Disease relevance of diazinon

• A completed termination event at tR2 requires both the nusA gene protein and the previously described E. coli termination factor rho [1].
• In mice whose oxidative metabolism had been increased with beta-ionone or in which esterase metabolism had been inhibited by diazinon, the severity of the toxicity was increased but the intraacinar origin of the lesion did not change [2].
• To determine the location of DNA sequences required for the utilization of rho factor in transcription termination at the tR1 terminator of phage lambda, we constructed and analyzed a series of deletion mutants affecting several distinct regions of the cro-gene sequence [3].
• Three groups of eight dogs each were studied to evaluate the early evolution of the hyperamylasemia, hyperlipasemia, and acinar cell pathology at the light and electron microscopic levels during acute Diazinon-induced pancreatitis [4].
• Treatment with diazinon (40 mg/kg, i.p.) resulted in hyperglycemia and depletion of glycogen from cerebral and peripheral tissues 2 hr after its administration in rats [5].

Psychiatry related information on diazinon

• These findings suggest that diazinon may interfere with airway defense mechanisms by reducing the activity of RARs [6].
• Core temperature (Tc) and motor activity (MA) were monitored by radiotelemetry in male and female rats of the Long-Evans strain dosed orally with diazinon (0 [corn-oil vehicle], 100, 200, or 300 mg/kg in males and 0, 50, 100, or 200 mg/kg in females) [7].
• 109 college man and 76 college women ranging in age from 17 to 50 years and having an average age of 21 yr. completed Coopersmith's Self-esteem Scale and Elison's Compass of Shame Scale which measures four shame-focused coping styles [8].
• Development and evaluation of a youth mental health community awareness campaign - The Compass Strategy [9].

High impact information on diazinon

• The high density lipoprotein (HDL)-associated enzyme paraoxonase (PON1) contributes significantly to the detoxication of several OPs (Fig. 1). The insecticides parathion, chlorpyrifos and diazinon are bioactivated to potent cholinesterase inhibitors by cytochrome P-450 systems [10].
• Understanding the molecular mechanism of specific and polarized termination of DNA replication at a sequence-specific replication terminus requires detailed analyses of the interaction of terminator protein (ter) with specific DNA sequences (tau), constituting the replication terminus [11].
• Furthermore, PCR analysis of pinned specimens of Australasian L. cuprina collected before the release of organophosphate insecticides reveals no cases of the diazinon-resistance change but several cases of those associated with malathion resistance [12].
• The pinned specimen analysis also shows much higher genetic diversity at the locus before organophosphate use, suggesting that the subsequent sweep of diazinon resistance in Australasia has compromised the scope for the locus to respond further to the ongoing challenge of the insecticides [12].
• Purified Tus protein alone is necessary and sufficient to arrest DNA replication on ColE1-type plasmid templates containing ter sites [13].

Chemical compound and disease context of diazinon

• The extent of growth of two Pseudomonas strains in media containing diazinon and malathion was in the range expected from the amount of insecticide supplied, and their proliferation resulted in disappearance of the chemical [14].
• Chlorpyrifos (CPF) and diazinon (DZN) are thionophosphorus organophosphate (OP) insecticides; their toxicity is mediated through CYP metabolism to CPF-oxon and DZN-oxon, respectively [15].
• The toxicity of two relevant pesticides (diazinon and methyl parathion) and two metals (chromium and mercury) to C. cornuta was evaluated and compared to the standard organisms for ecotoxicological testing: Daphnia magna and Vibrio fischeri [16].
• Atrazine concentrations as low as 5 microg/L in combination with diazinon significantly increased toxicity to C. dubia compared to diazinon alone [17].
• The toxicity of dimethoate, azinphos-methyl, diazinon, pirimiphos methyl, organophosphorus insecticides, and benomyl (a benzimidazole fungicide) singly and in mixture was studied in a human neuroblastoma cell line, SH-SY5Y [18].

Biological context of diazinon

• Tus protein-catalyzed termination depends upon the orientation of the ter site in the plasmid DNA [13].
• Three new potential Ter sites, referred to as TerH, TerI, and TerJ, were identified by searching the E. coli genome for sequence similarity to a consensus Ter site sequence [19].
• In this study, mutant Ter sites carrying single base pair substitutions at 16 different positions were examined for their ability to bind purified Tus protein and arrest DNA replication [19].
• Twenty-nine early promoters from bacteriophage T4 and 14 early promoters from bacteriophage T6 were isolated using vector M13HDL17, a promoterless derivative of M13mp8 carrying a linker sequence, the bacteriophage lambda-terminator tR1, and the lacZ' gene including part of its ribosome-binding site [20].
• Modified and susceptible phenotypes showed increased asymmetry score for temperatures and larval densities above and below standard rearing conditions; a positive correlation was observed between diazinon concentration and asymmetry score [21].

Anatomical context of diazinon

• Our results indicate that structural changes in the diazinone molecule shift the mechanism of action for the positive inotropic effect of the diazinone derivatives in the intact cell from a predominant myofilament sensitization (EMD 54622) to an enhancement in cell Ca2+ loading and an augmentation in the Cai transient (EMD 54650) [22].
• Novel diazinone derivatives separate myofilament Ca2+ sensitization and phosphodiesterase III inhibitory effects in guinea pig myocardium [22].
• Pretreatment of hepatocytes with diazinon (100 microM), an esterase inhibitor, enhanced PG-induced cytotoxicity [23].
• Light-activated destruction of cancer cell nuclei by platinum diazide complexes [24].
• Most notably, we observed decreases in both the splenic T-dependent antibody response to sheep erythrocytes and the splenic T-independent antibody response to DNP-ficoll and a dramatic thymic atrophy in mice exposed to cocaine + diazinon, which were not seen in mice exposed to cocaine alone [25].

Associations of diazinon with other chemical compounds

• We have investigated the effects and the mechanism of action of novel diazinone derivatives, EMD 54622, EMD 53998, and EMD 54650 (developed by E. Merck, Darmstadt), on guinea pig myocardial preparations [22].
• Odds ratios for organophosphates paralleled the World Health Organization hazard classifications, with parathion much higher than diazinon or malathion [26].
• These results indicate that T cells, especially immature thymocytes located in the thymus, are sensitive to effects associated with the combined treatment of cocaine + diazinon [25].
• The activities of the hepatic gluconeogenic enzymes fructose 1,6-diphosphatase and phosphoenolpyruvate carboxykinase were also increased significantly in diazinon-treated animals [5].
• Identification of photocatalytic degradation products of diazinon in TiO2 aqueous suspensions using GC/MS/MS and LC/MS with quadrupole time-of-flight mass spectrometry [27].

Gene context of diazinon

• DNA sequences of all the RET/GDNF/NTN coding regions were determined using a direct DyeDeoxy Terminator Cycle method [28].
• Diazinon is activated by CYP2C19 in human liver [29].
• These data indicate that CYP2C19 is the major enzyme involved in diazinon activation in human liver, while other enzymes including CYP1A2 may play a more minor role [29].
• Time- and money-saving one-directional Big Dye Terminator cycle sequencing is shown to provide reliable high resolution typing of the HLA-A alleles, even in a few cases of two amplicons in one primer reaction mixture [30].
• This research describes both the activation and detoxification of diazinon, chlorpyrifos and parathion by recombinant P450 isozymes and by human liver microsomes that had been characterised for P450 marker activities [31].

Analytical, diagnostic and therapeutic context of diazinon

• DESIGN AND SETTING: Retrospective cohort study of administrative and quality-of-care data on HMOs from the National Committee for Quality Assurance (NCQA) annual Quality Compass databases for 1997, 1998, and 1999, including Health Plan Employer Data and Information Set (HEDIS) quality scores [32].
• Modification of diazinon-induced changes in carbohydrate metabolism by adrenalectomy in rats [5].
• The impurities present in commercial diazinon preparations have been examined by high performance liquid chromatography with particular reference to the ability of these compounds to cause porphyrin accumulation in cultures of chicken embryo liver cells [33].
• Analysis of the diazinon metabolites G 27550 and GS 31144 by gas-liquid chromatography with nitrogen-specific detection after derivatization [34].
• The immunoassays were used as a tool to quantify diazinon in natural waters [35].

References