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At least 19 recordsLinked to original sources
PubMed1976

A study of the inhalation of pentachlorophenol by rats. Part I. A method for the determination of pentachlorophenol in rat plasma, urine and tissue and in aerosol samples.

Simple and flexible methods have been designed for the determination of pentachlorophenol in animal tissue, blood plasma, urine, and aerosol. The isolation of the pesticide is achieved through its extraction with benzene or hexane after acidification, derivatization, and its subsequent purification through florosil columns. A brief describption of the sampling methods is included. The described procedures are especially suited for exposure experiments where different types of samples with a large variety of PCP concentrations are encountered.

Aerosols↗
PubMed1992

Confirmation of oxidative dehalogenation of pentachlorophenol by a Flavobacterium pentachlorophenol hydroxylase.

Pentachlorophenol (PCP) hydroxylase purified from Flavobacterium sp. strain ATCC 39723 converted PCP or 2,3,5,6-tetrachlorophenol to tetrachloro-p-hydroquinone (TeCH) with the co-consumption of O2 and NADPH. The purified enzyme incorporated 18O from 18O2 but not from H218O into the reaction end product TeCH. The results clearly demonstrate that PCP is oxidatively converted to TeCH by a monooxygenase-type enzyme from Flavobacterium sp. strain ATCC 39723.

Flavobacterium↗
PubMed1976

A study of inhalation of pentachlorophenol by rats. IV. Distribution and excretion of inhaled pentachlorophenol.

It appears that in the rat repeated respiratory exposures to PCP do not result in an increase in the body burden of this compound as would be suspected from the 24 hour half-life determined from a single inhalation exposure. These results suggest some mechanism induced by prior exposure to PCP that increases the ability of the animals to remove this compound from its body. Increased excretion may be a factor in this activity, however, it cannot account for the total effect. Storage appears unlikely, since the elimination rate and time period remain unchanged after five doses as compared to after one. Increased matebolism may be the explanation, although this mechanism can only be inferred from these data. Quantitative metabolic results will be necessary to support this hypothesis.

Aerosols↗
PubMed1976

Electrical conductivity in lipid bilayer membranes induced by pentachlorophenol.

Electrical conductivity induced in thin lipid bilayer membranes by pentachlorophenol has been studied. The membranes were formed from phosphatidyl choline, phosphatidyl ethanolamine, or phosphatidyl glycerol and various amounts of cholesterol. The position and the magnitude of the maximum of the conductivity vs. pH curve depend on the type of lipids and cholesterol content. At low pentachlorophenol concentrations and low pH the concentration dependence of conductivity is quadratic and becomes linear at higher pH. Above 10(-5) M of pentachlorophenol the concentration dependence of the membrane conductivity tends to saturate. Presence of pentachlorophenol enhances membrane transport of nonactin-K+ complex. Increase of cholesterol content increases pentachlorophenol induced conductivity in all membranes and shifts the conductivity toward lower pH. For phosphatidyl choline the largest rate of change of membrane conductivity with cholesterol occurs at 1:1 phospholipid to cholesterol molar ratio. Pentachlorophenol is found to be a class II uncoupler and the experimental results are consistent with the hypothesis that the membrane permeable species are dimers formed by combination of neutral and dissociated pentachlorophenol molecules. Several schemes of membrane conduction, including dimer formation in the aqueous phase as well as at the membrane-water interface have been considered. Arguments are given in favor of the formation of dimers within the membrane surface.

Electric Conductivity↗
PubMed1978

Metabolism of pentachlorophenol in vivo and in vitro.

Pentachlorophenol has earlier been shown to be metabolized in mammals to tetrachloro-p-hydroquinone. The metabolite possesses pronounced inhibitory activity on bacterial beta-glucuronidase but not on beta-glucuronidase from liver. Indirect evidence for the occurrence of both pentachlorophenol and tetrachloro-p-hydroquinone as conjugates with glucuronic acid in the urine from pentachlorophenol-treated rats is now presented. Bovine liver beta-glucuronidase has been utlizied to split the conjugates present. The in vivo metabolism of pentachlorophenol has also been studied in rats treated with phenobarbital and beta-diethylaminoethylidiphenyl propylacetate (SKF 525-A). In vitro metabolism has been studied using liver microsomes from rats pretreated with pehnobarbital. Quantitative analysis of the compounds occurring in extracts of urine or extracts from the microsomal incubates was performed by means of mass fragmentography. Pretreatment with phenobarbital increased the metabolism of pentachlorophenol to tetrachloro-p-hydroquinone both in vivo and in vitro. SKF 525-A, however, inhibited the metabolism in vitro but enhanced the metabolism in vivo when given less frequently than every 6th h. Dechlorination of pentachlorophenol is mediated by microsomal enzymes that can be induced by phenobarbital. SKF 525-A does not inhibit the dechlorination in vivo but does so in vitro.

Animals↗
PubMed1976

Dinitrophenol, dicoumarol and pentachlorophenol as inhibitors and parasite substrates in the ATP phosphoribosyltransferase reaction.

Adenosine-triphosphate phosphoribosyltransferase from Escherichia coli is inhibited by dicoumarol and pentachlorophenol in competition with ATP. Ki was approximately 60 muM for dicoumarol and 50 muM for pentachlorophenol. Carbonylcyanide m-chlorphenylhydrazine did not seem to have any kinetic effect. Dicoumarol is bound to the extent of 6 sites per enzyme hexamer with a dissociation constant Kd of 50 muM. Dicoumarol and pentachlorophenol partly prevent the binding of ATP and AMP to the transferase. The reverse reaction is inhibited by dicoumarol and pentachlorophenol without changes in [s]0.5 for phosphoribostladenosine trophosphate. Dicumarol, dinitrophenol and pentachlorophenol diminish the yield of phosphoribosyladenosine triphosphate in the transferase reaction apparently by acting as parasite substrates; carbonylcyanide m-chlorophenylhydrazone had no effect.

ATP Phosphoribosyltransferase↗
PubMed1992

Reductive dechlorination of chlorophenols by a pentachlorophenol- acclimated methanogenic consortium.

Anaerobic digester sludge fed 5,300 mg of acetate per liter, 3.4 microM pentachlorophenol, and nutrients for 10 days biotransformed pentachlorophenol by sequential ortho dechlorinations to produce 2,3,4,5-tetrachlorophenol and 3,4,5-trichlorophenol. Upon acclimation to 3.4 microM pentachlorophenol for 6 months, the methanogenic consortium removed chlorines from the ortho, meta, and para positions of pentachlorophenol and its reductive dechlorination products. Pentachlorophenol was degraded to produce 2,3,4,5-tetrachlorophenol, 2,3,4,6-tetrachlorophenol, and 2,3,5,6-tetrachlorophenol. Dechlorination of 2,3,4,5-tetrachlorophenol produced 3,4,5-trichlorophenol, which was subsequently degraded to produce 3,4-dichlorophenol and 3,5-dichlorophenol. 2,3,4,6-Tetrachlorophenol was dechlorinated at the ortho and meta positions to produce 2,4,6-trichlorophenol and 2,4,5-trichlorophenol. 2,3,5,6-Tetrachlorophenol yielded 2,3,5-trichlorophenol, followed by production of 3,5-dichlorophenol. 2,4,6-Trichlorophenol was degraded to form 2,4-dichlorophenol, and 2,4,5-trichlorophenol was dechlorinated at two positions to form 2,4-dichlorophenol and 3,4-dichlorophenol. Of the three dichlorophenols produced (2,4-dichlorophenol, 3,4-dichlorophenol, and 3,5-dichlorophenol), only 2,4-dichlorophenol was degraded significantly within 3 weeks, to produce 4-chlorophenol.

Adaptation, Physiological↗
PubMed1978

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the in vivo and in vitro dechlorination of pentachlorophenol.

The metabolism of pentachlorophenol has been studied in the rat after pretreatments with phenobarbital, 3-methyl cholanthrene or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In addition to the previously identified metabolite, tetrachloro-p-hydroquinone, trichloro-p-hydroquinone has been identified in urine as a metabolite. The formation of the latter represents a type dechlorination different from that of the formation of tetrachlorohydroquinone. The inducing agents, 3-methylcholanthrene and TCDD have similar effects on the dechlorination and increase the formation of tetrachloro-p-hydroquinone more pronounced than does phenobarbital. In contrast to phenobarbital they also increase the formation of trichloro-p-hydroquinone and the total elimination of pentachlorophenol and its metabolites. The in vivo findings are supported by in vitro studies with microsomes from rats pretreated with phenobarbital or TCDD. Use of the inhibitor beta-diethylaminoethyl-diphenyl propylacetate (SKF 525-A) in vitro showed a more pronounced inhibition on microsomes from phenobarbital-treated rats than on microsomes from untreated or TCDD-treated rats. Gas chromatography-mass spectrometry have been used for the identification and quantification of pentachlorophenol and its metabolites.

Animals↗
PubMed1991

Chronic toxicity of a pure and technical grade pentachlorophenol to Daphnia magna.

Chronic toxicity test procedures (static, with renewal) were used to determine the chronic toxicity of sublethal concentrations of a technical formulation of pentachlorophenol (PCP) and pure pentachlorophenol to Daphnia magna. Test organisms 48 +/- 12 h old were exposed for their entire lifespan (i.e., until death) to 0.01, 0.05, 0.1 and 0.5 mg technical PCP/L and 0.01, 0.087 and 0.1 mg pure PCP/L. Criteria used to assess chronic toxicity were mean time to appearance of the primiparous instar in the brood chamber, mean number of days to release of the first brood, mean number of broods produced per female, mean brood size per female, mean number of reproductive days, mean number of young produced per reproductive day per female and survivorship. Pentachlorophenol differentially affected maturation and reproduction but not survivorship or longevity. Mean number of broods produced per daphnid, length of the reproductive period, longevity and survivorship were insensitive criteria relative to mean time to appearance of the primiparous instar, time to release of first brood, brood size, and number of young produced per daphnid per reproductive day. Generally, there was little difference in toxicity of the three concentrations of pure PCP, for they significantly reduced mean brood size and rate of reproduction of young and significantly but differentially affected maturation. Technical PCP, at the highest concentration of 0.5 mg/L, significantly reduced mean brood size and the rate of production of young, and significantly delayed both time to appearance of the primiparous instar and release of the first brood. When differences in toxicity occurred, generally, pure PCP was more toxic than comparable concentrations of technical PCP. Although enhanced maturation was observed there was no compensatory reproduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Acute toxicity of pure pentachlorophenol and a technical formulation to three species of Daphnia.

The acute toxicity of a technical formulation of pentachlorophenol (PCP) and pure pentachlorophenol to three age classes of Daphnia magna, and adult D. pulex and D. galeata mendotae was determined by static toxicity tests. The influence of a number of factors on toxicity of PCP was also examined. The 48-hr LC50 estimates for adult daphnids of the three species exposed to pure PCP were 1.78, 4.59 and 0.51 mg/L, respectively, while those for the technical formulation were 2.57, 3.66 and 0.33 mg/L, respectively. There was little difference in toxicity between the technical and pure PCP; however, toxicity of both forms of PCP was influenced by duration of exposure, age (and/or size) and species of test organism and pH of the test solution. Pentachlorophenol caused a toxic response over a very narrow range of concentrations, with the greatest response occurring immediately between 0 and 24 hr. Pure PCP was equally toxic to all age classes of D. magna but susceptibility to technical PCP decreased with maturation. D. g. mendotae was ten times more sensitive than D. pulex to PCP. Pure PCP was significantly more toxic to D. magna at pH 5.5 than 7.0 with mean 48-hr LC50 values of 0.082 and 1.78 mg PCP/L, respectively. At 12 degrees C, the toxicity of both forms of PCP to D. g. mendotae and D. pulex did not differ significantly from that at 20 degrees C; however, technical PCP was significantly more toxic to D. magna at 12 degrees C for an exposure duration of 48 hr.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1976

Alternating current studies of charge carrier transport in lipid bilayers. Pentachlorophenol in lecithin-cholesterol membranes.

Surface and interior electrical properties of lecithin-cholesterol bilayer membranes treated with the uncoupler pentachlorophenol have been determined on the basis of a.c. measurements over a wide range of frequencies (0.02 to 1000 kHZ). The method used depends on accurately determining the resistance of the aqueous solution in series with each individual membrane by extrapolating admittance data into infinite frequency. Loss tangent vs. frequency curves are corrected by subtracting out a loss contribution which is present in untreated membranes and is due, presumably, to dielectric relaxation. The results, which are useful below 100 kHZ, can be fitted to loss tangent curves computed for a three-element equivalent circuit consisting of frequency independent conductance-capacitance pairs, arranged in series to represent surface and interior properties of membranes. Interior conductances agree with net conductances obtained from d.c. measurements. The pH and concentration dependence of surface conductance is consistent with a scheme of transport in which a fixed number of surface binding sites are filled preferentially with neutral pentachlorophenol molecules, which in turn dissociate to supply protons to the aqueous phase. Surface capacitances range from 15 to 90 times that of interior capacitance and show a systematic increase with pentachlorophenol concentration at high pH, and a decrease with concentration at low pH.

Biological Transport, Active↗
PubMed1990

Liquid chromatographic determination of pentachlorophenol in serum, using pre-column phase-transfer catalysed dansylation and post-column photolysis with fluorescence detection.

Dansylation of pentachlorophenol was carried out after solid-phase extraction of acidified human serum and desorption with dichloromethane, in a dichloromethane-water two-phase system using tetrabutyl-ammonium bromide as the phase-transfer catalyst. Derivatisation was complete within 2 min at room temperature. After evaporation of an aliquot of the organic phase, the residue was dissolved in methanol and injected into a reversed-phase chromatographic system, equipped with a post-column photochemical reactor. In the reactor, dansylated pentachlorophenol is converted into highly fluorescent products. The recovery of the analyte from serum was 85 +/- 4%. Calibration graphs for horse and human serum were linear over two decades, with correlation coefficients ranging from 0.996 to 0.999. The detection limit of pentachlorophenol in horse and human serum was 400 pg ml-1. The reproducibility of the total procedure for a human serum sample containing 4 ng ml-1 was 4.5%.

Catalysis↗
PubMed1978

Inhibition of bacterial transport by uncouplers of oxidative phosphorylation. Effects of pentachlorophenol and analogues in Bacillus subtilis.

Analogues of the potent uncoupler of oxidative phosphorylation pentachlorophenol were tested as inhibitors of proline and glycine transport by Bacillus subtilis. These analogues included less highly substituted chlorophenols and pentachlorothiophenol. Like pentachlorophenol, they are non-competitive inhibitors of proline transport and uncompetitive inhibitors of glycine transport. However, the less highly substituted chlorophenols are weaker acids than pentachlorophenol and also weaker inhibitors. Analysis indicated that the anionic form of the uncouplers is the inhibiting species. Pentachlorothiophenol, a water-insoluble anion, is also a potent inhibitor. These results support previous studies that concluded that uncouplers of oxidative phosphorylation inhibit amino acid transport by binding at specific sites on proteins, the free energy of interaction stabilizing 'unproductive' conformations. Such specific interactions of uncoupler with protein are probably commonplace.

Bacillus subtilis↗
PubMed1976

[Detection of pentachlorophenol in natural rubber latex].

The method of detection of pentachlorophenol in natural rubber latex is proposed. Pentachlorophenol is isolated from other nonrubber-like substances by thin-layer chromatography and identified by spectroscopic method in UV-light. Isolation of pentachlorophenol is carried out from water extracts obtained from the dry caoutchouc films, so the same method can be used for examination of the rubber articles designed for the medicinetoo.

Chlorophenols↗
PubMed1979

Neurochemical effects of peroral administration of technical pentachlorophenol.

Administration of technical pentachlorophenol in drinking water (20 mg/l) to male Wistar rats caused significant liver concentration of tetrachlorophenol which remained stable during the exposure of 14 weeks. Pentachlorophenol and tetrachlorophenol accumulated to some extent in the perirenal fat whereas only pentachlorophenol could be found in brain. A period of four weeks of chlorophenol-free diet was sufficiently long to allow removal of the major part of the chlorophenol burden. The neurochemical effects included increased acid proteinase activity at the 8th week of exposure. It levelled off while superoxide dismutase activity increased to twice the control level. Glial glutathione peroxidase activity did not change whereas glial glutathione concentration was below the control range at the 12th week of exposure. Cerebral diaphorase activity was below the control range initially, and its activity increased above the control level during the recovery period whereas other biochemical changes levelled off.

Adipose Tissue↗