Avermectin Toxicity Research Articles

Placental telomere length decline with gestational age differs by sex and TERT, DNMT1, and DNMT3A DNA methylation

Despite increasing evidences pointing to residues of avermectin (AVM) pose toxic effects on non-target organisms in environment, but the data in pigeon is insufficient. The alteration of global DNA methylation and response of heat shock proteins (Hsps) are important for assessing the AVM toxicity in cardiac tissues of pigeon (Columba livia). To investigate the effects of AVM exposure in cardiac tissues of pigeon, we detected the expression levels of DNA methyltransferases (Dnmts), methylated DNA-binding domain protein 2 (MBD2), and Hsp 60, 70 and 90. Pigeons were exposed to feed containing AVM (0, 20, 40 and 60 mg/kg diet) for 30, 60, 90 days respectively, and cardiac tissues were collected and analyzed. We found the transcriptional levels of Dnmt1, Dnmt3a and Dnmt3b mRNA were down-regulated, but the transcriptional levels of MBD2 mRNA were up-regulated by AVM exposure in cardiac tissues of pigeon. Necrocytosis, hemorrhage, infiltration of inflammatory cells and abundant vacuoles appeared in cardiac tissues after AVM exposure. Accompanying this phenotype, the mRNA transcriptional and/or protein levels of Hsp30, Hsp60, Hsp70 and Hsp90 increased. In conclusion, these results underscored AVM exposure caused DNA methylation machinery malfunctions, and induced over-expression of Hsps to improve the protective function against cardiac injury.

Avermectin induced global DNA hypomethylation and over-expression of heat shock proteins in cardiac tissues of pigeon

Despite increasing evidences pointing to residues of avermectin (AVM) pose toxic effects on non-target organisms in environment, but the data in pigeon is insufficient. The alteration of global DNA methylation and response of heat shock proteins (Hsps) are important for assessing the AVM toxicity in cardiac tissues of pigeon (Columba livia). To investigate the effects of AVM exposure in cardiac tissues of pigeon, we detected the expression levels of DNA methyltransferases (Dnmts), methylated DNA-binding domain protein 2 (MBD2), and Hsp 60, 70 and 90. Pigeons were exposed to feed containing AVM (0, 20, 40 and 60mg/kg diet) for 30, 60, 90days respectively, and cardiac tissues were collected and analyzed. We found the transcriptional levels of Dnmt1, Dnmt3a and Dnmt3b mRNA were down-regulated, but the transcriptional levels of MBD2 mRNA were up-regulated by AVM exposure in cardiac tissues of pigeon. Necrocytosis, hemorrhage, infiltration of inflammatory cells and abundant vacuoles appeared in cardiac tissues after AVM exposure. Accompanying this phenotype, the mRNA transcriptional and/or protein levels of Hsp30, Hsp60, Hsp70 and Hsp90 increased. In conclusion, these results underscored AVM exposure caused DNA methylation machinery malfunctions, and induced over-expression of Hsps to improve the protective function against cardiac injury.

Effects of avermectin on heat shock proteins expression and histopathology in spleen tissues of pigeon

Avermectin (AVM) is the active component of some insecticidal and nematicidal product used in agriculture and veterinary medicine for the prevention of parasitic diseases. Residues of AVM in environment have toxic effects on non-target aquatic and terrestrial organisms. Heat shock proteins (Hsps) are commonly used by environmental toxicologists as biochemical markers of exposure to various chemical and other stressors. The objective of this study was to investigate whether sub-chronic AVM exposure would alter the levels of stress proteins, Hsps in the pigeon spleen after 30, 60 and 90days. Our results showed that Hsp60, Hsp70 and Hsp90, and their corresponding messenger RNA (mRNA) transcriptions (as well as Hsp30) significantly elevated, meanwhile, obviously histopathological changes were not observed in pigeons spleens after early AVM exposure. Then the expression of Hsps relatively decreased and obvious histopathological damages occurred in the spleen tissues with continued AVM exposure. So we suggest that the elevations of Hsps can be as a part of protective mechanism to reduce cellular damage, and important markers to help assess the toxicity induced by AVM. The reduction of Hsps in spleen implies that the tissues are damaged by long-term and excessive AVM exposure. Thus, the information presented in this study is believed to be helpful in supplementing data for further AVM toxicity study.

The effects of avermectin on amino acid neurotransmitters and their receptors in the pigeon brain

The objective of this study was to examine the effects of avermectin (AVM) on amino acid neurotransmitters and their receptors in the pigeon brain. Four groups two-month-old American king pigeons (n=20/group) were fed either a commercial diet or an AVM-supplemented diet (20mg/kg·diet, 40mg/kg·diet, or 60mg/kg·diet) for 30, 60, or 90days. The contents of aspartic acid (ASP), glutamate (GLU), glycine (GLY), and γ-aminobutyric acid (GABA) in the brain tissues were determined using ultraviolet high-performance liquid chromatography (HPLC). The expression levels of the GLU and GABA receptor genes were analyzed using real-time quantitative polymerase chain reaction (qPCR). The results indicate that AVM exposure significantly enhances the contents of GABA, GLY, GLU, and ASP in the cerebrum, cerebellum, and optic lobe. In addition, AVM exposure increases the mRNA expression levels of γ-aminobutyric acid type A receptor (GABAAR), γ-aminobutyric acid type B receptor (GABABR), N-methyl-d-aspartate 1 receptor (NR1), N-methyl-d-aspartate 2A receptor (NR2A), and N-methyl-d-aspartate 2B receptor (NR2B) in a dose- and time-dependent manner. Moreover, we found that the most damaged organ was the cerebrum, followed by the cerebellum, and then the optic lobe. These results show that the AVM-induced neurotoxicity may be associated with its effects on amino acid neurotransmitters and their receptors. The information presented in this study will help supplement the available data for future AVM toxicity studies.

Combined effects of temperature and avermectins on life history and stress response of the western flower thrips, Frankliniella occidentalis

Temperature and pesticide are two important factors that affect survival, reproduction and other physiological processes of insects. To determine interactions of elevated temperature and avermectins treatment on the western flower thrips, Frankliniella occidentalis, newly emerged adults were exposed to combinations of three temperatures (21, 26 and 33°C) and two avermectins concentrations (0, 45ppm), and survival rate, reproduction, longevity, antioxidant enzymes activities and heat shock proteins (hsps) induction were analyzed. The results showed that the survival, longevity and reproduction of F. occidentalis decreased with increased temperature and avermectins treatment. While elevated temperature and avermectins treatment significantly decreased activity of SOD, activities of POD and GST significantly increased after exposure to elevated temperature, avermectins or their combination. Elevated temperature had no effect on activity of CAT, but it was obviously improved by the combination of temperature and avermectins treatment. Expression analysis of hsps showed that four heat shock proteins (hsp90, hsc702, hsp60 and hop) were up-regulated by the induction of elevated temperature with small fold changes. After treatment with avermectins, expression levels of hsp90, hsc701, hsc702 and hop were significantly up-regulated with increased temperature and higher than those of their respective control at higher temperature. Surprisingly, expression level of hps60 was down-regulated with increased temperature, but the expression level at 21 or 26°C remained higher than that of control. Overall, our studies suggest that elevated temperature enhance toxicity of avermectins and their combination induced acute oxidative damage to F. occidentalis. Therefore, consideration of temperature in evaluating avermectins toxicity is necessary to make accurate prediction of its effect on F. occidentalis and other insects.

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Introduction: Multiple case reports with avermectin, a highly lipophilic insecticide, toxicity have been published in human and veterinary medicine. Intravenous treatment with lipid emulsion has been reported as a treatment option for a variety of lipophilic drug overdoses and toxicities. Extracorporeal blood purification with conventional hemodialysis or charcoal hemoperfusion has failed for the treatment of highly lipophilic toxins. Single pass albumin dialysis (SPAD) has shown promising effect for the treatment of highly protein bound drug overdoses, but has little or no effect against highly lipid bound toxins. We present a case of severe avermectin toxicity, which was treated with single pass lipid dialysis (SPLD). We replaced the albumin part of the dialysate with a 5% lipid solution to act as a second lipid sink for the extracorporeal removal of ivermectin. Case desription: A three year old, male Australian Shepherd presented to the emergency room with severe muscle tremors, hypersalivation, stupor and history of ivermectin ingestion 2 hours ago. Pertinent blood work showed a normal CBC and chemistry profile. His arterial blood gas analysis showed a respiratory acidosis with a pCO2 of 72 and a pH of 7.12. The patient was intubated, mechanical ventilation was initiated and he was treated with intravenous lipid emulsion. Despite the intravenous lipid therapy he remained comatose and ventilator depended. Due to the persistency of clinical signs, single pass lipid dialysis (SPLD) using a Gambro Prismaflex CRRT machine and a preparation of 5% lipid solution added to the dialysate was started. A six hour treatment with a projected Kt/V of 0.7 was prescribed. Blood samples were collected before and after 6 hours of treatment and submitted for ivermectin levels. The patient remained ventilator dependent for 3 more days and was successfully weaned of the ventilator on day 4. He made a full recovery, with normal physical exam and normal motor function after 4 weeks of supportive therapy. Discussion: To our knowledge this is the first case report of single pass lipid dialysis for a treatment of toxicity with a lipophilic substance. Pre-treatment level of ivermectin was 35 ppb and a drop to 25 ppb was noted after treatment, which represents an ivermectin reduction ratio of 29 %. The addition of a 5% lipid solution to the dialysate is believed to exert its beneficial effect by acting as a lipid "sink," causing lipophilic drugs to be redistributed into the expanded plasma lipid volume and decreasing free and tissue drug levels. The patient was an Australian Shepherd, who tested positive for multi –drug resistant gene (mdr1) mutation, which codes for the P-glycoprotein membrane transport molecule. This gene mutation disables the active removal of toxins through the blood-brain–barrier in this breed, explaining the long recovery for this patient. SPLD was efficient to decrease the amount of ivermectin with a relatively small dialysis dose (Kt/V of 0.7%) by 29 %. The normal plasma clearance in dogs is 2% per hour. This patient was initially treated with intravenous lipid therapy, which might have decreased the extracorporeal ivermectin reduction ratio. SPLD was an effective way to decrease the plasma levels of ivermectin in this patient. The lack of fast clinical response to the decreased plasma levels can partly be explained by the mdr1 gene mutation, which decreased the patient's ability of actively removing the drug from the brain tissue.

Avermectin induced inflammation damage in king pigeon brain

To determine the effect of Avermectin (AVM) on inflammation damage in king pigeon brain, eighty two-month-old American king pigeons were randomly divided into four groups, and were fed with either commercial diet or AVM-supplemented diet containing 20mgkg−1diet, 40mgkg−1diet, and 60mgkg−1diet AVM for 30, 60 and 90d, respectively. Then, the expression level of inflammatory factors (iNOS, PTGEs, NF-κB), histological damage, and ultra-structural damage were examined. It showed that AVM caused higher expressions (P<0.05) of iNOS, PTGEs, NF-κB with disorganized histological and ultra-structural structures in cerebrum, cerebellum, and optic lobe. Meanwhile, inflammatory and histopathological damage were induced by AVM in king pigeon brains. In addition, the main targeted organelle in nervous system was mitochondria, which indicated that mitochondria may be relevant to the process of inflammation induced by AVM. To our best knowledge, this is the first report to study the toxic effect of AVM on inflammatory damage in king pigeon. Thus, the information presented in this study is believed to be helpful in supplementing data for further AVM toxicity study.

Salmon lice (Lepeophtheirus salmonis) showing varying emamectin benzoate susceptibilities differ in neuronal acetylcholine receptor and GABA-gated chloride channel mRNA expression

BackgroundCaligid copepods, also called sea lice, are fish ectoparasites, some species of which cause significant problems in the mariculture of salmon, where the annual cost of infection is in excess of €300 million globally. At present, caligid control on farms is mainly achieved using medicinal treatments. However, the continued use of a restricted number of medicine actives potentially favours the development of drug resistance. Here, we report transcriptional changes in a laboratory strain of the caligid Lepeophtheirus salmonis (Krøyer, 1837) that is moderately (~7-fold) resistant to the avermectin compound emamectin benzoate (EMB), a component of the anti-salmon louse agent SLICE® (Merck Animal Health).ResultsSuppression subtractive hybridisation (SSH) was used to enrich transcripts differentially expressed between EMB-resistant (PT) and drug-susceptible (S) laboratory strains of L. salmonis. SSH libraries were subjected to 454 sequencing. Further L. salmonis transcript sequences were available as expressed sequence tags (EST) from GenBank. Contiguous sequences were generated from both SSH and EST sequences and annotated. Transcriptional responses in PT and S salmon lice were investigated using custom 15 K oligonucleotide microarrays designed using the above sequence resources. In the absence of EMB exposure, 359 targets differed in transcript abundance between the two strains, these genes being enriched for functions such as calcium ion binding, chitin metabolism and muscle structure. γ-aminobutyric acid (GABA)-gated chloride channel (GABA-Cl) and neuronal acetylcholine receptor (nAChR) subunits showed significantly lower transcript levels in PT lice compared to S lice. Using RT-qPCR, the decrease in mRNA levels was estimated at ~1.4-fold for GABA-Cl and ~2.8-fold for nAChR. Salmon lice from the PT strain showed few transcriptional responses following acute exposure (1 or 3 h) to 200 μg L-1 of EMB, a drug concentration tolerated by PT lice, but toxic for S lice.ConclusionsAvermectins are believed to exert their toxicity to invertebrates through interaction with glutamate-gated and GABA-gated chloride channels. Further potential drug targets include other Cys-loop ion channels such as nAChR. The present study demonstrates decreased transcript abundances of GABA-Cl and nAChR subunits in EMB-resistant salmon lice, suggesting their involvement in avermectin toxicity in caligids.

Doramectin toxicity in a group of lions (&lt;i&gt;Panthera leo&lt;/i&gt;)

Ten lions (Panthera leo) that were treated with a single injection of doramectin at a dose ranging between 0.2 mg/kg and 0.5 mg/kg showed clinical signs consistent with avermectin toxicity, namely ataxia, hallucinations, and mydriasis. Two subsequently died whereas the other eight lions recovered after 4-5 days with symptomatic therapy. Post-mortem examinations of the two that died showed cyanosis, severe pulmonary oedema, pleural effusion, and pericardial effusion, with histopathology not revealing any abnormalities. In both these lions, doramectin brain and liver tissue concentrations were elevated. Although doramectin is regularly used in wild felids, to date there have been no reports of avermectin toxicity in the literature. This article highlights the potential for doramectin toxicity in this species.

A Monoclonal Antibody-Based ELISA for Multiresidue Determination of Avermectins in Milk

Due to the widespread use and potential toxicity of avermectins (AVMs), multi-residue monitoring of AVMs in edible tissues, especially in milk, has become increasingly important. With the aim of developing a broad-selective immunoassay for AVMs, a broad-specific monoclonal antibody (Mab) was raised. Based on this Mab, a homologous indirect enzyme-linked immunosorbent assay (ELISA) for the rapid detection of AVMs in milk was developed. Under the optimized conditions, the IC50 values in assay buffer were estimated to be 3.05 ng/mL for abamectin, 13.10 ng/mL for ivermectin, 38.96 ng/mL for eprinomectin, 61.00 ng/mL for doramectin, 14.38 ng/mL for emamectin benzoate. Detection capability (CCβ) of the ELISA was less than 5 ng/mL and 2 ng/mL in milk samples prepared by simple dilution and solvent extraction, respectively. The optimized ELISA was used to quantify AVMs in milk samples spiked at different amounts. The mean recovery and coefficient of variation (CV) were 95.90% and 15.42%, respectively. The Mab-based ELISA achieved a great improvement in AVMs detection. Results proved this broad-selective ELISA would be useful for the multi-residue determination of AVMs in milk without purification process.

Effect of TBHQ on avermectin photo-degradation and its synergism on small brown planthopper

To delay avermectin photo-degradation, the paper studied the effects of different concentrations of antioxidant, terliary butyl hydroqulnon (TBHQ), on avermectin photo-degradation. The toxicity of avermectin and TBHQ mixture on small brown planthopper (SBPH) Laodelphax striatellus (Fallen) was also determined via rice-stem-dipping method. The results indicate that avermectin photo-degradation fits into the equation for first-order chemical reaction kinetics. Photolysis rate of avermectin photo-degradation under sunlight is slower than that under UV light. When TBHQ and avermectin ratio is 1︰1, photolysis rate is lowest for avermectin photo-degradation, and its half-life is 11.81 h. This is 167.19% increase compared with treatment without TBHQ. Laboratory bioassay results demonstrate that the synergistic effect of TBHQ and avermectin mixture on SBPH is significantly strong. After 3 h exposure to sunlight and UV light, the toxicity of avermectin and TBHQ mixture on SBPH increases significantly compared to that without TBHQ. The synergism ratio is 2.00 and 2.63, respectively.

Effects of avermectins on neurite outgrowth in differentiating mouse neuroblastoma N2a cells

Avermectins (AVMs) are macrocyclic lactone compounds that have been widely used as parasiticides in veterinary and human medicine and as pesticides in agriculture and horticulture. The multidrug resistance transporter, P-glycoprotein (P-gp), is associated with the efflux transport of AVMs and other drugs across the blood–brain and placental barrier, and plays an important role in attenuating the neurotoxicity and developmental toxicity of AVMs. In this study, the mouse neuroblastoma N2a cell line was used to investigate the neurotoxicity of two AVM derivatives: abamectin (ABM) and doramectin (DOR). We found that both these compounds caused significant dose-dependent inhibition of neurite growth in differentiating N2a cells. In addition, Western blotting analysis showed that ABM and DOR significantly inhibited the expression of not only P-gp but also the cytoskeletal proteins, β-actin and β-tubulin. This suggests ABM and DOR may inhibit neurite growth by down-regulating the expression of P-gp and cytoskeletal proteins. Furthermore, knockdown of P-gp expression by RNA interference in N2a cells reduced neurite growth even in the absence of ABM and DOR, and reduced it even more in the presence of low levels of these compounds. These results suggest that even subcytotoxic levels of ABM and DOR can be neurotoxic in differentiating cells and that this neurotoxicity may, at least in part, be the result of the down-regulation of P-gp and cytoskeletal proteins.

Interaction between short-term heat pretreatment and avermectin on 2nd instar larvae of diamondback moth, Plutella xylostella (Linn).

Based on the cooperative virulence index (c.f.), the interaction effect between short-term heat pretreatment and avermectin on 2(nd) instar larvae of diamondback moth (DBM), Plutella xylostella (Linnaeus), was assessed. The results suggested that the interaction results between short-term heat pretreatment and avermectin on the tested insects varied with temperature level as well as its duration and avermectin concentration. Interaction between heat pretreatment at 30 degrees C and avermectin mainly resulted in addition. Meanwhile, pretreatment at 35 degrees C for 2 or 4 h could antagonize the toxicity of avermectin at lower concentrations, which indicated a hormetic effect occurred. The results indicate that cooperative virulence index (c.f.) may be adopted in hormetic effect assessment.

Toxicity of abamectin and doramectin to soil invertebrates

This study aimed at determining the toxicity of avermectins to soil invertebrates in soil and in faeces from recently treated sheep. Abamectin was more toxic than doramectin. In soil, earthworms ( Eisenia andrei) were most affected with LC50s of 18 and 228 mg/kg dry soil, respectively, while LC50s were 67–111 and >300 mg/kg for springtails ( Folsomia candida), isopods ( Porcellio scaber) and enchytraeids ( Enchytraeus crypticus). EC50s for the effect on reproduction of springtails and enchytraeids were 13 and 38 mg/kg, respectively for abamectin, and 42 and 170 mg/kg for doramectin. For earthworms, NOEC was 10 and 8.4 mg/kg for abamectin and doramectin effects on body weight. When exposed in faeces, springtails and enchytraeids gave LC50s and EC50s of 1.0–1.4 and 0.94–1.1 mg/kg dry faeces for abamectin and 2.2–>2.4 mg/kg for doramectin. Earthworm reproduction was not affected. This study indicates a potential risk of avermectins for soil invertebrates colonizing faeces from recently treated sheep.

Potential impact of ABCB1 (p-glycoprotein) polymorphisms on avermectin toxicity in humans

Several members of the ATP binding cassette (ABC) transporter protein superfamily perform xenobiotic efflux functions in mammals, limiting gut absorption, mediating excretion, and controlling entry of a wide range of chemicals to sensitive compartments such as brain, testes and foetus. Perhaps the best characterised of these is p-glycoprotein (gene name ABCB1/MDR1), a barrier epithelia expressed protein with structurally diverse substrates, including the avermectin pesticides. In specific mouse and dog strains, ABCB1 mutations have been identified that result in loss of p-glycoprotein function in the blood brain barrier (BBB) and increased susceptibility to avermectin neurotoxicity. As yet no large rearrangements of the human ABCB1 gene analogous to those in the mouse and dog have been identified. However, numerous human ABCB1 single nucleotide polymorphisms (SNPs) have been identified, the allelic frequencies of which vary with ethnicity. There is no clear consensus on whether or not SNPs, or combinations of SNPs, reduce human p-glycoprotein functionality. However, recent in vivo human data indicate that the two commonest ABCB1 haplotypes both exhibit full BBB functionality. We discuss here the role of p-glycoprotein in limiting brain absorption of avermectin pesticides, as well as the potential impact of the reported functional effects and population frequencies of known ABCB1 polymorphisms on avermectin pesticide risk assessments.

Abamectin in the aquatic environment

Abamectin, widely used as a veterinary anthelmintic, medicine against a variety of animal parasites and insects, can runoff from the sites of application and becomes an aquatic pollutant. The aim of this study was to identify the toxicity of abamectin on bacteria, algae, daphnids, and fish. An extremely high toxicity of avermectin to the survival and reproduction of Daphnia magna was observed in 21-day exposure tests. Zebrafish and the algae Scenedesmus subspicatus are less sensitive to avermectin. The compound is expected to have adverse effects on the aquatic environment due to its high toxicity, even at very low concentrations, to daphnids and to fish.

Toxicity of Avermectins to Diamondback Moth (Lepidoptera: Plutellidae) Populations: Implications for Susceptibility Monitoring

The susceptibility of diamondback moth, Plutella xylostella (L.), larvae to 2 avermectins, abamectin and MK-243 (4-epi-methylamino-4 deoxyavermectin B 1 hydrochloride), was assessed through toxicity evaluations of 17-19 geographically diverse populations. Both avermectins were very potent to 3rd-instar diamondback moth ; LC 50 s for abamectin and MK-243 ranged from 0.4 to 44.0 ng (AI)/ml and 0.2 to 8.0 ng (AI)/ml, respectively. Although most populations showed resistance to methomyl and permethrin, the populations were not resistant to abamectin or MK-243. Pairwise correlations indicated lack of cross or multiple resistance between the avermectins and methomyl and permethrin. This information will serve as an aid for resistance monitoring programs and permit comparative changes in susceptibility during commercial use. Such data are necessary to assist in decisions to recommend product use appropriately in the context of resistance management.

Host plant preference and the influence of different cabbage cultivars on the toxicity of abamectin and cypermethrin against Plutella xylostella Lepidoptera: Plutellidae

SummaryThe toxicity of avermectin B, (abamectin) and cypermethrin was determined against fourth instar larvae of Plutella xylostella L. reared on three cabbage cultivars which differed in their suitability as host plants. Cabbage cultivars were assessed as hosts for P. xylostella on the basis of larval and pupal weight and adult fecundity. Larvae reared on the best host, the cabbage cv. Offenham Flower of Spring were significantly (P &gt; 0.01) less sensitive to topically‐applied abamectin (4.7‐fold at LD50) or cypermethrin (2.3‐fold) when compared with larvae reared on the intermediate host, the Savoy cabbage cv. Aquarius F1. Larvae reared on Offenham Flower of Spring were also significantly (P &gt; 0.01) less sensitive (4.5‐fold) to topically‐applied abamectin compared with larvae reared on the poorest host tested, the cabbage cv. Minicole Fl. In contrast, the residual/ingestion toxicity of abamectin against fourth instars was significantly (P &gt; 0.01) greater (2.5‐fold at LC50) on Offenham Flower of Spring than on Minicole F1. The results are discussed in terms of larval weight and larval feeding rates on the different cabbage cultivars.

Avermectin toxicity in calves and an evaluation of picrotoxin as an antidote.

Avermectin toxicity in calves and an evaluation of picrotoxin as an antidote.

Toxicity of Avermectin to Larva and Adult Soybean Looper (Lepidoptera: Noctuidae) and Influence on Larva Feeding and Adult Fertility and Fecundity

Effects of Avermectin (MK 936) on larval and adult soybean looper (SBL), Pseudoplusia includens (Walker), were investigated in the laboratory and in field-cage tests. Larvae were reared on one of three food types before treatment: artificial pinto bean diet, ‘Ransom’ soybean foliage, or P. includens-resistant ‘GATIR 81-327’ soybean foliage. Larvae reared on artificial diet were less susceptible to MK 936 than larvae reared on either type of soybean foliage. Little difference in larval susceptibility was noted between larvae reared on the two foliage types. Topical LD50 values at 48 h ranged from 0.024 μg per larva (larvae reared on ‘Ransom’ foilage) to 0.203 μg per larva (larvae reared on artificial diet). Moths allowed to feed on various concentrations of MK 936 in 8% sucrose solutions exhibited increased mortality and reduced fertility and fecundity compared with moths given 8% sucrose solutions only. The LC50 of MK 936 at 72 h was 6.1 mg/liter. Unfed and newly emerged moths released into small field cages (five male–female pairs per cage) containing cotton plants sprayed 24 h previously with MK 936 (0.16 kg [AI]/ha) oviposited an average of only 5.9 eggs per plant as compared to a mean of 31.9 eggs per plant in control cages. When moths were released into field cages 72 h postspray, no difference in eggs per plant was noted in sprayed and unsprayed cages.