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1.
小菜蛾对阿维菌素B1抗药性选育及交互抗性 总被引：6，自引：0，他引：6
用阿维菌素B1（abamectin)对小菜蛾敏感种群在室内进行抗性品系选育。经过25代连续汰选，获得抗性种群Laba-R，与选育前比较，抗性提高100倍，La-ba-R种群在不接触任何药剂条件下饲养20代，抗性逐渐下降，很难恢复到选育前的敏感状态。抗性汰选前后分别测定10种药剂的剂量-死亡率毒力回归线，发现Laba-R抗性种群对乙酰甲胺磷、锐劲特、灭多威、敌敌畏不存在交互抗性；对溴氰菊酯、氯氰菊酯、杀虫双、巴丹和Bt的第三性略有下降，但无明显交互抗性。活性增效剂试验表明，增效醚（PBO）和磷酸三苯酯（TPP）对阿维菌素B1均有明显的增效作用，其中PBO的增效活性尤为显著，它能使对阿维菌素B1产生100多倍抗药性的小菜蛾完全恢复其敏感性，说明多功能氧化酶解毒代谢增强可能是小菜蛾对阿维菌素B1产生抗性的主导因素之一。 相似文献
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为了明确小菜蛾Plutella xylostella对唑虫酰胺的抗性特征,采用生物生化方法测定了江西省5个蔬菜产区小菜蛾田间种群对唑虫酰胺的抗性水平,并研究了小菜蛾唑虫酰胺抗性品系对其它药剂的交互抗性和生化抗性机制。结果显示,分宜县和高安市小菜蛾田间种群对唑虫酰胺尚未产生明显抗性,永丰县、德安县和余江县小菜蛾种群对唑虫酰胺产生了低水平的抗性,抗性倍数为5.20~8.20倍;小菜蛾唑虫酰胺抗性品系对阿维菌素、氯虫苯甲酰胺、氟虫双酰胺和茚虫威有中低水平的交互抗性,抗性倍数分别为11.72、3.44、2.77和2.20倍,而对溴虫腈、定虫隆和丁醚脲无交互抗性;增效剂磷酸三苯酯和胡椒基丁醚对小菜蛾唑虫酰胺抗性品系均有显著增效作用,增效倍数分别为3.42倍和2.64倍;唑虫酰胺抗性品系的酯酶和多功能氧化酶活性均显著提高,分别为敏感品系的2.18倍和1.64倍。研究表明,小菜蛾对唑虫酰胺产生抗性可能与酯酶和多功能氧化酶活性的升高有关。 相似文献
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小菜蛾对阿维菌素B_1抗药性选育及交互抗性 总被引：1，自引：0，他引：1
用阿维菌素B_1(abamectin)对小菜蛾敏感种群在室内进行抗性品系选育。经过25代连续汰选,获得抗性种群Laba-R,与选育前比较,抗性提高100倍。Laba-R种群在不接触任何药剂条件下饲养20代,抗性逐渐下降,很难恢复到选育前的敏感状态。抗性汰选前后分别测定10种药剂的剂量-死亡率毒力回归线,发现Laba-R抗性种群对乙酰甲胺磷、锐劲特、灭多威、敌敌畏不存在交互抗性;对溴氰菊酯、氯氰菊酯、杀虫双、巴丹和Bt的敏感性略有下降,但无明显交互抗性。活体增效剂试验表明,增效醚(PBO)和磷酸三苯酯(TPP)对阿维菌素B_1均有明显的增效作用,其中PBO的增效活性尤为显著,它能使对阿维菌素B_1产生100多倍抗药性的小菜蛾完全恢复其敏感性。说明多功能氧化酶解毒代谢增强可能是小菜蛾对阿维菌素B_1产生抗性的主导因素之一。 相似文献
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用丁烯氟虫腈对小菜蛾敏感品系在室内经7代次药剂汰选,获得了抗性品系(R),与敏感品系(S)比较其抗性指数为77.58倍。抗性汰选前后,采用点滴法测定的结果表明,小菜蛾对阿维菌素、毒死蜱、灭多威、杀虫单和高效氯氰菊酯的敏感性并无明显变化,其抗性指数为0.80~1.36,均不存在交互抗性。通过构建种群生命表,观察比较了小菜蛾抗丁烯氟虫腈品系和敏感品系的一系列生长发育和繁殖特征。结果表明,抗丁烯氟虫腈品系较敏感品系幼虫期和蛹历期延长,低龄幼虫龄期转换时的虫口死亡率增加,蛹重减轻,化蛹率和羽化率降低;在繁殖上表现为产卵量增加,而孵化率和雌雄比降低,雌成虫的数量、寿命减少。抗丁烯氟虫腈种群相对于敏感种群的相对适合度为0.84,抗性种群在繁殖能力上存在明显的生存劣势。 相似文献
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药剂对小菜蛾抗性及敏感品系乙酰胆碱酯酶抑制作用比较 总被引：5，自引：1，他引：4
采用浸叶法测定了云南通海、元谋和澜沧的小菜蛾plutella xylostella田间种群对常用杀虫剂的抗药性。结果表明,云南上述地区小菜蛾田间种群对各类杀虫剂均产生了不同程度的抗性。对有机磷类药剂的抗药性为1.74~31.1倍;对菊酯类药剂的抗药性为7.41~764倍;对阿维菌素类药剂则产生了 5.60~4.06×104倍的抗性。通过离体和活体试验测定了药剂对小菜蛾头部乙酰胆碱酯酶(AChE)的抑制作用。敌敌畏和灭多威对通海抗性品系AChE离体和活体内的抑制中浓度(I50)分别是敏感品系的209、26.5倍和2.21、2.16倍;敌敌畏对通海小菜蛾种群的离体和活体内抑制中时间(IT50)小于敏感品系,分别是敏感品系的0.32和0.17倍;而灭多威对通海小菜蛾种群的离体和活体内抑制中时间(IT50)则大于敏感品系,分别是敏感品系的1.37和1.74倍。 相似文献
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以田间菜蚜茧蜂为试虫,采用药膜法研究了增效剂胡椒基丁醚(PB)、磷酸三苯酯(TPP)和马来酸二乙酯(DEM)对6种杀虫剂的增效作用。结果表明,三种增效剂对6种杀虫剂均有显著增效作用,其大小依次为PB>DEM>TPP。PB对甲胺磷、阿维菌素、氟虫腈、氰戊菊酯、氯氰菊酯和吡虫啉的增效比达5.0～9.6倍。TPP和DEM对甲胺磷、DEM对氟虫腈的增效比达2.6～3.0倍,但TPP和DEM对阿维菌素、氰戊菊酯和氯氰菊酯、TPP对氟虫腈的增效比均在1.9倍以下。PB、TPP和DEM对吡虫啉的增效比分别高达9.6、6.8和8.2倍。体内抑制试验结果显示,PB、TPP和DEM对菜蚜茧蜂AChE活性无明显抑制作用,而PB和TPP对羧酸酯酶(CarE)、DEM对谷胱甘肽S转移酶(CST)活性有显著抑制作用。由此认为,菜蚜茧蜂对所用的6种杀虫剂的耐药性与多功能氧化酶(MFO)、CarE和GST的解毒作用有关。 相似文献
10.
棉铃虫抗辛硫磷品系的代谢抗性机理 总被引：1，自引：0，他引：1
通过重复回交和药剂选择,将棉铃虫Phoxim-R抗性品系对辛硫磷的抗性导入到BK77敏感品系中,得到棉铃虫BK77-R抗性品系,BK77-R和BK77为一对近等基因系。BK77-R抗性品系对辛硫磷的抗性达155倍,对溴氰菊酯有高水平交互抗性(抗性倍数248倍),对灭多威和硫丹有中等水平交互抗性, 分别为31倍和11倍,对丙溴磷有低水平交互抗性(4倍)。在BK77-R抗性品系中,脱叶磷(DEF,酯酶抑制剂)对辛硫磷、灭多威和硫丹具有增效作用,增效倍数分别为7倍、2倍 和1.9倍;增效醚(PBO,氧化酶抑制剂)对溴氰菊酯、灭多威和辛硫磷的增效倍数分别为21倍、2.2倍和1.7倍。与BK77敏感品系相比,BK77-R抗性品系的酯酶和多功能氧化酶活性均显著提高,而谷胱甘肽S-转移酶活性没有明显变化。上述结果表明,酯酶解毒代谢在棉铃虫BK77-R品系对辛硫磷的抗性中起重要作用,酯酶和多功能氧化酶解毒作用增强是该抗性品系对不同类型药剂产生交互抗性的重要原因。 相似文献
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杀虫剂亚致死剂量对小菜蛾羧酸酯酶的影响 总被引：11，自引：2，他引：11
就阿维菌素和高效氯氰菊酯亚致死剂量对小菜蛾Plutella xylostella Linneae羧酸酯酶(CarE)活性的影响进行了研究。用亚致死剂量的阿维菌素和高效氯氰菊酯分别处理阿维菌素敏感和抗性小菜蛾,使敏感品系CarE比活力上升,抗性品系CarE比活力下降。酶动力学研究表明,两种药剂亚致死剂量处理对小菜蛾CarE与底物α-NA亲和力的影响存在差异。在敏感品系中,阿维菌素和高效氯氰菊酯处理前后CarE的Km值无明显变化;抗性品系中,用阿维菌素亚致死剂量处理后,小菜蛾体内CarE的Km值显著高于对照,即其对α-NA的亲和力比对照组明显降低,高效氯氰菊酯处理组CarE的Km值与对照相比无明显变化。 相似文献
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小菜蛾对阿维菌素的抗性选育及交互抗性研究 总被引：2，自引：1，他引：2
用阿维菌素对小菜蛾进行室内抗性汰选,选择压为约杀死种群70％的剂量。连续施药7～8次即表现抗性趋势,汰选至11代,获得抗性指数为80.71的抗性种群(ABM-R)。ABM-R种群对所测试的有机磷杀虫剂乙酰甲胺磷、有机氯类的硫丹、沙蚕毒素类的杀螟丹、氨基甲酸酯类的灭多威、微生物杀虫剂Bt、磺胺脲类衍生物丁醚脲、芳基取代的吡咯杂环化合物虫螨腈和昆虫生长调节剂定虫隆、虫酰肼无交互抗性(R/S为0.73～1.19),而对苯基吡唑类氟虫腈的敏感性却有所上升(R/S为0.22)。增效剂试验显示,PB和唧对ABM-S种群无增效作用,而对ABM-R种群增效作用显著,增效比分别为24.57和13.61,表明多功能氧化酶和羧酸酯酶在抗性机制中可能起重要作用。 相似文献
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The genetic basis of abamectin resistance was studied in a strain of the diamondback moth, Plutella xylostella (L), following laboratory selection of a field population collected at Xuanhua, Hebei Province, China. Data from the testing of F1 progeny from reciprocal crosses between abamectin-resistant and abamectin-susceptible strains indicated that resistance might be autosomal and incompletely recessive with a degree of dominance of -0.13. Chi-squared analyses from the response of a backcross of crossed F1 progeny and the resistant strain and F2 progeny were highly significant, suggesting that the resistance was probably controlled by more than one gene. The results of cross-resistance studies showed that there was little cross-resistance between abamectin and four pyrethroid insecticides (deltamethrin, beta-cypermethrin, fenvalerate and bifenthrin) and no cross-resistance between abamectin and the acylureas chlorfluazuron or flufenoxuron. 相似文献
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First-instar Earias vittella (Fab.) larvae were selected with fenvalerate and cypermethrin for 15 successive generations in the laboratory at 28(± 1)°C. The insect developed 7.8-fold resistance to fenvalerate and no resistance to cypermethrin. The fenvalerate-selected strain developed 2800-fold and 1200-fold cross-resistance to endosulfan and carbaryl, respectively. This strain, however, did not manifest cross-resistance to the organophosphorus insecticides, quinalphos, fenitrothion, monocrotophos and malathion, or to the synthetic pyrethroid, cypermethrin. The cypermethrin-selected strain acquired 5-, 4-, and 3-fold cross-resistance to endosulfan, fenvalerate and carbaryl, respectively and no cross-resistance to the above organophosphorus insecticides. 相似文献
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Christiane N. Gouamene-LamineKyong Sup Yoon J. Marshall Clark 《Pesticide biochemistry and physiology》2003,76(1):15-23
As resistance to currently used insecticides increases in the Colorado potato beetle (CPB), Leptinotarsa decemlineata (Say), abamectin and its 4″-epi and 8,9-oxide analogs may serve as likely replacements if proven effective. We previously selected an abamectin-resistant strain of CPB (AB-F) that is suitable for the determination of cross-resistance to these two bioactive avermectin analogs. Using bioassay and logit analysis, the present work shows that, on average and following normalization by weight, the larval stages of the insecticide-susceptible SS strain are equally sensitive to the toxic action of abamectin and its 4″-epi and 8,9-oxide analogs, indicating that all three compounds retain high bioactivity towards the susceptible larval stages. Abamectin and the two analogs also are similar in toxicity to the larval stages of the AB-F strain. However, the AB-F larval stages are significantly less sensitive on average to these insecticides than the SS larval stages, indicating resistance to abamectin and cross-resistance to both the two analogs tested. Likewise, adults of the AB-F strain are significantly less sensitive to the toxic action of abamectin and the two analogs compared to SS adults, also indicative of resistance and cross-resistance. Abamectin is significantly more toxic, however, to both SS and AB-F adults, respectively, than either of the two analogs. The reduction in sensitivity was particularly evident in SS adults to both the 4″-epi and 8,9-oxide analogs. Additionally, adults of the SS strain are significantly less sensitive to the toxic action of abamectin and the two analogs when compared to SS larval stages. There is no significant differences, however, in the toxicity of these three insecticides, respectively, between larval and adults stages of the AB-F strain. This phenomenon results in lower resistance ratio (RR) values calculated for the two avermectin analogs compared to those calculated for abamectin regardless of the insect stage examined but is particularly evident and significant in the adult stage. This relative decrease in resistance levels is primarily associated with SS adults that are less sensitive to the toxic action of these insecticides. The decrease in abamectin toxicity is apparently due to significantly increased levels of P450 associated with SS adults versus forth instars and to similar levels in adults of the SS and AB-F strains. Because abamectin resistance in CPB is due in large part to enhanced oxidative metabolism of abamectin, it is likely that the SS adults are more tolerant to abamectin due to an enhanced level of oxidative detoxification. Finally, neither abamectin nor the two analogs are structurally protected at the specific molecular locations, C3″, C24, and C26 carbons, which leads to enhanced oxidative metabolism, resistance and cross-resistance. Structurally-protected avermectin analogs at these vulnerable intramolecular sites are likely to be more effective insecticides in suppressing the development of oxidative detoxification-based resistance to abamectin, as would the use of oxidative synergists. 相似文献
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Synergism by Propynyl Aryl Ethers in Permethrin-Resistant Tobacco Budworm Larvae,Heliothis virescens
Synergists were used to diagnose possible mechanisms of permethrin resistance in permethrin-selected strains of the tobacco budworm, Heliothis virescens (F.). In addition to permethrin, these strains of the tobacco budworm were resistant to α-cyano-pyrethroid insecticides, organophosphorus insecticides and DDT. The monooxygenase-inhibiting prop-2-ynyl aryl ethers were the only effective synergists of permethrin among 16 candidates tested. The most effective synergist was 1,2,4-trichloro-3-(2-propynyloxy)benzene. Piperonyl butoxide, a common monooxygenase-inhibiting synergist in other species and tobacco budworm strains, was inactive. These results suggested the presence and contribution of an unusual monooxygenase in the enzymatic detoxication of permethrin. DDT cross-resistance, which was not synergized, and broad pyrethroid cross-resistance supported previous evidence for target site insensitivity as a second pyrethroid-resistance mechanism in these strains. The actions of S,S,S-tributyl phosphorotrithioate (TBPT) and triphenyl phosphate (TPP) suggested that hydrolytic detoxication, important in methyl parathion-resistance tobacco budworm strains, had little or no role in conferring pyrethroid resistance in these strains. 相似文献
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Lu Qian 《Pesticide biochemistry and physiology》2008,91(3):175-179
Experiments have been carried out to confirm the cross-resistance between abamectin and tebufenozide in Plutella xylostella and demonstrate its mechanism. The results showed that the resistant strain of P. xylostella selected by tebufenozide (RF 99.38) really showed high cross-resistance to abamectin (RF 29.25). When this strain was subjected to resistance decaying treatment, breeding without contacting any insecticides, and abamectin resistance selection for 20 generations, the former resulted in decrease of its resistance to both tebufenozide and abamectin to about one third of the original (RF 35.03 and 11.67, respectively), and the later enhanced its resistance to abamectin dramatically (RF 303.77), but not to tebufenozide(RF 50.04). PBO showed high synergism to abamectin (SR 2.11-12.23), and the synergism ratio positively related to the resistance level among different strains. Enzyme analysis also proved that the activity of cytochrome P450 monooxygenase (MFO) was notable enhanced in the strains resistant to both tebufenozide and abamectin (1.71- to 3.01-fold). Based on discussion, it was concluded that tebufenozide selection could resulted in significant cross-resistance of P. xylostella to abamectin. The major mechanism for the cross-resistance should be the enhancement of MFO activity. For resistance management, tebufenozide and abamectin would not recommend for rotational use. 相似文献
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The activities of the acylurea insect growth regulators, chlorfluazuron, teflubenzuron and difubenzuron, and the neurotoxic macrocyclic lactone, abamectin were assessed against a laboratory susceptible (FS) strain and a field (Cameron Highlands, Malaysia (CH)) strain of the diamondback moth, Plutella xylostella L. using a leaf-dip bioassay at 20°C. The time taken to achieve end-point mortality was found to vary considerably (9–17 days), being fastest with abamectin against the FS strain and slowest with difubenzuron against the CH strain. The order of activity (LC50 at F6/7) against second-instar larvae of both strains was: abamectin > chlorfluazuron = teflubenzuron ? difubenzuron. Subsequent assays (F14) with the acylureas, flufenoxuron and hexaflumuron against the FS strain suggested that the former was slightly more active than chlorfluazuron or teflubenzuron, the latter slightly less active. The CH population was found to be 12.6-, 6.7-, 6.4- and 2.3-fold less sensitive to difubenzuron, teflubenzuron, chlorfluazuron and abamectin respectively than the FS strain. Selection of sub-populations of the CH strain with chlorfluazuron (CHL-SEL) and teflubenzuron (TEF-SEL) for six generations (F6-11), resulted in LC50 resistance ratios of 109- and 315-fold respectively when compared with the FS strain, equivalent to an 18- and a 46-fold increase in resistance compared with the unselected CH strain. Marked cross-resistance was also demonstrated between chlorfluazuron and teflubenzuron in both sub-populations. However, there was no evidence of cross-resistance to dijlubenzuron and abamectin and little or no cross-resistance to flufenoxuron and hexaflumuron. Resistance to chlorfluazuron and teflubenzuron appeared to be relatively unstable in the TEF-SEL compared with the CHL-SEL sub-population (over 6–9 generations). However, reselection of the TEF-SEL population with chlorfluazuron (F18–20) led to a very rapid increase in resistance to chlorfluazuron and particularly teflubenzuron. For the latter compound, resistance factors of about 1000000 were obtained (F19, 21). Such values are probably only semi-quantitative, as above a certain level of resistance feeding bioassays with acylureas (compounds which are active to a significant extent by ingestion) are likely to become rate-limiting. 相似文献
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A housefly strain, originally collected in 1998 from a dump in Beijing, was selected with beta-cypermethrin to generate a resistant strain (CRR) in order to characterize the resistance and identify the possible mechanisms involved in the pyrethroid resistance. The resistance was increased from 2.56- to 4419.07-fold in the CRR strain after 25 consecutive generations of selection compared to a laboratory susceptible strain (CSS). The CRR strain also developed different levels of cross-resistance to various insecticides within and outside the pyrethroid group such as abamectin. Synergists, piperonyl butoxide (PBO) and S,S,S-tributyl phosphorotrithioate (DEF), increased beta-cypermethrin toxicity 21.88- and 364.29-fold in the CRR strain as compared to 15.33- and 2.35-fold in the CSS strain, respectively. Results of biochemical assays revealed that carboxylesterase activities and maximal velocities to five naphthyl-substituted substrates in the CRR strain were significantly higher than that in the CSS strain, however, there was no significant difference in glutathione S-transferase activity and the level of total cytochrome P450 between the CRR and CSS strains. Therefore, our studies suggested that carboxylesterase play an important role in beta-cypermethrin resistance in the CRR strain. 相似文献