Spinosad resistance in female Musca domestica L. from a field-derived population

BACKGROUND: Bait-formulated spinosad is currently being introduced for housefly (Musca domestica L.) control around the world. Spinosad resistance was evaluated in a multiresistant field population and strains derived from this by selection with insecticides. Constitutive and spinosad-induced expression levels of three cytochrome P450 genes, CYP6A1, CYP6D1 and CYP6D3, previously reported to be involved in insecticide resistance, were examined. RESULTS: In 2004 a baseline for spinosad toxicity of Danish houseflies where all field populations were considered to be susceptible was established. In the present study, females of a multiresistant field population 791a were, however, 27-fold spinosad resistant at LC₅₀, whereas 791a male houseflies were susceptible. Strain 791a was selected with spinosad, thiamethoxam, fipronil and imidacloprid, resulting in four strains with individual characteristics. Selection of 791a with spinosad did not alter spinosad resistance in either males or females, but counterselected against resistance to the insecticides thiamethoxam and imidacloprid targeting nicotinic acetylcholine receptors. A synergist study with piperonyl butoxide, as well as gene expression studies of CYP6A1, CYP6D1 and CYP6D3, indicated a partial involvement of cytochrome P450 genes in spinosad resistance. CONCLUSION: This study reports female-linked spinosad resistance in Danish houseflies. Negative cross-resistance was observed between spinosad and neonicotinoids in one multiresistant housefly strain. Spinosad resistance involved alterations of cytochrome P450 gene expression. Copyright © 2011 Society of Chemical Industry     

新疆北疆马铃薯甲虫成虫对新烟碱类杀虫剂的敏感性变化

采用点滴法于2009和2010年监测了新疆维吾尔自治区北疆马铃薯甲虫Leptinotarsa decemlineata 9个田间种群成虫对新烟碱类杀虫剂吡虫啉、啶虫脒、噻虫嗪和噻虫啉的敏感性变化,发现其对吡虫啉和噻虫嗪的敏感性逐年降低。2009年监测的6个种群中有3个对啶虫脒和噻虫嗪低抗(抗性倍数5.0~10.0);2010年监测的6个种群全部对噻虫嗪产生了抗性,其中中抗(抗性倍数10.1~40.0)和低抗种群各3个。噻虫嗪与高效氯氟氰菊酯可能存在交互抗性。     

烟粉虱细胞色素CYP6EM1基因的克隆及对吡虫啉抗性的作用

烟粉虱是一种世界性农业害虫,其防治手段以化学防治为主,新烟碱类杀虫剂吡虫啉常年用于防治烟粉虱,田间烟粉虱已经形成严重的抗药性。本研究通过分析烟粉虱吡虫啉抗性和敏感种群,发现细胞色素CYP6EM1基因在吡虫啉抗性品系中上调了4.7倍,进而克隆了其全长基因,进行了荧光定量PCR分析,发现该基因在吡虫啉抗性烟粉虱3龄若虫期和雄虫成虫期过量表达,并且在抗性成虫胸部和腹部过量表达。最后通过RNA干扰的方法使成虫的CYP6EM1基因表达量下降了54.8%,之后发现当烟粉虱暴露于吡虫啉时死亡率显著升高了39.65%,这表明CYP6EM1与烟粉虱对吡虫啉抗性的形成相关。研究结果对于揭示烟粉虱对吡虫啉产生抗性的机制有帮助,也为烟粉虱抗性水平田间监测及烟粉虱综合治理提供理论依据。     

Q型烟粉虱细胞色素P450 CYP6DV5基因克隆及其在烟粉虱对噻虫嗪抗性中的作用

烟粉虱Bemisia tabaci已严重危害农作物的正常生长,而新烟碱类杀虫剂噻虫嗪已被广泛用于烟粉虱的防治,但由于常年应用,致使烟粉虱对噻虫嗪产生了严重的抗性,而目前其抗药性分子机制尚不明确.本研究通过荧光定量PCR比较分析烟粉虱噻虫嗪抗性及敏感种群,发现细胞色素P450基因CYP6DV5在噻虫嗪抗性品系中的表达量为...     

Monitoring neonicotinoid resistance in biotype B of Bemisia tabaci in Florida

BACKGROUND: Biotype B of the sweetpotato whitefly, Bemisia tabaci (Genn.), is a worldwide pest that has developed resistance to many insecticides, including the neonicotinoid class. Florida field populations were monitored for susceptibility to the neonicotinoids imidacloprid and thiamethoxam using a cut leaf petiole bioassay method. RESULTS: Average RR₅₀ values for imidacloprid increased from 3.7 in 2000 to 12.0 in 2003; decreased to 5.0 and 2.5 in 2004 and 2005, respectively; and then increased to 26.3 and 23.9 in 2006 and 2007, respectively. Populations with RR₅₀ values of about 50 to 60 during generation one reverted to RR₅₀ values of ?4 in six generations, when reared without further exposure to imidacloprid. Average RR₅₀ values for thiamethoxam increased from 2.0 in 2003 to 24.7 in 2006 and decreased to 10.4 in 2007. Populations with RR₅₀ values of about 22, 32 and 53 during generation one declined to 8, 5 and 6, respectively, after being reared for five generations without exposure to thiamethoxam. The correlation coefficient from the 26 populations that were bioassayed both with imidacloprid and thiamethoxam showed a significant positive correlation (R² = 0.58) between these populations. CONCLUSION: The high level of RR₅₀ values to imidacloprid and thiamethoxam suggest an unstable decline in the susceptibility of B. tabaci to imidacloprid and thiamethoxam, with possible cross‐resistance or predisposition for dual resistance selection. Copyright © 2009 Society of Chemical Industry     

Susceptibility to thiamethoxam of Musca domestica from Danish livestock farms

BACKGROUND: Neonicotinoid baits are currently replacing anticholinesterase baits for control of adult houseflies (Musca domestica L.). Introduction of new insecticides includes evaluation of their cross-resistance potential, which was assessed for thiamethoxam in field populations from Denmark. RESULTS: In feeding bioassay with a susceptible strain, thiamethoxam LC(50) at 72 h was 1.7 microg thiamethoxam g(-1) sugar, making it 19-fold, 11-fold and threefold more toxic to houseflies than azamethiphos, methomyl and spinosad respectively. The field populations were 6-76-fold resistant to thiamethoxam. There was no correlation between the toxicities of thiamethoxam and spinosad, dimethoate, methomyl, bioresmethrin or azamethiphos. The toxicity in feeding bioassay at 72 h of imidacloprid in a susceptible strain was 32 microg imidacloprid g(-1) sugar at LC(50), making it 19-fold less toxic to houseflies than thiamethoxam. There was a strong significant correlation between the toxicities of thiamethoxam and imidacloprid in field populations.CONCLUSION: Neonicotinoid-resistant houseflies were present at a detectable and noticeable level before thiamethoxam and imidacloprid were introduced for housefly control in Denmark. The toxicity of thiamethoxam is explained by other parameters than the toxicities of spinosad, dimethoate, methomyl, bioresmethrin or azamethiphos. The cross-resistance between thiamethoxam and imidacloprid indicates a coincidence of mechanism of the toxicity and resistance in the field populations.     

Two cytochrome P450 genes are involved in imidacloprid resistance in field populations of the whitefly, Bemisia tabaci, in China

The sweet potato whitefly, Bemisia tabaci (Gennadius) (Hemiptera:Aleyrodidae), is an invasive and damaging pest of field crops worldwide. The neonicotinoid insecticide imidacloprid has been widely used to control this pest. We assessed the species composition (B vs. Q), imidacloprid resistance, and association between imidacloprid resistance and the expression of five P450 genes for 14–17 B. tabaci populations in 12 provinces in China. Fifteen of 17 populations contained only B. tabaci Q, and two populations contained both B and Q. Seven of 17 populations exhibited moderate to high resistance to imidacloprid, and eight populations exhibited low resistance to imidacloprid, compared with the most susceptible field WHHB population. In a study of 14 of the populations, resistance level was correlated with the expression of the P450 genes CYP6CM1 and CYP4C64 but not with the expression of CYP6CX1, CYP6CX4, or CYP6DZ7. This study indicates that B. tabaci Q has a wider distribution in China than previously reported. Resistance to imidacloprid in field populations of B. tabaci is associated with the increased expression of two cytochrome P450 genes (CYP6CM1 and CYP4C64).     

Toxicities and sublethal effects of seven neonicotinoid insecticides on survival, growth and reproduction of imidacloprid-resistant cotton aphid, Aphis gossypii

BACKGROUND: Imidacloprid has been a major neonicotinoid insecticide for controlling Aphis gossypii (Glover) (Homoptera: Aphididae) and other piercing–sucking pests. However, the resistance to imidacloprid has been recorded in many target insects. At the same time, cross‐resistance of imidacloprid and other insecticides, especially neonicotinoid insecticides, has been detected. RESULTS: Results showed that the level of cross‐resistance was different between imidacloprid and tested neonicotinoid insecticides (no cross‐resistance: dinotefuran, thiamethoxam and clothianidin; a 3.68–5.79‐fold cross‐resistance: acetamiprid, nitenpyram and thiacloprid). In the study of sublethal effects, imidacloprid at LC₂₀ doses could suppress weight gain and honeydew excretion, but showed no significant effects on longevity and fecundity of the imidacloprid‐resistant cotton aphid, A. gossypii. However, other neonicotinoid insecticides showed significant adverse effects on biological characteristics (body weight, honeydew excretion, longevity and fecundity) in the order of dinotefuran > thiamethoxam and clothianidin > nitenpyram > thiacloprid and acetamiprid. CONCLUSION: The results indicated that dinotefuran is the most effective insecticide for use against imidacloprid‐resistant A. gossypii. To avoid further resistance development, the use of nitenpyram, acetamiprid and thiacloprid should be avoided on imidacloprid‐resistant populations of A. gossypii. Copyright © 2011 Society of Chemical Industry     

Thiamethoxam is a neonicotinoid precursor converted to clothianidin in insects and plants

Neonicotinoid insecticides are compounds acting agonistically on insect nicotinic acetylcholine receptors (nAChR). They are especially active on hemipteran pest species such as aphids, whiteflies, and planthoppers, but also commercialized to control many coleopteran and some lepidopteran pest species. The most prominent member of this class of insecticides is imidacloprid. All neonicotinoid insecticides bind with high affinity (I₅₀-values around 1 nM) to [³H]imidacloprid binding sites on insect nAChRs. One notable ommission is the neonicotinoid thiamethoxam, showing binding affinities up to 10,000-fold less potent than the others, using housefly head membrane preparations. Electrophysiological whole cell voltage clamp studies using neurons isolated from Heliothis virescens ventral nerve cord showed no response to thiamethoxam when applied at concentrations of 0.3 mM, although the symptomology of poisoning in orally and topically treated noctuid larvae suggested strong neurotoxicity. Other neonicotinoids, such as clothianidin, exhibited high activity as agonists on isolated neurons at concentrations as low as 30 nM. There was no obvious correlation between biological efficacy of thiamethoxam against aphids and lepidopterans and receptor affinity in electrophysiological and binding assays. Pharmacokinetic studies using an LC-MS/MS approach to analyze haemolymph samples taken from lepidopteran larvae revealed that thiamethoxam orally applied to 5th instar Spodoptera frugiperda larvae was rapidly metabolized to clothianidin, an open-chain neonicotinoid. Clothianidin shows high affinity to nAChRs in both binding assays and whole cell voltage clamp studies. When applied to cotton plants, thiamethoxam was also quickly metabolized, with clothianidin being the predominant neonicotinoid in planta briefly after application, as indicated by LC-MS/MS analyses. Interestingly, the N-desmethylated derivative of thiamethoxam, N-desmethyl thiamethoxam, was not significantly produced in either lepidopteran larvae or in cotton plants, although it was often mentioned as a possible metabolite, being nearly as active as imidacloprid. In conclusion, our investigations show that thiamethoxam is likely to be a neonicotinoid precursor for clothianidin.     

新疆MEAM1烟粉虱隐种对吡虫啉的抗性遗传力分析及交互抗性测定

采用Tabashnik的域性状指标分析了新疆MEAM1(Middle-East-Asia-Minor l)烟粉虱隐种对吡虫啉的抗性现实遗传力(h2)和不同致死率下的抗性发展速率,同时测定了抗性种群对不同类型杀虫剂的交互抗性。结果表明,在30%~50%较低的选择压力下,新疆MEAM1烟粉虱隐种连续汰选8代后,对吡虫啉的抗性上升28.01倍,抗性现实遗传力h2为0.429 7。假设田间种群现实遗传力为实验室筛选估算值的1/2,即h2=0.214 9,对新疆MEAM1烟粉虱隐种对吡虫啉的抗性发展速率估算结果表明:在药剂选择压力为50%~60%下,若使其对吡虫啉的抗性增长10倍,则需要生长10~8代;而在药剂选择压力为70%~90%下,若使其抗性增长10倍,则仅需要生长6~4代。表明新疆MEAM1烟粉虱隐种对吡虫啉产生抗性的风险很大。交互抗性测定结果显示:抗性种群对同类型的杀虫剂吡虫清和噻虫嗪分别产生了10.78倍和4.75倍的中等至低水平交互抗性;对多杀菌素、毒死蜱、吡丙醚和高效氯氰菊酯的敏感性有所降低;对阿维菌素、氟啶虫胺腈和乙基多杀菌素等杀虫剂则无交互抗性。     

Resistance and cross-resistance to imidacloprid and thiamethoxam in the Colorado potato beetle Leptinotarsa decemlineata

One of the major challenges in managing the Colorado potato beetle, Leptinotarsa decemlineata (Say) is its remarkable ability to develop resistance to virtually every insecticide that has ever been used against it. Resistance is particularly common throughout northeastern USA as far north as Maine. The first instances of resistance to imidacloprid have already been reported from several locations in New York, Delaware and southern Maine. Rotating insecticides with different modes of action may delay insecticide resistance, but successful implementation of this technique depends on a good understanding of resistance and cross-resistance patterns in populations of target pests. LC(50) values were measured for imidacloprid and thiamethoxam in Colorado potato beetle populations from a variety of locations in the USA and Canada using diet incorporation bioassays. The field performance of imidacloprid, thiamethoxam and clothianidin against imidacloprid-resistant beetles on a commercial potato farm in southern Maine was also evaluated. Correlation between LC(50) values for imidacloprid and thiamethoxam was highly significant, even when populations previously exposed to thiamethoxam were excluded from the analysis. There was no statistically detectable difference in the LC(50) values between populations exposed to both insecticides and to imidacloprid alone. Applications of neonicotinoid insecticides at planting delayed build-up of imidacloprid-resistant beetle populations on field plots by 1-2 weeks but failed to provide adequate crop protection. Consistently with bioassay results, there was also substantial cross-resistance among the three tested neonicotinoid insecticides. Results of the present study support the recommendation to avoid rotating imidacloprid with thiamethoxam as a part of a resistance management plan.     

Characterisation of imidacloprid resistance mechanisms in the brown planthopper, Nilaparvata lugens Stål (Hemiptera: Delphacidae)

Effective control of the brown planthopper, Nilaparvata lugens Stål, across rice-growing regions of Asia has been seriously compromised over the last 2 years by the appearance of widespread resistance to the neonicotinoid insecticide, imidacloprid. Sequence analysis of the ligand-binding domain of the nicotinic acetylcholine receptor α1 subunit from two field-collected resistant strains (CHN-2 and IND-11) did not reveal the Y151S point mutation previously implicated in conferring target-site resistance in this species. This result was supported by ligand-binding studies with [³H]-imidacloprid that showed no significant change in insecticide binding to isolated membranes from susceptible and resistant strains. In contrast, there was an approximate 5-fold increase in the mixed function oxidase activity for the two resistant strains suggesting that imidacloprid metabolism by increased cytochrome P450 monooxygenase activity is the major mechanism of resistance in these strains.     

Low expression of nicotinic acetylcholine receptor subunit Mdα2 in neonicotinoid‐resistant strains of Musca domestica L.

BACKGROUND: Neonicotinoid action as well as resistance involves interaction with nicotinic acetylcholine receptors (nAChRs). In the housefly, neonicotinoid resistance also involves cytochrome P450, as indicated by bioassay with synergist as well as altered expression. In bioassay, synergism was only partial and indicated possible target‐site resistance. The nAChR α2 subunit is important in neonicotinoid toxicity to insects, and gene expression of the Mdα2 subunit was investigated in field populations and laboratory strains of neonicotinoid‐resistant and insecticide‐susceptible houseflies, Musca domestica L. The genomic sequence covering exon III–VII of Mdα2 was analysed for mutations. RESULTS: Gene expression profiling of Mdα2 revealed notable differences between neonicotinoid‐resistant and insecticide‐susceptible houseflies. On average, the neonicotinoid‐resistant field population 766b and the imidacloprid selected strain 791imi had 60% lower copy numbers of Mdα2 compared with the susceptible reference strain. Sequencing of exon III–VII of the Mdα2, encoding acetylcholine binding‐site regions and three out of four transmembrane domains, did not reveal any mutations explaining the increased neonicotinoid tolerance in the strains examined. CONCLUSION: Previous discoveries and the results of this study suggest that the neonicotinoid resistance mechanism in Danish houseflies involves both cytochrome P450 monooxygenase‐mediated detoxification and reduced expression of the nAChR subunit α2. Copyright © 2010 Society of Chemical Industry     

P450-mediated resistance in Myzus persicae (Sulzer) (Hemiptera: Aphididae) reduces the efficacy of neonicotinoid seed treatments in Brassica napus

BACKGROUND

The prophylactic use of seeds treated with neonicotinoid insecticides remains an important means of controlling aphid pests in canola (Brassica napus) crops in many countries. Yet, one of the most economically important aphid species worldwide, the peach potato aphid (Myzus persicae), has evolved mechanisms which confer resistance to neonicotinoids, including amplification of the cytochrome P450 gene, CYP6CY3. While CYP6CY3 amplification has been associated with low-level resistance to several neonicotinoids in laboratory acute toxicity bioassays, its impact on insecticide efficacy in the field remains unresolved. In this study, we investigated the impact of CYP6CY3 amplification on the ability of M. persicae to survive neonicotinoid exposure under laboratory and semi-field conditions.

RESULTS

Three M. persicae clones, possessing different copy numbers of CYP6CY3, were shown to respond differently when exposed to the neonicotinoids, imidacloprid and thiamethoxam, in laboratory bioassays. Two clones, EastNaernup209 and Osborne171, displayed low levels of resistance (3–20-fold), which is consistent with previous studies. However, in a large-scale semi-field trial, both clones showed a surprising ability to survive and reproduce on B. napus seedlings grown from commercial rates of neonicotinoid-treated seed. In contrast, an insecticide-susceptible clone, of wild-type CYP6CY3 copy number, was unable to survive on seedlings treated in the same manner.

CONCLUSION

Our findings suggest that amplification of CYP6CY3 in M. persicae clones substantially impairs the efficacy of neonicotinoid seed treatments when applied to B. napus. These findings highlight the potentially important real-world implications of resistances typically considered to be ‘low level’ as defined through laboratory bioassays. © 2023 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.     

Resistance and cross-resistance to neonicotinoid insecticides and spinosad in the Colorado potato beetle, Leptinotarsa decemlineata (Say) (Coleoptera: Chrysomelidae)

The Colorado potato beetle, Leptinotarsa decemlineata (Say), has developed resistance to many insecticides used for its control, recently including imidacloprid, a neonicotinoid compound. Other neonicotinoids are now being deployed to control this pest. A key point in the strategies of resistance management is the monitoring of resistance and cross-resistance. In the summer of 2003, imidacloprid-resistant adult Colorado potato beetles collected from Long Island, New York, USA were bioassayed using topical applications of imidacloprid and nine other neonicotinoids. Compared to a standard susceptible strain, the Long Island beetles showed 309-fold resistance to imidacloprid, and lower levels of cross-resistance to all other neonicotinoids, despite these never having been used in the field, i.e., 59-fold to dinotefuran, 33-fold to clothianidin, 29-fold to acetamiprid, 28-fold to N-methylimidacloprid, 25-fold to thiacloprid, 15-fold to thiamethoxam, 10-fold to nitenpyram, but less than 2-fold to nicotine. In injection bioassays, high resistance to imidacloprid was also found (116-fold). Piperonyl butoxide partially suppressed resistance to imidacloprid, but the resistance level was still over 100-fold, indicating that other mechanisms were primarily responsible for resistance. Low levels of resistance (8- to 10-fold) were found to the nicotinic activator, spinosad, in an imidacloprid-resistant strain collected from the same field in 2004. The cross-resistance seen with all the neonicotinoids tested suggests that the rotation of imidacloprid with other neonicotinoids may not be an effective long-term resistance management strategy. Rotation with spinosad also carries some risk, but it is unlikely that spinosad resistance in this case is mechanistically related to that for the neonicotinoids.     

Toxicological and mechanistic studies on neonicotinoid cross resistance in Q-type Bemisia tabaci (Hemiptera: Aleyrodidae)

The tobacco whitefly, Bemisia tabaci Gennadius (Homoptera: Aleyrodidae) is a serious pest in numerous cropping systems and has developed a high degree of resistance against several chemical classes of insecticides. One of the latest group of insecticides introduced to the market were the neonicotinoids (chloronicotinyls), acting agonistically on insect nicotinic acetylcholine receptors. Resistance to neonicotinoid insecticides has recently been shown to occur, especially in Q-type B tabaci in some places in Almeria, Spain, whereas control of B-type B tabaci in many other intense cropping systems worldwide has remained on high levels. Our study revealed that neonicotinoid-resistant Q-type strains from Almeria were often more than 100-fold less susceptible to thiamethoxam, acetamiprid and imidacloprid when tested in discontinuous systemic laboratory bioassays. The resistance factors were generally 2- to 3-fold lower in leaf-dip bioassays. In addition to the Spanish strains, we obtained two other highly neonicotinoid-cross-resistant B tabaci greenhouse populations, one from Italy (December 1999) and one from Germany (June 2001). A molecular diagnostic analysis revealed that both strains also belong to the (Spanish) subtype Q of the B tabaci species complex. The resistance levels of Q-type whitefly strains derived from Almeria greenhouses in 1999 remained stable for at least two years, even when maintained in the laboratory without any selection pressure. The biochemical mechanisms conferring resistance to neonicotinoids have not yet been elucidated in detail, but synergist studies suggested a possible involvement of microsomal monooxygenases. Furthermore, we checked two Almerian strains of B tabaci isolated in 1998 and 1999 and demonstrated that neonicotinoid resistance is not due to an altered [3H]imidacloprid binding site of nicotinic acetylcholine receptors.     

吡虫啉和噻虫嗪对苜蓿盲蝽的防治效果及其在苜蓿中的残留

为了评价新烟碱类杀虫剂吡虫啉和噻虫嗪对苜蓿盲蝽的防治效果及安全性,采用田间喷雾法测定了20%吡虫啉可溶液剂(SL)和30%噻虫嗪悬浮剂(SC)对苜蓿盲蝽的防治效果,使用超高效液相色谱-串联质谱法(UPLC-MS/MS)测定了施药1、2、3次后(间隔7 d),药剂在苜蓿中的残留情况。结果表明,当吡虫啉和噻虫嗪在施药剂量分别为25.02 g/hm²和18.00 g/hm²时,药后3～7 d对苜蓿盲蝽的防治效果分别为80.01%～82.01%和77.54%～83.29%。吡虫啉和噻虫嗪连续施药3次后,在苜蓿中的最终残留量分别为1.90 mg/kg和0.08 mg/kg,吡虫啉已超过我国食品安全国家标准GB 2763-2021规定的果蔬中的最大残留限量(0.5 mg/kg)。因此建议每茬苜蓿生长期,可选用吡虫啉和噻虫嗪防治苜蓿盲蝽,吡虫啉和噻虫嗪喷施次数分别不宜超过2次和3次。     

北京、山东和湖南地区烟粉虱抗药性及CYP4v2和CYP6CX1 mRNA水平表达量分析

于2011年采集北京、山东和湖南三地的烟粉虱,进行B、Q隐种鉴定,并测定4种杀虫剂的抗药性,同时通过荧光定量PCR分析CYP4v2和CYP6CX1两个基因的mRNA水平的表达量。结果表明,北京、湖南和长沙烟粉虱均为Q隐种。抗药性监测表明,北京和湖南种群对阿维菌素敏感,山东种群抗性水平较低,而对烟碱类药剂噻虫嗪出现不同程度的抗药性,其中湖南地区烟粉虱对噻虫嗪的抗药性达到49.08倍的高抗水平,北京和山东地区也达到中抗水平。另外,这3个地区的种群对毒死蜱和联苯菊酯抗性水平都较低。通过qRT-PCR分析三地的CYP4v2和CYP6CX1基因表达量,发现相对于敏感种群CYP4v2基因在北京、山东和湖南3个地理种群中分别过量表达3.85倍、19.57倍和10.78倍,而CYP6CX1基因在北京种群中过量表达20.55倍。结果提示田间烟粉虱的细胞色素P450基因CYP4v2和CYP6CX1过量表达可能会是烟粉虱抗药性的形成机制之一。     

四种新烟碱类杀虫剂对蜜蜂的急性毒性及初级风险评估

采用饲喂管法和点滴法,分别测定了吡虫啉、噻虫嗪、噻虫胺、啶虫脒4种原药及其制剂对意大利蜜蜂成年工蜂的急性毒性,并采用危害商值(HQ)法进行了初级风险评价。结果表明:饲喂管法测得97.3%吡虫啉原药、25%吡虫啉可湿性粉剂、96%噻虫嗪原药、30%噻虫嗪悬浮剂、97%噻虫胺原药、5%噻虫胺可湿性粉剂、96%啶虫脒原药及40%啶虫脒可溶性粉剂的经口毒性48 hLD50值分别为有效成分8.04×10-3、9.46×10-3、7.04×10-3、4.64×10-3、11.8×10-3、5.25×10-3、5.22和6.31μg/蜂;点滴法测得各药剂的接触毒性48 h-LD50值分别为有效成分2.46×10-2、1.33×10-2、3.63×10-2、9.27×10-3、1.52×10-2、2.21×10-2、5.82和5.07μg/蜂。按《化学农药环境安全评价试验准则》的毒性等级划分标准,啶虫脒原药及其可溶性粉剂对蜜蜂的急性毒性均为中等毒,其他6种药剂对蜜蜂的急性毒性均为高毒;根据危害商值(HQ),啶虫脒对蜜蜂为低风险,吡虫啉、噻虫嗪和噻虫胺对蜜蜂均存在高风险。