Disease relevance of aldicarb

• In contrast, GOA-1 (Goalpha) and DGK-1 (diacylglycerol kinase) appear to negatively regulate synaptic transmission, because reducing their function results in strong aldicarb hypersensitivity and hyperactive locomotion [1].
• The toxicity of aldicarb to adult males was significantly lowered by E2 and T whereby the mortality percentage was reduced to 23.3 +/- 5.8% and 3.3 +/- 5.8%, respectively, compared to the fish not receiving steroids (46.7 +/- 5.8% mortality) [2].
• Aldicarb was tested for its ability to induce chromosomal aberrations in human peripheral lymphocytes in vitro, in the presence of an exogenous metabolic activation system [3].
• Enzyme and locomotion changes due to carbamate treatment were investigated during and following oral administration of aldicarb (0.2 mg/kg body weight/day x 7) to six-day-old chicks [4].
• Analysis of the hydrolysis/dehydration rate constants showed that anaerobic cultures enhanced the rate of conversion of aldicarb by 4-fold for acclimated cultures and by 2-fold for unacclimated cultures compared to the rate of abiotic hydrolysis (p < 0.05) [5].

Psychiatry related information on aldicarb

• Motor activity assessment showed that aldicarb did not produce any activity depression in PND17 rats, whereas the data for the PND27 and adult rats overlapped [6].
• The neuropharmacologic effects of chronic dosing with aldicarb, AChE inhibition and dopaminergic modulation could be useful for treatment of memory deficits related to CNS disorders [7].

High impact information on aldicarb

• We sought other components of the Goalpha-G(q)alpha signaling network by screening for aldicarb-resistant mutants with phenotypes similar to egl-30 (G(q)alpha) mutants [8].
• Release of acetylcholine from motor neurons was assayed by measuring the sensitivity of intact animals to the acetylcholinesterase inhibitor aldicarb [9].
• EGL-30 and EGL-8 appear to positively regulate synaptic transmission because reducing their function results in strong aldicarb resistance and slow locomotion rates [1].
• Furthermore, rab-3 animals were resistant to the acetylcholinesterase inhibitor aldicarb, suggesting that cholinergic transmission was generally depressed [10].
• The down-regulation of ceGAT-1 by RNAi leads to an interesting phenotype associated with altered function of body muscles (as evident from changes in thrashing frequency) and enteric muscles (as evident from the rates of defecation failure) and also with altered sensitivity to aldicarb-induced paralysis [11].

Chemical compound and disease context of aldicarb

• Discovery of aldicarb and its oxidative sulfoxide and sulfone metabolites in well or ground water in Florida, Wisconsin, and New York, and accidental poisonings from ingesting contaminated watermelons and cucumbers in the South and West have spurred interest and concern about this pesticide [12].
• These positive results demonstrate that propoxur, methomyl, and aldicarb are capable of inducing structural and/or numerical chromosomal aberrations in mammalian cells either in vitro or in vivo [13].
• The toxicity of Temik (aldicarb) in Nubian goats [14].
• Individual and combined toxicity of three pesticides, endosulfan, phosphamidon, and aldicarb was evaluated in P. conchonius [15].
• The findings, however, did reveal a spatial association between the breast cancer incidence rates and the application of three selected pesticides [Aldicarb, Atrazine and Lindane (thought to potentially mimic oestrogen)] in rural Leicestershire [16].

Biological context of aldicarb

• The resistance to aldicarb was rescued by introducing a ric-19 transgene into the ric-19 mutant background [17].
• The current study examines the toxicity, AChE inhibition, plasma kinetics, and in vivo metabolism of aldicarb in channel catfish [18].
• The aim of this work was to investigate the effects of Aldicarb on human lymphocytes in vitro in the presence of an exogenous metabolic activation system [19].
• Muscle AChE activity showed no significant relationship with salinity, although the IC50 of aldicarb to muscle AChE differed significantly between 6.21 +/- 1 [20].
• Isocratic high-performance liquid chromatographic separation and multiple-wavelength ultraviolet detection of aldicarb and its soil degradation products. Optimization of stationary phase selectivity [21].

Anatomical context of aldicarb

• (2) Laboratory study: The direct effect of obidoxime and of pralidoxime on acetylcholinesterase activity in vitro was investigated in normal human packed red blood cells pretreated with an organophosphate (paraoxon) or a carbamate (aldicarb or methomyl) [22].
• These data together suggested that aldicarb affects the macrophage functions by interfering with IL-1 production and that it does not affect the T cell functions directly [23].
• Also, the decreased stimulation of D10.G4 clone by aldicarb-treated macrophages was reconstituted when exogenous recombinant IL-1 was added to the cultures [23].
• Salinity increased flavin-containing monooxygenase (FMO) mRNA expression and catalytic activities in microsomes of liver, gill, and kidney of rainbow trout, which was consistent with the salinity-induced enhancement of aldicarb toxicity [24].
• Induction of sister-chromatid exchanges in cultured human lymphocytes by Aldicarb, a carbamate pesticide [19].

Associations of aldicarb with other chemical compounds

• A method is described for the determination of aldicarb and its metabolites (the sulphoxide and sulphone) in urine by gas chromatography with flame photometric detection (GC-FPD) [25].
• Assessment of the ability of propoxur, methomyl, and aldicarb, three carbamate insecticides, to induce micronuclei in vitro in cultured Chinese hamster ovary cells and in vivo in BALB/c mice [13].
• A reversed-phase high-performance liquid chromatographic (HPLC) method has been developed for the determination of trace concentrations of benomyl, carbendazim, aldicarb, aldicarb sulphoxide and aldicarb sulphone in drinking water [26].
• Less NTE inhibition was observed when either aldicarb or verapamil was included in the incubation of SY-5Y cells with mipafox [27].
• We propose an uptake pathway for aldicarb, levamisole, peptide mimetics and other soluble molecules by retrograde transport along dendrites of chemoreceptive neurons to the cell bodies and synapses where they act [28].

Gene context of aldicarb

• On the basis of the aldicarb resistance phenotype, we named the gene ric-19 (resistance to inhibitors of cholinesterase-19) [17].
• Finally, the dys-1 mutants are hypersensitive to acetylcholine and to the acetylcholinesterase inhibitor aldicarb, suggesting that dys-1 mutations affect cholinergic transmission [29].
• Methyl paraoxon and aldicarb had a higher affinity for plasma AChE than for BChE or CaE [30].
• When BChE was absent, aldicarb toxicity was not affected [30].
• Concentration-response curves for the toxicants arsenite and aldicarb, both of which affect motility, were determined for wild-type and several mutant strains, identifying P-glycoprotein mutants as not significantly more sensitive to either compound, while cat-4 mutants are more sensitive to arsenite but not aldicarb [31].

Analytical, diagnostic and therapeutic context of aldicarb

• Determination of aldicarb and its derivatives in groundwater by high-performance liquid chromatography with UV detection [32].
• Aldicarb administered at concentrations less than 0.005 microgram/kg body wt failed to cause significant immunosuppression [23].
• Construction of an acetylcholinesterase-choline oxidase biosensor for aldicarb determination [33].
• No correlation existed between CYP isoform expression (determined by western blot) and aldicarb sulfoxidation rates, suggesting the involvement of an unmeasured CYP isoform or involvement of several isoforms with low specificity [34].
• Adding a fourth sensor (neuronal microelectrode array) to the test battery allowed detection of two additional chemicals (aldicarb and methamidophos), but the neuronal microelectrode array was overly sensitive to paraquat [35].

References