Abamectin: Toxicity to House Flies (Diptera: Muscidae) Resistant to Synthetic Organic Insecticides

Rt, Roush; Je, Wright

doi:10.1093/jee/79.3.562

Cited by 30 publications

(14 citation statements)

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“…Roush and Wright (1986) found full susceptibility to abamectin in two cyclodiene-resistant strains of the housefly. Similarly, cyclodiene-resistant red flour beetles were susceptible to abamectin and also to methoxychlor (Beeman and Stuart, 1990), a compound with a mode of action similar to Type I pyrethroids (Wu et al, 1975).…”

Section: Discussionmentioning

confidence: 95%

Cyclodiene resistance at the insect GABA receptor/chloride channel complex confers broad cross resistance to convulsants and experimental phenylpyrazole insecticides

Bloomquist

1994

Arch Insect Biochem Physiol

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This study investigated the pharmacological profile of cyclodiene resistance in Drosophila melanogaster and the mode of action of a phenylpyrazole insecticide, JKU 0422. Toxicological studies were performed with a sucrose bait assay containing the synergist piperonyl butoxide. The Maryland strain of D. melanogaster was resistant to dieldrin, lindane, picrotoxinin, TBPS, p-CN-TBOB, and JKU 0422. In contrast, this strain was susceptible to cypermethrin and the avermectins MK-243, abamectin, and abamectin 8,9-oxide. Neurophysiological studies showed that both TBPS and JKU 0422 reversed the inhibitory action of GABA in central nerve preparations from susceptible D. melanogaster. However, the response to these compounds was attenuated in nerve preparations from the resistant Maryland strain, which indicated that the resistance was expressed at the level of the nerve. Topical toxicity bioassays with JKU 0422 on susceptible (CSMA) and cyclodiene-resistant (LPP) strains of German cockroach revealed a resistance ratio of 553-fold for this compound. These studies demonstrate that cyclodiene resistance in D. melanogaster confers broad cross resistance toward compounds thought to block the GABA-gated chloride channel in a manner similar to the cyclodienes. Moreover, the cross resistance extends to JKU 0422, and resistance to this compound is also present in a strain of cyclodiene-resistant German cockroach. These toxicological results, along with the neurophysiological studies, confirm that JKU 0422 has a mode of action that is similar to the cyclodienes and TBPS. These findings suggest that the introduction and use of new chloride channel antagonists as insecticides should be managed carefully in order to prevent the rapid development of resistance in the field.

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Section: Discussionmentioning

confidence: 95%

Cyclodiene resistance at the insect GABA receptor/chloride channel complex confers broad cross resistance to convulsants and experimental phenylpyrazole insecticides

Bloomquist

1994

Arch Insect Biochem Physiol

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“…There is no cross‐resistance to abamectin in numerous insect strains resistant to conventional insecticides (Roush and Wright 1986; Argentine and Clark 1990; Cochran 1990; Clark et al. 1995; Liang et al.…”

Section: Discussionmentioning

confidence: 99%

Cross‐resistance and biochemical mechanisms of abamectin resistance in the B‐type Bemisia tabaci

Wang

2007

J Applied Entomology

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To understand the risk of resistance and the possible mechanisms of resistance to abamectin in B-type Bemisia tabaci (Gennadius) better, a resistant strain of B. tabaci was selected in the laboratory and cross-resistance pattern and resistance mechanisms to abamectin were investigated. The NJ-Abm strain of B. tabaci was derived from a field population (NJ) collected in Nanjing, China in 2002 with 18 generations of selection with abamectin in the laboratory. Compared with the unselected NJ strain, the selected NJ-Abm strain developed 14.5-fold resistance to abamectin and showed significant cross-resistance to emamectin benzoate (4.4-fold) and imidacloprid (3.4-fold), but no crossresistance to fipronil. The oxidase inhibitor piperonyl butoxide (PBO) and glutathione S-transferase inhibitor diethyl maleate (DEM) produced significant synergism on abamectin in the NJ-Abm strain (with synergistic ratios of 3.9-and 4.1-fold respectively); however, the esterase inhibitor triphenyl phosphate (TPP) did not act synergistically with abamectin. Biochemical analysis confirmed that P450 monooxygenase activity and glutathione S-transferase activity of the NJ-Abm strain were elevated to 2.1-and 2.0-fold, respectively, compared with that of the NJ strain. This indicated that enhanced metabolism mediated by P450 monooxygenase and glutathione S-transferase is likely to be involved in abamectin resistance and cross-resistance to imidacloprid and emamectin benzoate in the NJ-Abm strain.

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“…It has a broad spectrum of activities against arthropods, including insects and mites (Argentine and Clark, 1990; Strong, 1992). However, its extensive use over many years has led to the development of resistance in several insect pests (Rousw and Wright, 1986; Liang et al, 2003; Xin et al, 2010). A survey of pesticide resistance of T. cinnabarinus in Southern China revealed that field strains had different levels of resistance to three acaricides, including fenproathrin, omethoate, and propargite (Chen et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

High Gama-Aminobutyric Acid Contents Involved in Abamectin Resistance and Predation, an Interesting Phenomenon in Spider Mites

Liu

Peng

et al. 2017

Front. Physiol.

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Abamectin has been widely used as an insecticide/acaricide for more than 30 years because of its superior bioactivity. Recently, an interesting phenomenon was identified in the carmine spider mite, Tetranychus cinnabarinus, an important pest in agriculture. The gamma aminobutyric acid (GABA) contents in a laboratory abamectin resistant strain of T. cinnabarinus (AbR) were significantly increased. Decreases in activity and mRNA expression of GABA transaminase (GABA-T) were responsible for GABA accumulation in AbR mites. To clarify the mechanism of GABA accumulation mediated abamectin resistance, three artificial approaches were conducted to increase GABA contents in susceptible mites, including feeding of vigabatrin (a specific inhibitor of GABA-T), feeding of exogenous GABA, and inhibition of GABA-T gene expression. The results showed that susceptible mites developed resistance to abamectin when the GABA contents were artificially increased. We also observed that the mites with higher GABA contents moved more slowly, which is consistent with the fact that GABA is an inhibitory neurotransmitter in arthropods. Subsequently, functional response assays revealed that predation rates of predatory mites on GABA accumulated abamectin-resistant mites were much higher than control groups. The tolerance to abamectin, slow crawling speed, and vulnerability to predators were all resulted from GABA accumulation. This relationship between GABA and predation was also confirmed in a field-collected population. Our finding indicates that predatory mites might be used as a tool for biological control to circumvent the development of abamectin resistance in mites.

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Abamectin: Toxicity to House Flies (Diptera: Muscidae) Resistant to Synthetic Organic Insecticides

Cited by 30 publications

References 0 publications

Cyclodiene resistance at the insect GABA receptor/chloride channel complex confers broad cross resistance to convulsants and experimental phenylpyrazole insecticides

Cyclodiene resistance at the insect GABA receptor/chloride channel complex confers broad cross resistance to convulsants and experimental phenylpyrazole insecticides

Cross‐resistance and biochemical mechanisms of abamectin resistance in the B‐type Bemisia tabaci

High Gama-Aminobutyric Acid Contents Involved in Abamectin Resistance and Predation, an Interesting Phenomenon in Spider Mites

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