peripheral blood, liver, heart, and spleen cells or induce nitric oxide synthesis in spleen cells. Twenty Balb/c mice were distributed into four groups: control (non-infected animals); Trypanosoma cruzi infected; T. cruzi infected and submitted to benznidazole therapy; and only treated with benznidazole. The results obtained with the single cell gel (comet) assay showed that T. cruzi was able induce DNA damage in heart cells of both benznidazole treated or untreated infected mice. Similarly, T. cruzi infected animals showed an increase of DNA lesions in spleen cells. Regarding nitric oxide synthesis, statistically significant differences (p<0.05) were observed in all experimental groups compared to negative control, the strongest effect observed in the T. cruzi infected group. Taken together, these results indicate that T. cruzi may increase the level of DNA damage in mice heart and spleen cells. Probably, nitric oxide plays an important role in DNA damaging whereas benznidazole was able to minimize induced T. cruzi genotoxic effects in spleen cells.     

Trimetazidine protects low-density lipoproteins from oxidation and cultured cells exposed to H2O2 from DNA damage

Trimetazidine is a well-established anti-ischemic drug, which has been used for long time in the treatment of pathological conditions related with the generation of reactive oxygen species. However, although extensively studied, its molecular mode of action remains largely unknown. In the present study, the ability of trimetazidine to protect low-density lipoproteins (LDL) from oxidation and cultured cells from H₂O₂-induced DNA damage was investigated. Trimetazidine, tested at concentrations 0.02 to 2.20 mM, was shown to offer significant protection to LDL exposed to three different oxidizing systems, namely copper, Fe/ascorbate, and met-myoglobin/H₂O₂. The oxidizability of LDL was estimated by measuring, (i) the lag period, (ii) the maximal rate of conjugated diene formation, (iii) the total amount of conjugated dienes formed, (iv) the electrophoretic migration of LDL protein in agarose gels (REM), and (v) the inactivation of the enzyme PAF-acetylhydrolase present in LDL. In addition, the presence of trimetazidine decreased considerably the DNA damage in H₂O₂-exposed Jurkat cells in culture. H₂O₂ was continuously generated by the action of glucose oxidase at a rate of 11.8 ± 1.5 μM per min (60 ng enzyme per 100 μl), and DNA damage was assessed by the single cell gel electrophoresis assay (also called comet assay). The protection offered by trimetazidine in this system (about 30% at best) was transient, indicating modification of this agent during its action. These results indicate that trimetazidine can modulate the action of oxidizing agents in different systems. Although its mode of action is not clarified, the possibility that it acts as a lipid barrier permeable transition metal chelator is considered.     

Protection by tropolones against H2O2-induced DNA damage and apoptosis in cultured Jurkat cells

Tropolones, the naturally occurring compounds responsible for the durability of heartwood of several cupressaceous trees, have been shown to possess both metal chelating and antioxidant properties. However, little is known about the ability of tropolone and its derivatives to protect cultured cells from oxidative stress-mediated damage. In this study, the effect of tropolones on hydrogen peroxide-induced DNA damage and apoptosis was investigated in cultured Jurkat cells. Tropolone, added to the cells 15 min before the addition of glucose oxidase, provided a dose dependent protection against hydrogen peroxide induced DNA damage. The IC₅₀ value observed was about 15 μM for tropolone. Similar dose dependent protection was also observed with three other tropolone derivatives such as trimethylcolchicinic acid, purpurogallin and β-thujaplicin (the IC₅₀ values were 34, 70 and 74 μM, respectively), but not with colchicine and tetramethyl purpurogallin ester. Hydrogen peroxide-induced apoptosis was also inhibited by tropolone. However, in the absence of exogenous H₂O₂ but in the presence of non-toxic concentrations of exogenous iron (100 μM Fe³⁺), tropolone dramatically increased the formation of single strand breaks at molar ratios of tropolone to iron lower than 3 to 1, while, when the ratio increased over 3, no toxicity was observed. In conclusion, the results presented in this study indicate that the protection offered by tropolone against hydrogen peroxide-induced DNA damage and apoptosis was due to formation of a redox-inactive iron complex, while its enhancement of iron-mediated DNA damage at ratios of [tropolone]/[Fe³⁺] lower than 3, was due to formation of a lipophilic iron complex which facilitates iron transport through cell membrane in a redox-active form.     

Trimetazidine protects low-density lipoproteins from oxidation and cultured cells exposed to H(2)O(2) from DNA damage

Trimetazidine is a well-established anti-ischemic drug, which has been used for long time in the treatment of pathological conditions related with the generation of reactive oxygen species. However, although extensively studied, its molecular mode of action remains largely unknown. In the present study, the ability of trimetazidine to protect low-density lipoproteins (LDL) from oxidation and cultured cells from H₂O₂-induced DNA damage was investigated. Trimetazidine, tested at concentrations 0.02 to 2.20 mM, was shown to offer significant protection to LDL exposed to three different oxidizing systems, namely copper, Fe/ascorbate, and met-myoglobin/H₂O₂. The oxidizability of LDL was estimated by measuring, (i) the lag period, (ii) the maximal rate of conjugated diene formation, (iii) the total amount of conjugated dienes formed, (iv) the electrophoretic migration of LDL protein in agarose gels (REM), and (v) the inactivation of the enzyme PAF-acetylhydrolase present in LDL. In addition, the presence of trimetazidine decreased considerably the DNA damage in H₂O₂-exposed Jurkat cells in culture. H₂O₂ was continuously generated by the action of glucose oxidase at a rate of 11.8 ± 1.5 μM per min (60 ng enzyme per 100 μl), and DNA damage was assessed by the single cell gel electrophoresis assay (also called comet assay). The protection offered by trimetazidine in this system (about 30% at best) was transient, indicating modification of this agent during its action. These results indicate that trimetazidine can modulate the action of oxidizing agents in different systems. Although its mode of action is not clarified, the possibility that it acts as a lipid barrier permeable transition metal chelator is considered.     

DNA damage and integrity of UV-induced DNA repair in lymphocytes of smokers analysed by the comet assay

DNA damage was assessed in smoker lymphocytes by subjecting them to the single cell gel electrophoresis (SCGE) assay. In addition to the appearance of comet tails, smoker cells exhibited enlarged nuclei when analysed by the comet assay. On comparing basal DNA damage among smokers and a non-smoking control group, smoker lymphocytes showed higher basal DNA damage (smokers, 36.25±8.45 μm; non-smokers, 21.6±2.06 μm). A significant difference in DNA migration lengths was observed between the two groups at 10 min after UV exposure (smokers, 65.5±20.34 μm; non-smokers, 79.2±11.59 μm), but no significant differences were seen at 30 min after UV exposure (smokers, 21.13±10.73 μm; non-smokers, (27.2±4.13 μm). The study thus implies that cigarette smoking perhaps interferes with the incision steps of the nucleotide excision repair (NER) process. There appeared be no correlation between the frequency of smoking and DNA damage or the capacity of the cells to repair UV-induced DNA damage that suggests inherited host factors may be responsible for the inter-individual differences in DNA repair capacities. The study also suggests monitoring NER following UV insult using the SCGE assay is a sensitive and simple method to assess DNA damage and integrity of DNA repair in human cells exposed to chemical mutagens.     

氯化钇和氯化镨引起的人淋巴细胞DNA分子损伤的研究

用单细胞凝胶电泳法检测了稀土化合物氯化钇和氯化镨对人外周血淋巴细胞的ＤＮＡ损伤效应。结果表明,与对照相比,３种不同浓度的氯化钇和氯化镨均可引起淋巴细胞ＤＮＡ受损后ＤＮＡ迁移率的显著升高,受损伤细胞的百分率与对照差异明显,提示氯化钇和氯化镨具有一定的遗传毒性。     

Assessment of oxidative DNA damage formation by organic complex mixtures from airborne particles PM10

The free radical generating activity of airborne particulate matter (PM₁₀) has been proposed as a primary mechanism in biological activity of ambient air pollution. In an effort to determine the impact of the complex mixtures of extractable organic matter (EOM) from airborne particles on oxidative damage to DNA, the level of 8-oxo-2′-deoxyguanosine (8-oxodG), the most prevalent and stable oxidative lesion, was measured in the human metabolically competent cell line Hep G2. Cultured cells were exposed to equivalent EOM concentrations (5–150 μg/ml) and oxidative DNA damage was analyzed using a modified single cell gel electrophoresis (SCGE), which involves the incubation of whole cell DNA with repair specific DNA endonuclease, which cleaves oxidized DNA at the sites of 8-oxodG. EOMs were extracted from PM₁₀ collected daily (24 h intervals) in three European cities: Prague (Czech Republic, two monitoring sites, Libuš and Smíchov), Košice (Slovak Republic) and Sofia (Bulgaria) during 3-month sampling periods in the winter and summer seasons. No substantial time- and dose-dependent increase of oxidative DNA lesions was detected in EOM-treated cells with the exception of the EOM collected at the monitoring site Košice, summer sampling. In this case, 2 h cell exposure to EOM resulted in a slight but significant increase of oxidative DNA damage at three from total of six concentrations. The mean 8-oxodG values at these concentrations ranged from 15.3 to 26.1 per 10⁶ nucleotides with a value 3.5 per 10⁶ nucleotides in untreated cells. B[a]P, the positive control, induced a variable but insignificant increase of oxidative DNA damage in Hep G2 cell (approximately 1.6-fold increase over control value).Based on these data we believe that EOM samples extracted from airborne particle PM₁₀ play probably only a marginal role in oxidative stress generation and oxidative lesion formation to DNA. However, adsorbed organic compounds can undergo various interactions (additive or synergistic) with other PM components or physical factors (UV-A radiation) and in this way they might enhance/multiply the adverse health effects of air pollution.     

Evaluation of DNA damage and mutagenicity induced by lead in tobacco plants

Tobacco (Nicotiana tabacum L. var. xanthi) seedlings were treated with aqueous solutions of lead nitrate (Pb²⁺) at concentrations ranging from 0.4 mM to 2.4 mM for 24 h and from 25 μM to 200 μM for 7 days. The DNA damage measured by the comet assay was high in the root nuclei, but in the leaf nuclei a slight but significant increase in DNA damage could be demonstrated only after a 7-day treatment with 200 μM Pb²⁺. In tobacco plants growing for 6 weeks in soil polluted with Pb²⁺ severe toxic effects, expressed by the decrease in leaf area, and a slight but significant increase in DNA damage were observed. The tobacco plants with increased levels of DNA damage were severely injured and showed stunted growth, distorted leaves and brown root tips. The frequency of somatic mutations in tobacco plants growing in the Pb²⁺-polluted soil did not significantly increase. Analytical studies by inductively coupled plasma optical emission spectrometry demonstrate that after a 24-h treatment of tobacco with 2.4 mM Pb²⁺, the accumulation of the heavy metal is 40-fold higher in the roots than in the above-ground biomass. Low Pb²⁺ accumulation in the above-ground parts may explain the lower levels or the absence of Pb²⁺-induced DNA damage in leaves.