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At least 19 recordsLinked to original sources

PubMed2000

Effects of sustained-release methoprene and a combined formulation of liquid methoprene and Bacillus thuringiensis israelensis on insects in salt marshes.

Aquatic insects are an important component of the food web in salt marshes, therefore it is necessary to test whether pesticides used to control mosquitoes in salt marshes are safe for nontarget insects. We tested the nontarget effects of a combined formulation (duplex) of Bacillus thuringiensis israelensis (B.t.i.) and liquid methoprene (an insect development regulator) or sustained-release methoprene pellets (Altosid(R) pellets) by applying these materials to replicated salt marsh ponds at maximum label rates. Untreated ponds served as controls. We measured effects of the pesticides by rearing immature mosquitoes (Aedes dorsalis) and water boatmen (Trichocorixa reticulata) in predator-exclusion cages and by monitoring uncaged populations of invertebrates using replicated sweep-net samples. Both pesticides killed caged mosquitoes, and the activity of the Altosid(R) pellets continued through 99 days. There were no detectable effects of either pesticide on the survival or maturation of T. reticulata, or on abundances of uncaged invertebrates. The long-term activity of the pellets could help minimize mosquito abatement activity in salt marshes where there are breeding birds or endangered species. However, other studies suggest that this advantage needs to be balanced against the risks that sustained-release formulations could lead to development of resistance in mosquitoes or that initially undetected nontarget effects could build over time.

Aedes↗

PubMed2003

Developmental toxicity of methoprene and several degradation products in Xenopus laevis.

Methoprene is an insect juvenile growth hormone mimic, which inhibits pupation and is used for the control of emergent insect pests such as mosquitoes. Researchers have hypothesized that methoprene use in US may be a contributing factor to the recent increase in malformed amphibians. However, little is known concerning the developmental toxicity of methoprene and its degradation products in amphibians. In these studies, the aqueous stability and developmental toxicity of methoprene and several degradation products (methoprene acid, methoprene epoxide, 7-methoxycitronellal, and 7-methoxycitronellic acid) were examined. Xenopus laevis embryos (stage 8) were exposed to the test chemicals for 96 h. Assays were conducted under static renewal (24 h) conditions and chemical concentrations in water were measured at the beginning and end of the renewal periods. Methoprene exposure did not result in developmental toxicity at concentrations up to 2 mg/l, which is slightly higher than its water solubility. Methoprene acid, a relatively minor degradation product, produced developmental toxicity when concentrations exceeded 1.25 mg/l. Methoprene epoxide and 7-methoxycitronellal caused developmental toxicity at concentrations of 2.5 mg/l and higher. 7-Methoxycitronellic acid was not developmentally toxic at a test concentration as high as 30 mg/l. The five test chemicals had differential stability in aqueous solution that was in some instances affected by the presence of test organisms. These data indicate that methoprene and its degradation products are not potent development toxicants in X. laevis. This, in combination with the fact that field applications of sustained-release formulations of methoprene result in methoprene concentrations that do not typically exceed 0.01 mg/l, suggests that concerns for methoprene-mediated developmental toxicity to amphibians may be unwarranted.

Abnormalities, Drug-Induced↗

PubMed2001

Low exposure concentration effects of methoprene on endocrine-regulated processes in the crustacean Daphnia magna.

Methoprene is a growth-regulating insecticide that manifests its toxicity to target organisms by acting as a juvenile hormone agonist. Methoprene similarly may exert toxicity to crustaceans by mimicking or interfering with methyl farnesoate, a crustacean juvenoid. We hypothesized that methoprene interferes with endocrine-regulated processes in crustaceans by several mechanisms involving agonism or antagonism of juvenoid receptor complexes. In the present study, we evaluated this hypothesis, in part, by characterizing and comparing the concentration-response curves for methoprene and several endpoints related to development and reproduction of the crustacean Daphnia magna. Our results demonstrate that methoprene has multiple mechanisms of toxicity and low-exposure concentration effects. Methoprene reduced the growth rate of daphnids with evidence of only a single concentration-response line, having a threshold of 12.6 nM. Molt frequency was reduced by methoprene in a concentration-dependent manner, with a response curve corresponding to a 2-segmented line and thresholds at 4.2 and 0.21 nM. An endpoint related to reproductive maturation, the time of first brood deposition, was also affected by methoprene, with a clear concentration-dependent response and a NOEC of 32 nM. Methoprene reduced fecundity according to a 2-segmented line, with thresholds of 24 and < or =0.18 nM. These results demonstrate that methoprene elicits significant toxicity to endocrine-related processes in the 5-50 nM concentration range. Furthermore, molting and reproduction were impacted at significantly lower methoprene concentrations, with a distinct concentration response and a threshold of < or =0.2 nM. The different concentration-dependent response from that of methoprene could involve agonism or antagonism of various juvenoid receptor configurations.

Animals↗

PubMed2005

Evaluation of methoprene effect on Aedes aegypti (Diptera: Culicidae) development in laboratory conditions.

Several Brazilian Aedes aegypti populations are resistant to the larvicidae temephos. Methoprene, that inhibits adult emergence, is one of the alternatives envisaged by the Brazilian Dengue Control Program (PNCD). However, at Brazil vector infestation rates are measured through larvae indexes and it has been claimed that methoprene use in the field could face operational problems. In order to define a standardized protocol, methoprene effect was evaluated in laboratory conditions after continuous exposure of larvae (Rockefeller strain) to a methoprene formulation available to the PNCD. Methoprene-derived mortality occurs mainly at the pupa stage and pupa development is inversely proportional to methoprene concentration. Number and viability of eggs laid by treated and control females are equivalent. A methoprene dose-dependent delay in the development was noted; however, strong correlations were found for total mortality or adult emergence inhibition if data obtained when all control mosquitoes have emerged are compared to data obtained when methoprene-treated groups finish development. The cumulative record of total methoprene-induced mortality at the time control adults emerge is proposed for routine evaluation of field populations. Mortality of all specimens, but not of larva, could account for adult emergence inhibition, confirming the inadequacy of larvae indexes to evaluate methoprene effect.

Aedes↗

PubMed2004

Effects of methoprene, its metabolites, and breakdown products on retinoid-activated pathways in transfected cell lines.

Methoprene (isopropyl (2E,4E)-11-methoxy-3,7,11-trimethyl-2,4-dodecadienoate) is an insect juvenile hormone agonist that blocks metamorphosis in some insects. Recent evidence suggests that a metabolite, methoprene acid, activates vertebrate retinoid X receptors (RXRs), and may interfere with retinoic acid-regulated developmental processes. Methoprene, methoxy-methoprene acid, and two major breakdown products were tested for their ability to interfere with retinoid-regulated pathways when using transfected cells. The CV-1 cells were transiently transfected with genes encoding RXRs and response elements attached to luciferase reporters, and retinoic acid-sensitive F9 cells were stably transfected with retinoic acid receptor (RAR)/RXR response elements attached a lacZ reporter (Sil-REM/beta-gal-NEO). Experiments confirmed that methoxy-methoprene acid acted as a ligand for RXRs and was capable of activating transcription through RAR/RXR response elements. However, neither methoprene nor the breakdown products, 7-methoxycitronellal and 7-methoxycitronellic acid, activated transcription in transfected CV-1 or F9 cells. Methoprene and methoxy-methoprene acid may interfere with the conversion of all-trans-retinol and all-trans-retinaldehyde to all-trans-retinoic acid in the F9-derived cell line. Methoprene was as effective as the retinol dehydrogenase inhibitor citral in blocking the retinol-induced transcription of RAR/RXR-regulated reporter genes, whereas methoxy-methoprene acid blocked transcription stimulated by retinaldehyde.

Acyclic Monoterpenes↗

PubMed2003

Methoprene interferes with mosquito midgut remodeling during metamorphosis.

Many juvenile hormone analogs interfere with insect metamorphosis, a property that makes them useful in insect control and as investigatorial tools with which to study metamorphic mechanisms. We report that one such analog, methoprene, interferes with mosquito metamorphic midgut remodeling. Methoprene treated Aedes aegypti (L.), Aedes albopictus (Skuse), and Culex quinquefasciatus (Say) fourth instars pupate, but the pupal midguts are morphologically similar to larval midguts. The degree of midgut remodeling is affected by the dose of methoprene applied and the extent of fourth instar development when methoprene exposure is initiated. DNA staining indicates that high methoprene concentrations interfere with diploid cell division and programmed death of polytene cells. Lower methoprene concentrations do not interfere with diploid cell division but the removal of polytene cells is incomplete. The effect of methoprene dose on the extent of midgut remodeling correlates well with its effect on pupal and adult survival. Metamorphic midgut remodeling offers a mosquito system with which to study the effect of ecdysone, juvenile hormone and juvenile hormone analogs on metamorphosis. An understanding of the molecular mechanisms by which methoprene affects mosquito metamorphosis might lead to the development of more effective mosquito control chemicals having fewer deleterious environmental effects and to genetic strategies by which mosquito populations might be controlled.

Aedes↗

PubMed1997

Trypanosoma brucei: effects of methoprene and other isoprenoid compounds on procyclic and bloodstream forms in vitro and in mice.

Drug therapy for the treatment of African sleeping sickness is limited by toxicity and resistance and in the last 50 years only one new drug has been introduced for the treatment of the human disease. We report that the juvenile hormone analog, methoprene, and several structurally related isoprenoid compounds kill Trypanosoma brucei in culture. Of the other isoprenoids tested, juvenile hormone III and mammalian retinoid X receptor ligands were the most potent trypanocides. Both the procyclic forms and the bloodstream trypomastigotes are killed by these compounds with LD50 values of 5-30 microM. Of the two methoprene stereoisomers, the EE form was the most active, suggesting that a protein target may be involved in mediating effects of these analogues against the parasite. Methoprene was not, however, able to clear trypanosomes from the blood of infected mice. Methoprene acid, the immediate downstream metabolite of methoprene, is not an effective anti-trypanosomal agent, suggesting that in the mice methoprene is converted to an inactive compound. Since methoprene and its analogues have low and well characterized toxicity in mammals these studies stress the importance of further exploring these isoprenoids as lead compounds for the treatment of African sleeping sickness.

Animals↗

PubMed1994

Integrated management of waste tire mosquitoes utilizing Mesocyclops longisetus (Copepoda: Cyclopidae), Bacillus thuringiensis var. israelensis, Bacillus sphaericus, and methoprene.

This study evaluated the compatibility and efficacy of using a predatory copepod, Mesocyclops longisetus in concert with 3 "biorational" compounds for mosquito control in waste tires. The toxicity of Bacillus thuringiensis var. israelensis (B.t.i), Bacillus sphaericus, and methoprene to Mesocyclops longisetus was assessed in the laboratory using concentrations 10 times the maximum labeled or suggested rate and based on a water depth of 7.6 cm. Microbials were tested using mature copepods exposed for durations of 24, 48, and 72 h. Methoprene bioassays consisted of individually exposing newly hatched copepods (i.e., nauplius larvae) and monitoring their development to maturity. The toxicity tests indicated B.t.i., B. sphaericus, and methoprene were not deleterious to copepods at concentrations exceeding those expected in the field. Copepods exposed to methoprene matured normally, and when mated, 50% developed egg sacs. A 5-month field test, integrating the copepod and B.t.i., B. sphaericus, and methoprene provided better mosquito reduction together than either copepods or control agents alone. When copepods were combined with B.t.i. or methoprene, overall reduction of 3rd- and 4th-instar larvae during the 5-month interval was equal to or greater than 90%. Bacillus thuringiensis var. israelensis alone temporarily produced a high degree of larval reduction (up to 100%), however reapplications were necessary to maintain that level of control. Of all the treatments, B. sphaericus alone produced the lowest degree of mosquito suppression due to lack of toxicity to Aedes albopictus, the predominant species during the study. It is recommended that mosquito control managers consider integrating M. longisetus and B.t.i. or methoprene against mosquitoes in waste tires.

Aedes↗

PubMed2002

High level methoprene resistance in the mosquito Ochlerotatus nigromaculis (Ludlow) in central California.

In the summer of 1998, failures of methoprene field applications to control the mosquito Ochlerotatus nigromaculis (Ludlow) were noticed in several pastures in the outskirts of Fresno, California, USA. Effective control with methoprene had been achieved for over 20 years prior to this discovery. Susceptibility tests indicated that the Fresno Oc nigromaculis populations had developed several thousand-fold higher LC50 and LC90 tolerance levels to methoprene compared with methoprene-naïve populations. The synergists piperonyl butoxide (PBO), S,S,S-tributyl phosphorotrithioate and 3-octylthio-1,1,1-trifluoro-2-propanone had little synergistic effect, suggesting that the mechanism of methoprene tolerance was not mediated by P450 monooxygenase or carboxylesterase enzyme degradation. As part of initiating a resistance management strategy, partial reversion back to methoprene susceptibility was achieved in a resistant population after six consecutive applications of Bacillus thuringiensis israelensis Goldberg & Marga coupled with two oil and two pyrethrum + PBO applications.

Acetone↗

PubMed2005

Efficacy of imidacloprid/permethrin and fipronil/(S)-methoprene combinations against Haemaphysalis longicornis ticks evaluated under in vitro and in vivo conditions.

Haemaphysalis longicornis is one of the most important ticks infesting a wide range of mammals including dogs in Japan. H. longicornis is recorded to be a vector of, for example, Babesia gibsoni. It was the aim of the study presented here to evaluate the efficacy of imidacloprid/permethrin and fipronil/(S)-methoprene against larval, nymphal and adult stages of H. longicornis under in vitro as well as in vivo conditions. In the in vitro part of the study, ticks showed avoidance behaviour to imidacloprid/permethrin-treated filter papers. The onset of acaricidal efficacy in the imidacloprid/permethrin group was recorded earlier than in the fipronil/(S)-methoprene group. In the in vivo experiment three beagles per group were treated with either imidacloprid/permethrin, fipronil/(S)-methoprene or left untreated. Each dog was infested with 30 adult female H. longicornis. Ticks were place on a shaved area of skin of the treated dogs and behaviour of the ticks was recorded as before. After 3 h all ticks were removed and placed in Petri dishes. Ticks were further examined until day 4 post-treatment (p.t.). All ticks recovered from the untreated dogs survived. At 4 h p.t. (1 h post-removal) 40 of the 90 ticks exposed to the imidacloprid/permethrin treatment and 25 of the 90 ticks in the fipronil/(S)-methoprene-treated group were found dead. At day 1 p.t., 61 ticks in the imidacloprid/permethrin- and 81 ticks in the fipronil/(S)-methoprene-treated group were recorded dead. At the final examination day 4 p.t., all 90 ticks were found dead in the imidacloprid/permethrin group, while five ticks remained alive in the fipronil/(S)-methoprene group.

Administration, Topical↗

PubMed2006

Mechanisms of midgut remodeling: juvenile hormone analog methoprene blocks midgut metamorphosis by modulating ecdysone action.

In holometabolous insects such as mosquito, Aedes aegypti, midgut undergoes remodeling during metamorphosis. Insect metamorphosis is regulated by several hormones including juvenile hormone (JH) and 20-hydroxyecdysone (20E). The cellular and molecular events that occur during midgut remodeling were investigated by studying nuclear stained whole mounts and cross-sections of midguts and by monitoring the mRNA levels of genes involved in 20E action in methoprene-treated and untreated Ae. aegypti. We used JH analog, methoprene, to mimic JH action. In Ae. aegypti larvae, the programmed cell death (PCD) of larval midgut cells and the proliferation and differentiation of imaginal cells were initiated at about 36h after ecdysis to the 4th instar larval stage (AEFL) and were completed by 12h after ecdysis to the pupal stage (AEPS). In methoprene-treated larvae, the proliferation and differentiation of imaginal cells was initiated at 36h AEFL, but the PCD was initiated only after ecdysis to the pupal stage. However, the terminal events that occur for completion of PCD during pupal stage were blocked. As a result, the pupae developed from methoprene-treated larvae contained two midgut epithelial layers until they died during the pupal stage. Quantitative PCR analyses showed that methoprene affected midgut remodeling by modulating the expression of ecdysone receptor B, ultraspiracle A, broad complex, E93, ftz-f1, dronc and drice, the genes that are shown to play key roles in 20E action and PCD. Thus, JH analog, methoprene acts on Ae. aegypti by interfering with the expression of genes involved in 20E action resulting in a block in midgut remodeling and death during pupal stage.

Aedes↗

PubMed2005

Toxicity of methoprene as assessed by the use of a model microorganism.

Methoprene is an insect juvenile growth hormone mimic, commonly used as a pesticide. Although widely used for the control of several pests, toxic effects on organisms of different phyla have been reported. These events triggered studies to clarify the mechanisms of toxicity of this insecticide putatively involved in ecological issues. Here we show the effect of methoprene on the normal cell growth and viability of a strain of the thermophilic eubacterium Bacillus stearothermophilus, previously used as a model for toxicological evaluation of other environment pollutants. Respiration studies were also carried out attempting to identify a putative target for the cytotoxic action of methoprene. Cell growth was affected and a decrease of the number of viable cells was observed as a result of the addition of methoprene to the growth medium, an effect reverted by the presence of Ca(2+). Methoprene also inhibited the redox flow of B. stearothermophilus protoplasts before the cytochrome oxidase segment, an effect further studied by individually assessing the enzymatic activities of the respiratory complexes. This study suggests that methoprene membrane interaction and perturbation of cell bioenergetics may underlie the mechanism of toxicity of this compound in non-target organisms.

Calcium↗

PubMed2004

Efficacy of fipronil/(S)-methoprene combination spot-on for dogs against shed eggs, emerging and existing adult cat fleas (Ctenocephalides felis, Bouché).

The inhibitory activities of fipronil (10% (w/v) solution), (S)-methoprene (9% (w/v) solution), and fipronil/(S)-methoprene (10 and 9% (w/v) solution, respectively) combination against eggs and emerging adult cat fleas (Ctenocephalides felis) and adulticidal activity were tested on experimentally infested dogs. Thirty-two Beagle dogs were selected for this study and eight replicates of four animals were formed based on body weight within sex. One dog in each replicate was randomly allocated to treatment with: (1) untreated control; (2) fipronil 10% (w/v) solution, (3) (S)-methoprene 9% (w/v) solution, and (4) fipronil 10% (w/v) and (S)-methoprene 9% (w/v) combination solution. Treatments were applied once topically on Day 0 at the rate of 0.067 ml/kg. On Days -12, -1, 21, and weekly to Day 84 each dog was infested with approximately 200 fleas and comb counted approximately 24h later, or 2 days (our 48 h) after in the case of Day -1 infestation. On Days -11, 1, 22, and weekly to Day 85 each dog was again infested with approximately 200 fleas. Flea eggs were collected over approximately 24 h beginning 3 days after infestation. Fleas were combed off of the dogs and counted at the end of the egg collection period (approximately 96 h count). One aliquot of up to about 100 eggs, if available, from each animal at each infestation time was incubated for approximately 72 h to determine larval hatch and the other for 35 days to determine the number of adults that developed. The 10% (w/v) fipronil spot-on provided excellent control (>95%) of adult fleas on dogs for 5 weeks. Similarly, the combination spot-on of 10% (w/v) fipronil and 9% (w/v) (S)-methoprene provided excellent control of adult fleas, i.e., >95% for 5 weeks. From week 6 post-treatment onward, the relatively low inhibition of adult flea emergence substantiated the lack of significant ovicidal/larvicidal activity in the fipronil (10%, w/v) treatment group. However, the combination product provided excellent (>90%) ovicidal activity for 8 weeks and high (91.4%) inhibition of adult flea emergence for 12 weeks. In addition, a synergistic effect of the two compounds in combination was demonstrated with fipronil enhancing the ovicidal and inhibition of adult flea emergence activity of (S)-methoprene against cat flea eggs. When all stages of the life cycle of the cat flea are considered, the combination spot-on product provided a high level of total flea control yielding a curative effect against adult fleas and inhibition of flea development stages with little to no potential reinfestation pressure on the animal or in the environment for 12 weeks.

Administration, Topical↗

PubMed2005

Development of a HPLC/tandem-MS method for the analysis of the larvicides methoprene, hydroprene, and kinoprene at trace levels using Diels-Alder derivatization.

The invasion and subsequent spread of the mosquito-borne West Nile virus in the United States has resulted in increased use of methoprene. With the increased need for sensitive detection and monitoring of methoprene in the environment, an analytical LC/ESI-MS/MS method has been developed for the analysis of methoprene and two analogues, kinoprene and hydroprene, in water. To improve the ionization efficiency of the nonpolar analytes, a derivatization step with the Cookson-type reagent 4-phenyl-1,2,4-triazoline-3,5-dione (PTAD) was used. Derivatization improved the limit of detection 100-fold. For tandem MS analyses, limits of detection in environmental water samples (S/N = 3) are about 6 pg/mL for methoprene and 20 pg/mL for kinoprene and hydroprene, resulting in limits of quantification (S/N = 10) of 20 pg/mL for methoprene and 60 pg/mL for hydroprene and kinoprene extracted from 10 mL of water. This method was applied to measure methoprene concentrations in water samples from a treated site.

Chromatography, High Pressure Liquid↗

PubMed1995

Activation of mammalian retinoid X receptors by the insect growth regulator methoprene.

We report that methoprene and its derivatives can stimulate gene transcription in vertebrates by acting through the retinoic acid-responsive transcription factors, the retinoid X receptors (RXRs). Methoprene is an insect growth regulator in domestic and agricultural use as a pesticide. At least one metabolite of methoprene, methoprene acid, directly binds to RXR and is a transcriptional activator in both insect and mammalian cells. Unlike the endogenous RXR ligand, 9-cis-retinoic acid, this activity is RXR-specific; the methoprene derivatives do not activate the retinoic acid receptor pathway. Methoprene is a juvenile hormone analog that acts to retain juvenile characteristics during insect growth, preventing metamorphosis into an adult, and it has been shown to have ovicidal properties in some insects. Thus, a pesticide that mimics the action of juvenile hormone in insects can also activate a mammalian retinoid-responsive pathway. This finding provides a basis through which the potential bioactivity of substances exposed to the environment may be reexamined and points the way for discovery of new receptor ligands in both insects and vertebrates.

Animals↗

PubMed1992

The competitive ability and fitness components of the Methoprene-tolerant (Met) Drosophila mutant resistant to juvenile hormone analog insecticides.

The Methoprene-tolerant (Met) mutation of Drosophila melanogaster results in a high (100-fold) level of resistance to the insecticide methoprene, a chemical analog of juvenile hormone. Pest species that are under control with methoprene may therefore have the potential to evolve resistance via a mutation homologous to Met. To evaluate the potential of such mutants to persist in wild populations, we must understand the fitness of flies carrying Met. In the absence of methoprene, Met flies were outcompeted by a wild-type strain both in a multigeneration population cage and in single-generation competition experiments. To determine which fitness component(s) is responsible for the competitive disadvantage, the survival, time of development, and fecundity of flies homozygous for each of five Met alleles were compared with wild type. Small but significant differences were found between the pooled Met alleles and wild type for pupal development time, pupal mortality, and early adult fecundity. These differences result in a large competitive disadvantage. Although Met flies were found to have reduced fitness by these measures, the phenotype is not as severe as might be expected from a knowledge of the disruption of juvenile hormone regulation seen in Met flies. It is concluded that (1) although Met flies have a large advantage under methoprene selection, they will quickly become outcompeted upon relaxation of methoprene usage, (2) even a seemingly severe disruption of juvenile hormone regulation has no drastic effect on the vital functions of the insect and (3) small differences in fitness components can translate into a large competitive disadvantage.

Alleles↗

PubMed1985

Effects of cyromazin and methoprene on the developmental stages of Anopheles dirus, Aedes aegypti and Culex quinquefasciatus (Diptera : Culicidae).

The effects of two chemical compounds, cyromazin and methoprene, on the developmental stages of Anopheles dirus, Aedes aegypti and Culex quinquefasciatus were investigated under laboratory conditions, with the mean temperature of 24 degrees +/- 1 degree C and the relative humidity at 65-75%. Both compounds were tested against the second, third and fourth instar larvae. The concentrations of cyromazin used for An. dirus and Cx. quinquefasciatus ranged from 0.0008 to 0.5 mg/l; and for Ae. aegypti from 0.004 to 2.5 mg/l. The concentrations of methoprene used for An. dirus, Ae. aegypti and Cx. quinquefasciatus ranged from 0.00016 to 0.1 mg/l. The mortality rates were found to be relatively high in larval and pupal stages when treated with cyromazin and methoprene. The primary toxic effects of cyromazin were on the second stage larvae. The LC50 values for cyromazin on the second, third and fourth stage larvae were, respectively, 0.0027, 0.0042 and 0.0114 mg/l for An. dirus, and 0.1662, 0.2307 and 0.3005 mg/l for Ae. aegypti. Cx. quinquefasciatus was the most sensitive species to cyromazin with LC50 values for second, third and fourth stage larvae of 0.0015, 0.0068 and 0.0130 mg/l, respectively. The primary toxic effects of methoprene were in the fourth stage larvae. The LC50 values for methoprene on the second, third and fourth stage larvae were, respectively, 0.0110, 0.0041 and 0.0022 mg/l for An. dirus, and 0.0077, 0.0034 and 0.0025 mg/l for Ae. aegypti. Cx. quinquefasciatus was the most sensitive species to methoprene, with LC50 values for second, third and fourth stage larvae of 0.0013, 0.0008 and 0.0006 mg/l, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aedes↗

PubMed1996

Genetic evidence that mutants of the methoprene-tolerant gene of Drosophila melanogaster are null mutants.

The Methoprene-tolerant (Met) mutation of Drosophila melanogaster results in resistance to juvenile hormone (JH) or JH analogs and appears to alter JH reception during late larval development. Several alleles of Met have been recovered from methoprene selection screens after mutagenesis with ethyl methanesulfonate, X-rays, or transposable genetic elements. The phenotype of files carrying any of these alleles is similar-resistance to the toxic and morphogenetic effects of methoprene-but otherwise is essentially wild-type. Understanding the function of the Met gene requires that we know whether these alleles are hypomorphic, producing some functional gene product, or amorphic, producing no functional gene product. This determination was made by comparing the methoprene-resistance phenotype produced by representative Met alleles with that produced by a chromosome carrying a deficiency that deletes the Met gene. The level of resistance to either the toxic or the morphogenetic effect of methoprene was similar among files heterozygous for either the deficiency chromosome or for any of the alleles. The results provide genetic evidence that the Met alleles recovered to date are amorphic and suggest that the Met gene may not be mutable to a more severe Met allele that affects the viability, development, or reproduction of the flies.

Animals↗