Disease relevance of Methoprene

• Finally, feeding males with fluvastatin, a juvenile hormone (JH) inhibitor, also led to start/stop feminization, and this effect is reversible by the simultaneous application of methoprene, a JH analog, suggesting the existence of a neuroendocrine control, by JH, of such behavioral dimorphism [1].
• These results demonstrate that methoprene elicits significant toxicity to endocrine-related processes in the 5-50 nM concentration range [2].
• 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 [3].
• Methoprene exposure resulted in a concentration-dependent increase in the metabolic androgenization ratio [4].
• The invasion and subsequent spread of the mosquito-borne West Nile virus in the United States has resulted in increased use of methoprene [5].

Psychiatry related information on Methoprene

• Exposure to 160 nM methoprene along with food deprivation and crowding caused a significant reduction in the percentage of males produced during the early phase of the sexual cycle and significantly increased the percentage of males produced during the later stages of the cycle [6].

High impact information on Methoprene

• Transformation of Met flies with a Met+ cDNA resulted in susceptibility to methoprene, indicating that the cDNA encodes a functional Met+ protein [7].
• Although Met27 homozygotes have reduced oogenesis, they are viable, demonstrating that Met is not a vital gene [8].
• The Met mutant of Drosophila melanogaster is highly resistant to juvenile hormone III (JH III) or its chemical analog, methoprene, an insect growth regulator [9].
• This protein and a second 29-kDa protein (pI 6.0) were labeled by MDK, but excess unlabeled methoprene or MDK only prevented binding to the latter [10].
• In similar studies, methoprene and hydroprene competed for [125I]IVMA binding sites but JH I, JH II, and JH III were all ineffective [11].

Chemical compound and disease context of Methoprene

• Methoprene similarly may exert toxicity to crustaceans by mimicking or interfering with methyl farnesoate, a crustacean juvenoid [2].
• 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 [12].
• Bacillus thuringiensis var. israelensis and pyriproxyfen produced LC50 values of 6.1 x 10(11) International Toxic Units (477 times the EFC) and 0.854 ppm (106 times the EFC), respectively. s-Methoprene was the least toxic compound, with no mortality recorded at 500 times the EFC [13].
• In 1992, Altosid (methoprene) pellets, Abate (temephos) 5 CG, and Bactimos (Bacillus thuringiensis serovar israelensis) granules were applied aerially to small field plots within a Culiseta breeding swamp [14].
• Determination of toxicity of danitol, methoprene and neem formulation against stored grain pest, sitophilus oryzae L [15].

Biological context of Methoprene

• Previous results have demonstrated a mechanism of resistance involving an intracellular JH binding protein that has reduced ligand affinity in Met flies [8].
• In competition studies, JH II and JH III competed for 3H-JH I binding sites, whereas IVMA, hydroprene, and methoprene did not [11].
• Furthermore, topical methoprene application to pupae leads to the ectopic accumulation of JhI-1 and JhI-26 transcripts [16].
• The juvenile hormone analogue, methoprene, inhibits ecdysterone induction of small heat shock protein gene expression [17].
• When Vg synthesis was prematurely induced by injection of methoprene into fifth-stage female larvae, the kinetics of mRNA accumulation were similar to those of primary stimulation in the adult [18].

Anatomical context of Methoprene

• Levels of vitellogenin (Vg) mRNA in Locusta migratoria fat body were determined as indicators of gene expression induced by the juvenile hormone analog methoprene [18].
• Here we show that application of the juvenile hormone analogue methoprene mimics the Sex-Peptide-mediated stimulation of vitellogenic oocyte progression in sexually mature virgin females [19].
• During the primary response to methoprene (in female locusts in which the corpora allata had been destroyed immediately after emergence), Vg mRNA was first detected after 18-24 hr and accumulated rapidly between 36 and 48 hr [18].
• Treatment of another subset of dark-reared bees with the JH analog, methoprene, also had no effect of the growth of the MB neuropil [20].
• To study the effect of flight experience and juvenile hormone on these changes within the mushroom bodies, young worker bees were treated with the juvenile hormone analog methoprene but a subset was prevented from foraging (big back bees) [21].

Associations of Methoprene with other chemical compounds

• Using an ethyl methane sulfonate mutagenesis screen, we have selected two noncomplementing mutants, one of which is nearly 100 times more resistant than wild-type to either methoprene or juvenile hormone III topically applied or incorporated into the diet [22].
• The methoprene-resistant mutations, Met1 and Met2, were 10 and 6 times more resistant to S31183 in the white puparial assay and about 20 times more resistant in the larval feeding experiments than the wild-type, indicating that the effects seen are typical of JH [23].
• Effects of methoprene, its metabolites, and breakdown products on retinoid-activated pathways in transfected cell lines [24].
• Competition between juvenile hormone antagonist precocene II and juvenile hormone analog: methoprene in the nematode Caenorhabditis elegans [25].
• A solid phase extraction reversed-phase HPLC method for the simultaneous determination of methoprene, permethrin and selected metabolites in rat plasma and urine [26].

Gene context of Methoprene

• As we predicted, methoprene phenocopies a subset of previously described BRC defects; it also phenocopies Deformed and produces abnormalities not associated with known mutations [27].
• In Drosophila melanogaster L57 cells, the JHRE-regulated reporter gene was induced by JH I, JH III, methoprene, and hydroprene [28].
• Since the Met mutation also confers resistance to methoprene-induced abnormalities in adult cuticle formation, the autonomy of Met expression could be evaluated in flies mosiac for this mutation [22].
• Treatment of blood-fed females with methoprene, an analogue of JH, resulted in decrease of the Tsf message [29].
• The JH analog, methoprene, increased both JH esterase and EH activity as high as 2.5-fold [30].

Analytical, diagnostic and therapeutic context of Methoprene

• 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 [31].
• Here, I present evidence that the JH analog methoprene applied to final instar larvae of a stalk-eyed fly (Cyrtodiopsis dalmanni) can induce males to produce larger eye-stalks relative to their body size [32].
• Ecdysteroid-dependent proliferative arrest and differentiation are blocked by coculture with methoprene but methoprene has no effect on ecdysteroid-dependent proliferation [33].
• Results from the field trials and comparison bioassays indicated that the causes of the poor inhibition were an existing cross-resistance to methoprene followed by an induction of resistance resulting from the continuous exposure to methoprene [34].
• Vg-1 mRNA appeared after treatment with the juvenile hormone analogue, methoprene, implying transcriptional regulation [35].

References