Disease relevance of diuron

• Deletion of fesM (fesM-D) led to an inability for Synechococcus cells to grow in the presences of glycerol and 3-(3,4-dichlorophenyl)-1,1-dimethylurea [1].
• Quenching was investigated in both a photosystem II-less mutant, and DCMU-poisoned wild-type Synechocystis sp. PCC 6803 [2].
• Medaka embryos exposed to diuron, desmethyl diuron, or siduron displayed dose-dependent delays in hatch, and elevated concentrations of diuron and desmethyl diuron produced developmental toxicity [3].
• However, no H2 production was measured in photoautotrophy if PSII was not inhibited by DCMU, due to the fact that anoxia was not reached [4].
• A smaller subclone of this gene (2.5 kb) expressed in E. coli coded for the protein that degraded diuron [5].

Psychiatry related information on diuron

• During the first six days, a latency period was observed both in the algal and the bacterial communities despite favorable abiotic conditions and independently of diuron exposure [6].

High impact information on diuron

• Similarly, inhibition of photosynthesis and hence of the release of photosynthetic products as a result of prolonged darkness and 3-(3,4-dichlorophenyl)-1,1-dimethyl urea (DCMU) treatment also abolishes persistence [7].
• In contrast, DCMU had no effect on either the abundance or the polyribosome profiles of endogenous histone H1 or transgenic P35S::CAT transcripts [8].
• The Fed-1 mRNA has a half-life of approximately 2.4 hr in the light and a half-life of only 1.2 hr in the dark or in the presence of the photosynthetic electron transport inhibitor 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) [9].
• Preincubation of thylakoids with diuron leads to a conformational change in the 32,000-dalton protein, modifying its trypsin digestion and preventing expression of diuron insensitivity [10].
• Thus, the rapidly metabolized 32,000-dalton thylakoid protein in Spirodela chloroplasts fulfills the requirements of the hypothesized "proteinaceous shield" [Renger, G. (1976) Biochim. Biophys. Acta 440, 287-300] regulating electron flow through photosystem II and mediating diuron sensitivity [10].

Chemical compound and disease context of diuron

• We have carefully characterized and reexamined the motility and phototactic responses of Synechocystis sp. adenylyl cyclase (Cya1) and catabolite activator protein (SYCRP1) mutants to different light regimens, glucose, 3-(3,4-dichlorophenyl)-1,1-dimethylurea, and cyclic AMP [11].
• The expression of group 2 sigma factors is characterized in a cyanobacterium Synechocystis sp. PCC 6803 grown in culture, changing light conditions (white, red and blue light, and darkness), or the presence of drugs (rifampicin, chloramphenicol, DCMU, and DBMIB), and the roles of these sigma factors are elucidated [12].
• We have cloned and sequenced a gene of the cyanobacterium Synechocystis sp. strain PCC 6803 named dspA (encoding drug sensory protein A; DspA), mutations in which result in cross-resistance to the herbicides difunon and diuron, as well as to the calmodulin antagonists chlorpromazine and trifluoperazine [13].
• The following increasing order of toxicity was obtained: Cd < Zn < Cu < Diuron < Zn pyrithione < Irgarol 1051 [14].
• Targeted pesticide analysis identified simazine and diuron as the major pesticides present and, using a toxicity unit (TU) approach. were shown to be responsible for a significant amount of the observed concentrate toxicity during a runoff event [15].

Biological context of diuron

• The rapidly metabolized 32,000-dalton polypeptide of the chloroplast is the "proteinaceous shield" regulating photosystem II electron transport and mediating diuron herbicide sensitivity [10].
• Analysis of QA- decay kinetics in the absence of 3-(3,4-dichlorophenyl)-1,1-dimethyl urea indicated a defect in electron transfer from QA- to QB, whereas experiments performed in the presence of this herbicide indicated that the recombination rate between QA- and the S2 state was strongly retarded [16].
• Degradation of the mutated kinase and cell death in bright light can be suppressed by inhibiting photosynthetic electron flow (PS-EF) with 3-(3,4-dichlorophenyl)-1,1-dimethylurea [17].
• Interfering with D1 function by mutations or by incubation with DCMU prevented the increase in ROS formation at HL and the concomitant down-regulation of LSU synthesis [18].
• 3. The inhibition by DCMU of palmitoylcarnitine oxidation by isolated liver mitochondria was used to calculate a flux control coefficient of the respiratory chain towards gluconeogenesis [19].

Anatomical context of diuron

• The protection exerted by DCMU is seen only in Cl(-)-depleted thylakoid membranes [20].
• Impact of diuron on aneuploidy and hemocyte parameters in Pacific oyster, Crassostrea gigas [21].
• The innovative bioassay described here involves chlorophyll a fluorescence measurements of gametes from the macroalgae, Hormosira banksii, where gametes (eggs) were exposed to Diuron, Irgarol and Bromacil [22].
• On the other hand, the number of fetuses in the litters from diuron-treated rats was slightly smaller than litters from control rats [23].
• Fertilisation of Acropora millepora and Montipora aequituberculata oocytes were not inhibited at diuron concentrations of up to 1000 microg l(-1) [24].

Associations of diuron with other chemical compounds

• Under these conditions, photoreduction of ferricyanide becomes insensitive to diuron [3-(3,4-dichlorophenyl)-1,1-dimethylurea], an inhibitor of photosystem II electron transport [10].
• In the present work the mutated amino acid residues from nine antimycin- and three diuron-resistant mutants have been identified by sequencing the relevant segments of the resistant cytochrome b gene [25].
• In light-, but not in dark-grown spinach seedlings, the mRNAs for the nuclear-encoded photosystem I subunits D, F and L are associated with polyribosomes and this association is prevented by the application of 3-(3',4'-dichlorophenyl)-1,1'-dimethyl urea (DCMU), an inhibitor of the photosynthetic electron transport [26].
• The activation of a fraction of PSII population (about 20%-30%) was light and temperature-dependent but did not require electron flow to plastoquinone [was not inhibited by 3-(3,4-dichlorophenyl)-1,1-dimethylurea] [27].
• In PS II samples at pH 6 in the presence of PMS, NH2OH, and DCMU, EPR measurements show that QA- is formed with high yield upon a 1 s illumination at 10 degrees C, while no radical from the electron donor side of PS II is detected [28].

Gene context of diuron

• The psbA gene of DCMU-resistant Euglena gracilis has an amino acid substitution at serine codon 265 [29].
• Diuron induced CYP1A1 mRNA levels in mouse hepatoma (Hepa1c1c7) cells and AhR-dependent luciferase reporter gene expression in stably transfected mouse, rat, guinea pig, and human cell lines [30].
• The increase in Arf1 mRNA at the beginning of the light period, however, was shown to be light-dependent, and, moreover, dependent on photosynthesis, since it was prevented by DCMU [31].
• Mitochondrial heredity of resistance to 3-(3,4-dichlorophenyl)-1,1-dimethylurea, an inhibitor of cytochrome b oxidation, in Saccharomyces cerevisiae [32].
• In addition, ligand binding and gel retardation analysis demonstrated the ability of diuron to competitively bind to and stimulate AhR transformation and DNA binding in vitro and in intact cells [30].

Analytical, diagnostic and therapeutic context of diuron

• The simetric triazines and bromacil were analyzed by gas chromatography and diuron by HPLC [33].
• An on-line immunoaffinity column with liquid chromatography/tandem mass spectrometry (IAC-LC-MS/MS) method for the determination of diuron in water matrices was described [34].
• The use of highly active PSII particles in combination with the flow system resulted in a reusable herbicide biosensor with good stability (50% of initial activity was still remaining after 35-h use at 25 degrees C) and high sensitivity (detection limit for diuron was 5 x 10(-10) M) [35].
• Combined supercritical-fluid chromatography/mass spectrometry in the analysis of diuron in plasma using on-line phase-system switching [36].
• The SPE materials were obtained by thermal immobilization of appropriate polysiloxanes onto 40 microm silica surfaces and were used in sample preparation for multiresidue analysis of the following pesticides: tebuthiuron and diuron (urea herbicides), simazine, atrazine and ametryn (triazines herbicides) and benomyl (benzimidazol fungicide) [37].

References