Disease relevance of Phenaclor

• Purification, cloning and sequencing of an enzyme mediating the reductive dechlorination of 2,4,6-trichlorophenol from Desulfitobacterium frappieri PCP-1 [1].
• Genetic and biochemical characterization of a 2,4,6-trichlorophenol degradation pathway in Ralstonia eutropha JMP134 [2].
• The other type includes strains belonging to the genera Pseudomonas, Sphingomonas, or Sphingopixis, which do not have tcp-like gene sequences and degrade this pollutant less efficiently and which therefore grow only as small colonies on plates with 2,4,6-TCP [3].
• Rhodococcus percolatus sp. nov., a bacterium degrading 2,4,6-trichlorophenol [4].
• Degradation of 2,4,6-trichlorophenol by Azotobacter sp. strain GP1 [5].

High impact information on Phenaclor

• The analysis of chlorinated phenols (2-chlorophenol, 3-chlorophenol, 4-chlorophenol, 2,4-dichlorophenol, 2,4,6-trichlorophenol, pentachlorophenol) in river water was accomplished using off-line solid-phase extraction (SPE) and capillary electrophoresis coupled with electrochemical detection [6].
• Investigations currently focus on a wider range of CP substrates (PCP, 2,4,6-trichlorophenol (2,4,6-TCP), 2,4,5-TCP, and 2,4-dichlorophenol (2,4-DCP)) to establish their reactivity toward dG and duplex DNA (calf thymus (CT)) following activation by HRP/H2O2, as a representative peroxidase system [7].
• We report here the ability of a previously unexposed forest soil microbiota to degrade high levels of 2,4,6-TCP and describe the changes in the soil microbial community found by terminal restriction fragment length polymorphism (T-RFLP) analysis [8].
• Three enzyme activities encoded by tcp genes, 2,4,6-TCP monooxygenase (tcpA), 6-chlorohydroxyquinol 1,2-dioxygenase (tcpC), and maleylacetate reductase (tcpD), are involved in this catabolic pathway [3].
• Ralstonia eutropha JMP134 can grow on several chlorinated aromatic pollutants, including 2,4-dichlorophenoxyacetate and 2,4,6-trichlorophenol (2,4,6-TCP) [2].

Chemical compound and disease context of Phenaclor

• Resting cells of 2,4,5-trichlorophenoxyacetic acid-grown Pseudomonas cepacia AC1100 metabolize both dichlorophenols, such as 2,4-dichlorophenol, 2,6-dichlorophenol, 3,4-dichlorophenol, and 3,5-dichlorophenol, and more highly substituted phenols, such as 2,4,6-trichlorophenol and pentachlorophenol, to the corresponding chlorohydroquinones [9].
• A bacterial strain that was able to mineralize 2,4,6-trichlorophenol was isolated from a chlorophenol-fed percolator and was identified as a member of the genus Rhodococcus on the basis of chemotaxonomic characteristics and 16S RNA phylogenetic inference data [4].
• Following subcultivation with thiosulfate as alternative electron acceptor and cocultivation with Clostridium celerecrescensT, the 2,4,6-trichlorophenol-dehalogenating bacterium Desulfitobacterium frappieri strain TCP-A was isolated and characterized regarding its taxonomic properties and the spectrum of chlorophenols that it dehalogenated [10].
• The acute and life cycle toxicities of acenaphthene and 2,4,6-trichlorophenol (2,4,6-TCP) were evaluated using the parthenogenic dipteran larva, Paratanytarsus parthenogeneticus, of the family Chironomidae [11].
• A gene encoding hydroxyquinol 1,2-dioxygenase was cloned from 2,4,6-trichlorophenol-degrading Ralstonia (Pseudomonas) pickettii strain DTP0602 [12].

Biological context of Phenaclor

• The maintenance of a steady-state biofilm in a continuous-flow fixed-bed reactor, as a consequence of the reproduction-detachment of cells (an interfacial cell physiology phenomenon of steady-state biofilm) during the biodegradation of 2,4,6-trichlorophenol by Pseudomonas cells, was determined [13].
• 2,4,6-Trichlorophenol (TCP) induces chromosome breakage and aneuploidy in vitro [14].
• The genotoxicity of the rodent carcinogen 2,4,6-trichlorophenol (TCP) was studied without exogenous metabolic activation in V79 Chinese hamster cells [15].
• A microwave-assisted extraction (MAE) method was optimised for extracting 2,4,6-trichloroanisole (TCA), 2,3,4,6-tetrachloroanisole (TeCA), pentachloroanisole (PCA), 2,4,6-trichlorophenol (TCP), 2,3,4,6-tetrachlorophenol (TeCP) and pentachlorophenol (PCP) from oak barrels [16].
• Prochloraz, but not the metabolites 2,4,6-trichlorophenoxyacetic acid or 2,4,6-trichlorophenol, inhibited the R1881-induced response in an androgen receptor reporter gene assay [17].

Anatomical context of Phenaclor

• The dysfunction of liver cells described here may therefore be explained by the effect of PCP and 2,4,6-T on the energy production of the cells [18].
• 2. Under the same conditions, rat liver microsomes produce 3,6/4,5-HCCH, 2,4,6-TCP and 2,3,4,6-TCCP at rates similar to human liver microsomes [19].
• Hexachlorophene (HCP), pentachlorophenol (PCP), 2,4,5-trichlorophenol (2,4,5-TCP) and 2,4,6-trichlorophenol (2,4,6-TCP) all hemolyzed washed human erythrocytes and inhibited acetylcholinesterase (AchE) activities in erythrocyte membrane [20].
• In the organic soluble fraction the 2,4,6-trichlorophenol was the major metabolite in urine and the only metabolite detected in feces [21].

Associations of Phenaclor with other chemical compounds

• Suspensions of cells grown in the presence of 2,4,6-trichlorophenol or 2,3,5,6-tetrachlorophenol did not show a lag period for mineralization of PCP, 2,4,6-trichlorophenol, or 2,3,5,6-tetrachlorophenol, indicating that one enzyme system probably was induced for the biodegradation of all three compounds [22].
• Increasing fungistatic activities were seen with 3,5-dichlorophenol, four trichlorophenols, and 2,3,4,5-tetrachlorophenol for all of the strains, with four dichlorophenols, 2,4,6-trichlorophenol, and two tetrachlorophenols for some strains, and with 2,3,6-trichlorophenol for only one strain (M. circinelloides PC 1) [23].
• A fluidized bed bioreactor (FBBR) was operated for more than 1000 days under two regimes, Methanogenic (M) and Methanogenic-Aerobic (M-A), to remove 2,4,6-trichlorophenol (TCP) and phenol (Phe) from a synthetic wastewater, containing different amounts of TCP and Phe, using different aeration flow-rates (0, 2.13, and 1.06 NL O(2)/L.day) [24].
• The use of a carefully selected internal standard permitted the estimation of (sub) parts per million levels of pentachlorophenol, 2,3,4,6-tetrachlorophenol and 2,4,6-trichlorophenol in several samples of adhesives and various sections of cardboard food containers [25].
• The effects of beta-HCH were compared to those of estradiol-17 beta (E2) and 2,4,6-trichlorophenol (TCP), a major urinary metabolite of beta-HCH in rats. beta-HCH in concentrations higher than 1 microM caused induction of PgRc whereas TCP was essentially without effect up to a cytotoxic concentration of 100 microM [26].

Gene context of Phenaclor

• Dual-wavelength spectrophotometry. Part VI. Determination of phenol in industrial waste and the determination of 2,4-dichlorophenol and 2,4,6-trichlorophenol in mixtures by first derivative spectra [27].
• Through measurements on the respective methylethers (anisoles) the O-H bond of 2,4,6-TCP turns out to be 5 kcal/ mol, and that in PCP 4 kcal/mol, less strong than O-H in phenol itself [28].
• PCP (4-6 microM) as well as 2,4,6-T (50-100 microM) interferes with the disposition of BSP [18].
• 3,5-Dichlorocatechol, 2,6-dichloro-1,4-benzoquinone and 2,6-dichloro-1,4-hydroquinone were found to be the primary products of 2,4,6-TCP oxidation by laccase; oligo- and polymeric compounds were also found [29].

Analytical, diagnostic and therapeutic context of Phenaclor

• For this purpose, an indirect enzyme-linked immunosorbent assay (ELISA) for 2,4,6-trichlorophenol detection has been developed using polyclonal antisera raised against 3-(3-hydroxy-2,4,6-trichlorophenyl)propanoic acid (hapten 5) covalently coupled by the mixed anhydride (MA) method to keyhole limpet hemocyanin (KLH) [30].
• Impact of long-term partial aeration on the removal of 2,4,6-trichlorophenol in an initially methanogenic fluidized bed bioreactor [24].
• Pentachlorophenol (50 ng) and 2,4,6-trichlorophenol (20 ng) gave significant HPLC peaks, readily permitting their detection in parts per billion from 100-g samples [25].
• Cells starved for 24, 48 or 72 h were incubated with 25 microm of 2,4,6-TCP and PHA in cells investigated by spectrofluorimetric and flow cytometry [31].
• Acute toxicity tests were performed on nine different domestic species indigenous to China to determine 48 h LC(50) and 96 h LC(50) values for 2,4,6-TCP [32].

References