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[Surgical treatment of onychomycoses, leukonychias, recessive mycoses and mycotic paronychias combined with 1 per cent solution of alcoholic pentachlorophenol solution].
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A turbidimetric method for the determination of pentachlorophenol in urine.
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[Studies on pentachlorophenol].
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Effect of thyroxine and pentachlorophenol on the metabolism of 14C labelled substrates in the tissues of the albino rat.
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[Quantitative method for urinary pentachlorophenol].
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Hygienic guide series. Pentachlorophenol and sodium pentachlorophenate.
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Influence of pentachlorophenol on fatty acids of Coho salmon (Onchorynchus kisutch).
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Thyroxine antagonism of pentachlorophenol poisoning in cichlid fish.
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[Autopsy case of acute pentachlorophenol poisoning].
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The microsomal metabolism of hexachlorobenzene. Origin of the covalent binding to protein.
The microsomal metabolism of hexachlorobenzene is studied, with special attention to the covalent binding to protein. The metabolites formed are pentachlorophenol and tetrachlorohydroquinone. In addition, a considerable amount of covalent binding to protein is detected (250 pmoles pentachlorophenol, 17 pmoles tetrachlorohydroquinone and 11 pmoles covalent binding in an incubation containing 50 mumoles of hexachlorobenzene). In order to establish the potential role of reductive dechlorination in the covalent binding, the anaerobic metabolism of hexachlorobenzene was investigated. At low oxygen concentrations no pentachlorobenzene was detected, and only very small amounts of pentachlorophenol as well as covalent binding, indicating a relationship between covalent binding and the microsomal oxidation of hexachlorobenzene. Incubations with 14C-pentachlorophenol at low concentrations showed that a conversion-dependent covalent binding occurs to the extent of 75 pmole binding per nmole pentachlorophenol. This is almost enough to account for the amount of label bound to protein observed in hexachlorobenzene incubations. This indicates that less than 10% of the covalent binding occurs during conversion of hexachlorobenzene to pentachlorophenol, and the remainder is produced during conversion of hexachlorobenzene to pentachlorophenol, and the remainder is produced during conversion of pentachlorophenol. The major product of microsomal oxidation of pentachlorophenol is tetrachlorohydroquinone, which is in redox-equilibrium with the corresponding semiquinone and quinone (chloranil). The covalent binding is inhibited by addition of ascorbic acid or glutathione to the hexachlorobenzene incubations. Ascorbic acid decreases the covalent binding with a simultaneous increase in formation of tetrachlorohydroquinone, probably due to a shift in the redox-equilibrium to the reduced side. Glutathione does not act as a reducing agent, since the inhibition of covalent binding is not accompanied by an increase in tetrachlorohydroquinone formation. Instead, glutathione reacts with chloranil, producing at least three stable products, probably in a Michael-type reaction. These results strongly indicate the involvement of chloranil or the semiquinone radical in the covalent binding during microsomal hexachlorobenzene metabolism.
Urinary excretion of chlorinated phenols in saw-mill workers.
The excretion and conjugation of chlorophenols were studied in workers exposed to 2,4,6-tri-, 2,3,4,6-tetra-, and pentachlorophenolates, the main components of the chlorophenolate product manufactured by direct chlorination of phenol. The workers were exposed in two different saw mills in which sodium chlorophenolate was used for treatment of lumber during the warm season. Urine specimens were collected at the end of the treatment season as well as at the start of a new treatment period in the spring. Serum specimens were collected towards the end of the treatment period. Total and unconjugated chlorophenols were analyzed with a gas chromatographic method. The maximal concentrations of urinary 2,4,6-tri-, 2,3,4,6-tetra- and pentachlorophenol at the end of the lumber-treatment period were 1-11.8, 3.4-17.3, and 0.2-0.9 mumol/l, respectively, and the average apparent half-times calculated using a one-compartment model were 18 h, 4.3 days and 16 days, respectively. For 2,3,4,6-tetrachlorophenol, the data of some subjects showed a better fit with a two-compartment model; the corresponding half-times were 5.3 and 26 days. During the continuous-exposure period the average serum levels of tetra- and pentachlorophenol were rather similar before and after the working day: 2.79 +/- 1.78 mumol/l for tetrachlorophenol and 0.85 +/- 0.4 mumol/l for pentachlorophenol. Renal clearance values for tetra- and pentachlorophenol were related to urine flow and indicated tubular reabsorption. At low concentrations, sulfate conjugation was dominant. With increasing chlorophenol concentrations the proportion of glucuronide conjugation was increased, especially for pentachlorophenol.
Metabolism of the "mixed" cytochrome P-450 inducer hexachlorobenzene by rat liver microsomes.
Hexachlorobenzene (HCB) was metabolised by phenobarbital-induced liver microsomes from male rats to pentachlorobenzene, pentachlorophenol, tetrachloro-1,2-benzenediol and tetrachloro-1,4-benzenediol (1:88:2:9). Metabolites were identified and quantified by electron capture g.l.c. Structures were confirmed by selective ion monitoring g.l.c.-m.s. The formation of pentachlorophenol was dependent on the presence of NADPH and O2 and inhibited by CO, SKF 525A and metyrapone. Conversion of HCB to pentachlorophenol was stimulated by pretreatment of rats with phenobarbital (PB) but not by 3-methylcholanthrene (3-MC), or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In contrast, the conversion of pentachlorophenol to tetrachloro-1,4-benzenediol was markedly induced by 3-MC but poorly by PB. HCB, Aroclor 1254 and isosafrole stimulated both hydroxylations. The cytochrome P-450c inhibitor 9-hydroxyellipticine inhibited conversion of pentachlorophenol to tetrachlorobenzenediols by HCB and beta-naphthoflavone induced micromes. In addition to hydroxylation reactions, evidence was obtained for the conjugation of HCB with glutathione catalysed by a microsomal glutathione transferase. Radioactivity from [14C]HCB was bound to microsomal protein during aerobic incubations. Binding was inhibited by GSH and N-acetyl-cysteine. Preliminary studies suggested that the reactive species was derived from tetrachloro-1,4-benzoquinone. No correlation was found between levels of metabolites or covalent binding produced by the two sexes and the marked sex dependent hepatic porphyrogenic and carcinogenic effects of HCB.
Studies on benzyl acetate. II. Use of specific metabolic inhibitors to define the pathway leading to the formation of benzylmercapturic acid in the rat.
Specific metabolic inhibitors were used to define the route of metabolism of benzyl acetate leading to the formation of benzylmercapturic acid. Male Fischer 344 rats were dosed by gavage with [methylene-14C]benzyl acetate (500 mg/kg) alone or together with pyrazole (200 mg/kg), pentachlorophenol (10 mg/kg) or both pentachlorophenol (10 mg/kg) and pyrazole (200 mg/kg), given in each case ip. Urine and faeces were collected and urinary metabolites were assayed by radio-TLC and HPLC. The excretion of 14C was rapid in all cases, with most of the dose excreted in the urine within 24 hr. Co-administration of pyrazole (an inhibitor of alcohol dehydrogenase) with benzyl acetate caused an 11-fold increase in the excretion of benzylmercapturic acid and halved the percentage of the dose excreted as benzoyl glucuronide. Pretreatment with pentachlorophenol, an inhibitor of sulphotransferase activity in vivo, abolished the excretion of benzylmercapturic acid, while excretion of the mercapturate following treatment with both pyrazole and pentachlorophenol was higher than in control or pentachlorophenol-treated rats, but much lower than in the animals given pyrazole alone. Taken together, these results suggest very strongly that the formation of benzylmercapturic acid involves the sulphate ester of benzyl alcohol as an obligatory intermediate and does not appear to involve a metabolic intermediate with sufficient reactivity to have toxicological relevance.
EPA site demonstration of BioTrol aqueous treatment system.
BioTrol's pilot scale, fixed-film biological system was evaluated, under the EPA's SITE program, for its effectiveness at removing pentachlorophenol from groundwater. The demonstration was performed in the summer of 1989 at a wood preserving site in New Brighton, Minnesota. The system employs indigenous microorganisms amended with a specific pentachlorophenol-degrading bacterium. Groundwater from a well on the site was fed to the system at 1, 3, and 5 gpm with no pretreatment other than pH adjustment, nutrient addition, and temperature control. Each flowrate was maintained for about two weeks while samples were collected for extensive analyses. At 5 gpm, the system was capable of eliminating about 96 percent of the pentachlorophenol in the groundwater and producing effluent with pentachlorophenol concentrations of about 1 ppm. At the lower flows (1 and 3 gpm) removal was higher (about 99 percent) and effluent pentachlorophenol concentrations were well below 0.5 ppm. The system consistently produced a completely nontoxic effluent at all three flowrates. Review of other data provided by BioTrol indicates that the process is also effective on other hydrocarbons, including solvents and fuels. The system appears to be a compact and cost-effective treatment for contaminated wastewaters requiring minimal operating attention once acclimated.
Organic compounds adsorption onto activated carbon: the effect of association between dissolved humic substances and pesticides.
The quantitative determination of pesticide binding to dissolved humic substances is relevant to both water treatment operation using activated carbon adsorption process and the application of transport models that predict the environmental distribution patterns of a given hydrophobic contaminant. In this study and in a first set of experiments, the extent of binding between (i) three pesticides of environmental concern, aldicarb, lindane and pentachlorophenol, and (ii) dissolved commercial humic acid and soil extracted fulvic acid, was determined using dialysis experiments and water solubility enhancement tests. In a second set of experiments, the influence of dissolved humic substances or pesticide on the retention of the other co-adsorbate onto activated carbon was investigated in binary systems. It was found that association was negligible for aldicarb and that the pesticide sorption onto activated carbon was not affected by humic acid (8.5 mg liter(-1) DOC). The association constants K for lindane and pentachlorophenol were identical in the presence of fulvic acid (logK=4.1) but lower than that observed with humic acid. In the presence of humic acid, binding affinity for pentachlorophenol (logK=4.6) was higher than the one observed for lindane (logK=4.4), despite its much higher water solubility. This observation suggests that the aromatic character of the pentachlorophenol molecule contributes to association interactions with humic acid. From co-adsorption experiments onto activated carbon it was found that fulvic acid (7.7 mg litre(-1) DOC) slightly enhances sorption kinetics of pentachlorophenol. Lindane (1 mg litre(-1)) does not affect sorption kinetics for fulvic acid but markedly enhances both the sorption kinetics and adsorptive capacity for humic acid. Activated carbon retention of dissolved humic substances or pesticide appears to be enhanced by the association potential that exists between these co-adsorbates in some binary systems.
Diversity of chlorophenol-degrading bacteria isolated from contaminated boreal groundwater.
Chlorophenol-degrading bacteria from a long-term polluted groundwater aquifer were characterized. All isolates degraded 2,4,6-trichlorophenol and 2,3,4,6-tetrachlorophenol at concentrations detected in the contaminated groundwater (< 10 mg 1(-1)). Pentachlorophenol was degraded by three isolates when present alone. In two gram-positive isolates, 2,3,4,6-tetrachlorophenol was required as an inducer for the degradation of pentachlorophenol. The gram-positive isolates were sensitive to pentachlorophenol, with an IC50 value of 5 mg/l. Isolates belonging to the Cytophaga/Flexibacter/Bacteroides phylum had IC50 values of 25 and 63 mg/l. Isolates belonging to alpha-, beta- and gamma-Proteobacteria generally tolerated the highest pentachlorophenol concentrations (> 100 mg/l). Polychlorophenol-degrading capacity was found in strains of Nocardioides, Pseudomonas, Ralstonia, Flavobacterium, and Caulobacter previously not known to degrade polychlorophenols. In addition, six polychlorophenol-degrading sphingomonads were found.
The relation between the oxidative biotransformation of hexachlorobenzene and its porphyrinogenic activity.
The relation between the major toxic effect of hexachlorobenzene, hepatic porphyria, and its oxidative biotransformation was studied in vivo, by observing the effect of modulating its biotransformation on the expression of porphyria. This modulation was achieved by selective in vivo inhibition of the major cytochrome P450 isoenzyme involved in both the hydroxylation of hexachlorobenzene and its primary oxidative metabolite, pentachlorophenol. The involvement of this isoenzyme, cytochrome P450p, was established by in vitro biotransformation studies using microsomes derived from rats treated with various inducers of cytochrome P450 isoenzymes and selective in vitro inactivation of cytochrome P450p by triacetyloleandomycin (TAO), resulting in a strong inhibition of the microsomal conversion of hexachlorobenzene and pentachlorophenol. In vivo inactivation of cytochrome P450p was achieved by coadministration of hexachlorobenzene and TAO. Female rats which were treated with this diet for 10 weeks showed a strongly diminished urinary excretion of the major oxidative metabolites, pentachlorophenol and tetrachloro-1,4-hydroquinone, as compared to rats treated with hexachlorobenzene alone. The TAO coadministration was found to result in complexation of 70% of the total amount of hepatic microsomal cytochrome P450. The group treated with hexachlorobenzene alone displayed a 600-fold increase in the amount of hepatic porphyrins, whereas an almost complete absence of hepatic porphyrins was observed after administration of hexachlorobenzene together with TAO. The urinary excretion of porphyrins was also significantly lowered by cotreatment with TAO. A strong correlation was found to exist between the amount of porphyrins excreted and the amount of oxidative metabolites excreted, as a function of exposure time. Glucuronidation of pentachlorophenol was observed to an average extent of 30%. This percentage was not influenced by either TAO or phenobarbital. These results suggest that oxidative biotransformation, and thus the formation of the very reactive tetrachloro-1,4-benzoquinone, is directly related to the porphyrinogenic action of hexachlorobenzene.