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This study examined the effects on PCP binding to BSA by varying the temperature, pH ionic strength, PCP concentration and BSA concentration. It also compared the albumin binding of PCP to the plasma binding of PCP for the rat and human.
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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.
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.
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.
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.
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.
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.
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.
A case of intentional intoxication with pentachlorophenol has been described. Salient features observed included pyrexia, diaphoresis, hyperkinesis, muscle twitching, tremors, epigastric tenderness, leg pain, tachypnea, and tachycardia. The patient's restlessness and agitation were controlled with phenytoin and phenobarbital. Forced diuresis with furosemide and mannitol resulted in a large increase in urinary excretion of pentachlorophenol. It is suggested that such therapy may be life saving in such intoxications.
Analytical methods have been implemented to measure levels of polychlorodibenzo-p-dioxins, and polychlorodibenzofurans in pentachlorophenol solutions used in the Boulton wood treatment process. When normalized against the pentachlorophenol (PCP) content, the octachlorodibenzo-p-dioxin level was 34% higher in the recirculating PCP solution than in the fresh PCP solution, and in the sludge it was 90% higher. A smaller concentration increase was observed for the heptachlorodibenzo-p-dioxin in the recirculating solution, but a similar increase was observed in the sludge.
A pharmacokinetic study of an intentional pentachlorophenol ingestion by an elderly human has been undertaken. Information on the presence or absence of forced diuresis either continuously or for a short restricted period indicates that such treatment would materially reduce the body burden of pentachlorophenol. It is suggested that forced diuresis is the treatment of preference for such intoxication at this time.
The toxicity of technical grade pentachlorophenol to rumen microorganisms was tested by an in vitro fermentation procedure. Rumen fluid was collected from a fistulated mature steer fed a diet of all alfalfa hay. The compound was dissolved in absolute ethanol and added in vitro at concentrations ranging from 0 to 100 ppm. Digestion of cellulose and production of volatile fatty acids over 24 and 48 h of incubation was used to assess toxicity. Both cellulose digestion and propionic acid production were decreased at the 10 ppm concentration. The results suggest that technical grade pentachlorophenol has the potential to interfere with utilization of cellulose in ruminants.
Pentachlorophenol (PCP) is a potent uncoupler of mitochondrial phosphorylation in vitro and also interferes with microsomal detoxication functions in vitro. This favours flavin mediated oxygenation compared with flavin cytochrome P-450 dependent reactions. Gas chromatographic analysis of subcellular fractions, obtained by zonal centrifugation showed markedly lower PCP concentration in mitochondria and a high accumulation in microsomes compared with cytosol. This increases the likelihood that PCP in vivo causes a malfunction in microsomal detoxication.
The application of hexachlorobenzene (HCB), pentachlorophenol (PCP) and 2,4,5-trichlorophenol (TCP) to female rats led to an induction of both the microsomal and the nuclear cytochrome P-450 system in the liver. The increase of th mixed-function hydroxylase activities examined (7-ethoxycoumarin deethylase, 7-ethoxyresorufin deethylase, NADPH-dependent cytochrome c reductase, aminopyrine demethylase, benzpyrene hydroxylase) did not correlate strictly with the cytochrome P-450 content. Depending on the inducers and the substrates used, the content and the activity of the cytochrome P-450 were essentially smaller in the nuclei than in the microsomes. It was striking that in the nuclei those activities (benzpyrene hydroxylase, 7-ethoxyresorufin deethylase, 7-ethoxycoumarin deethylase) were preferably induced which can be attributed to the methyl-cholanthrene-induced form of the cytochrome P-450 (cytochrome P-448). These results suggest, also in the light of findings of other authors, the induction of different species of cytochrome P-450 in the nuclei and microsomes.
Metabolism of pentachlorophenol (PCP)-ring-14C(U) by a microorganism (Pseudomonas sp.) isolated from soil was examined. The microorganism degraded PCP-14C rapidly, and released 14CO2 equivalent to approximately 50% of the PCP-14c added to the bacterial cell suspension in 1 hour of incubation. The results of amino acid analysis of the bacterial cells incubated with PCP-14C showed that radioactive carbon derived from PCP-14C was incorporated rapidly into the cell constituents, and that the pattern of 14C-amino acids in the cell constituents was not much different between the 15 minute and 24 hour incubation periods. Intermediate metabolities of PCP isolated from the incubation medium were identified as tetrachlorocatechol and tetrachlorohydroquinone by spectral analyses.
Aerobic and anaerobic degradation of 14C-labeled pentachlorophenol (PCP) was examined in nitrogen aerated, moist Hagerstown silty clay loam with or without cellulose amendments. In anaerobic soil, PCP reduced soil respiration in the presence of cellulose; volatilization losses accounted for only 0.5% of the PCP added to soil; no 14CO2 was detected; and organic solvent extractable radioactivity was the same from all treatments. Gas and thin-layer chromatographic analysis of the soil extracts showed the presence of pentachloroanisole in both aerobic and anaerobic soils. 2,3,5,6- and 2,3,4,5-tetrachlorophenols and 2,3,6-trichlorophenol were also detected as degradation products by gas chromatography after methylation. Further degradation of pentachloroanisole was examined in both aerobic and anaerobic soils.