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PubMedDate not supplied

Biotransformation of dichloroaromatic compounds in nonadapted and adapted freshwater sediment slurries.

Nonadapted freshwater sediment slurries and sediment slurries adapted to dechlorinate 2,3-dichloropyridine (2,3-Cl2Pyd), 2,3-dichloroaniline (2,3-Cl2Anl), 2,3-dichlorophenol (2,3-Cl2PhOH), 3,5-dichloropyridine (3,5-Cl2Pyd), 3,5-dichloroaniline (3,5-Cl2Anl) and 3,5-dichlorophenol (3,5-Cl2PhOH) were studied to determine the rate, range and extent of biotransformation of structurally related compounds under anaerobic conditions. 2,3-dichloroanisole (2,3-Cl2Ans) and 3,5-dichloroanisole (3,5-Cl2Ans) were initially demethylated, producing 2,3-Cl2PhOH and 3,5-Cl2PhOH as intermediate transformation products. All other dichloroaromatic compounds examined were initially dechlorinated. The rates of dechlorination of 2,3-Cl2PhOH, 2,3-Cl2Anl, and 2,3-Cl2Pyd were significantly lower (5-15 times) in nonadapted sediment slurries compared to sediment slurries adapted to 2,3-Cl2Anl or 2,3-Cl2Pyd. In 2,3-Cl2PhOH adapted sediment, the rate of dechlorination of 2,3-Cl2PhOH was 15 times greater than in nonadapted sediment; however, the rates of dechlorination of 2,3-Cl2Anl and 2,3-Cl2Pyd were similar for 2,3-Cl2PhOH-adapted and nonadapted sediment slurries. In adapted and nonadapted sediment slurries, 2,3-Cl2PhOH, 2,3-Cl2Anl, and 2,3-Cl2Pyd were preferentially dechlorinated at the ortho, meta, and meta positions, respectively. Additionally, 2,3-Cl2Pyd adapted sediment slurries dechlorinated 2,3-Cl2PhOH and 2,3-Cl2Pyd at both ortho and meta positions. Rates of dechlorination of 3,5-Cl2PhOH, 3,5-Cl2Anl, and 3,5-Cl2Pyd were lower (2-4 times) in nonadapted sediment slurries compared to sediment slurries adapted to 3,5-Cl2Anl or 3,5-Cl2Pyd. In 3,5-Cl2PhOH adapted sediment, the rate of dechlorination of 3,5-Cl2PhOH was approximately 10 times greater than in nonadapted sediment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aniline Compounds↗
PubMed1995

Hydrophobic adsorption of aromatic compounds on polyurethane foam as a carbon source for Pseudomonas growth.

The use of polyurethane foam appears to be efficient to extract hydrophobic pollutants from aqueous media. Their adsorption is the result of spontaneous hydrophobic interactions with the foam, The rate of adsorption is a function of the diffusion of the molecules into the foam as well as their hydrophilic/lipophilic balance. A mixture of different molecules modifies the adsorption capacities of each type of molecule on the foam, probably resulting from stacking phenomena between the molecules. The Pseudomonas species can grow in the presence of the polyurethane foam and be adsorbed on it. Moreover, a strain of Pseudomonas pseudoalcaligenes tested in this study can use adsorbed biphenyl as the sole carbon source. Polyurethane foam therefore shows favorable characteristics for being chosen as a method of concentrating aromatic compounds and optimizing the rate of degradation of these molecules by bacteria.

Adsorption↗
PubMed1995

Estimation of selected phenols in drinking water with in situ acetylation and study on the DNA damaging properties of polychlorinated phenols.

Gas chromatography/mass spectrometry with selected-ion monitoring (GC/MS-SIM) method were used to analyze 23 selected phenols in natural and drinking waters by an in situ acetylation technique. This method was suitable for determining phenol concentrations at the ng/L level because of less background interference and better recoveries. The application range for all these phenols was from 0.01 or 0.04 to 10 micrograms/L, using a 800 ml water sample. The levels of trace phenols in four Taiwan water treatment plants were in the range of 12-312 ng/L. The polychlorinated phenols, namely 2,4,6-trichlorophenol, 2,3,4,6-tetrachlorophenol, and pentachlorophenol, were evaluated for their ability to induce deoxyribonucleic acid (DNA) damage using a DNA precipitation assay employing mouse embryonic fibroblast cells (C3H10T1/2) with or without a liver microsomal activation system. These agents exhibited a weak positive response when microsomal activation enzymes were present in this assay. When the tetrachlorohydroquinone, a toxic metabolite of pentachlorophenol, was measured by the same method without the activation system, a significant and dose-dependent DNA damage was found. This result indicates that in the evaluation of the carcinogenic potential of these agents, their corresponding metabolites should be taken into consideration. DNA strand breakage caused by these active metabolites may play an important role in the tumorigenetic process of polychlorinated phenols.

3T3 Cells↗
PubMed1992

A comparison of the relative sensitivities of factor VII and prothrombin time measurements in detecting drug interactions with warfarin.

We have studied the comparative abilities of the prothrombin time and factor VII clotting activity, measured using a chromogenic assay, to detect drug interactions with warfarin. Pharmacokinetic and pharmacodynamic data were collected from studies involving the single administration of 25 mg of warfarin in the absence and presence of fengabin, cimetidine, ranitidine, and enoxacin. Fengabin caused changes in both the pharmacokinetics and pharmacodynamics of warfarin, whereas cimetidine and enoxacin only caused changes in its pharmacokinetics. Ranitidine had no effect on either the pharmacokinetics or pharmacodynamics of warfarin. In general, factor VII clotting activity showed greater sensitivity but also greater variability than the prothrombin time to changes in clotting activity. Consequently, factor VII clotting activity did not have greater discriminatory power than the prothrombin time in detecting drug interactions involving warfarin.

Adult↗
PubMed1980

Ultrastructural morphometric investigations on rat liver of young and adult rats after treatment with technical pentachlorophenol (PCP).

Age-dependent effects of technical pentachlorophenol (PCP) on male rat livers were investigated after a 15 day treatment with PCP, 30 mg/kg/d body weight. The liver tissues were investigated morphometrically at light and electron microscopical levels. Statistically significant alterations of nuclei and organelles of the hepatocytes were described.

Adipose Tissue↗
PubMed1980

Effects of pentachlorophenol and 2,4,6-trichlorophenol on the disposition of sulfobromophthalein and respiration of isolated liver cells.

The effect of pentachlorophenol (PCP) and 2,4,6-tricholorphenol (2,4,6-T) on the disposition of the hepatodiagnostic dye, sulfobromophthalein (BSP) has been studied in isolated liver cells. PCP (4-6 microM) as well as 2,4,6-T (50-100 microM) interferes with the disposition of BSP. The main effect apparently occurs at the secretion step as both drugs severely impair the release of the glutathione conjugate of BSP into the medium. As a consequence, BSP and its conjugate accumulate in the cell. High doses of PCP did not increase the release of lactate dehydrogenase from the hepatocytes. Concentrations of the two phenols which interfere with the secretion of BSP also completely uncouple the oxidative phosphorylation of hepatocellular mitochondria. 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. The higher toxicity of PCP as compared to 2,4,6-T observed in our system corresponds well with the higher LD50 of the latter compound.

Animals↗
PubMed1986

Pharmacokinetics of pentachlorophenol in man.

Pentachlorophenol (PCP) was given orally to three volunteers at single doses of 3.9, 4.5, 9, and 18.8 mg. Daily urinary excretion of PCP and PCP conjugated to glucuronic acid was monitored using gas chromatography with electron capture detection (GC/ECD). Based on first-order elimination kinetics an elimination half-life of 20 days was derived. To eliminate interference by the uncontrolled absorption of PCP from the environment 0.98 mg 13C-PCP was taken by one of the volunteers. PCP levels in urine and plasma were determined using mass spectrometry (GC/MS) with negative chemical ionization. An elimination half-life of 17 days was found in both urine and blood. The collected data were used to calculate the clearance of PCP: a value of 0.07 ml/min was found. The long elimination half-life of PCP is explained by the low urinary clearance due to the high plasma protein binding (greater than 96%) and the tubular reabsorption. The pH-dependency of the elimination of PCP was investigated, and a distinct increase in the daily excretion was observed following alkalinization by oral administration of sodium bicarbonate. In order to elucidate the role of the enterohepatic circulation as a possible pool for PCP in humans, the bile of cholelithiasis patients with postoperative T-drainage was investigated for PCP and compared with the corresponding urine and plasma levels, but no accumulation of PCP in the enterohepatic circulation could be observed. The daily elimination and plasma levels of PCP in a group of individuals without a specific exposition were found to range from 10 to 48 micrograms/day and 19 to 36 micrograms/1, respectively.

Adult↗
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↗
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↗
PubMed1978

Metabolism of tetrachlorophenols in the rat.

The three isomers of tetrachlorophenol were administrated intraperitoneally to rats and the urinary excretion products studied. Tetrachloro-p-hydroquinone was identified as a major metabolite of 2,3,5,6-tetrachlorophenol, constituting about 35% of the dose given. Trichloro-p-hydroquinone was identified as a minor metabolite of both 2,3,4,5- and 2,3,4,6-tetrachlorophenol. 2,3,5,6-tetrachlorophenol was eliminated within 24 h, 2,3,4,6-tetrachlorophenol within 48 h while only 60% of the given dose of 2,3,4,5-tetrachlorophenol could be recovered within 72 h. The acute toxicity of the tetrachlorophenols and tetrachloro-p-hydroquinone was studied in mice upon oral and intraperitoneal administration. 2,3,5,6-tetrachlorophenol (LD50p.o. 109 mg . kg-1) was the most toxic compound followed by 2,3,4,6- and 2,3.4,5-tetrachlorophenol (LD50p.o. 131 and 400 mg . kg-1, respectively). Tetrachloro-p-hydroquinone proved to have low oral toxicity (LD50p.o. 500 mg . kg-1) but was more toxic than the tetrachlorophenols when administered intraperitoneally. The oral LD50 for pentachlorophenol, under identical experimental conditions was found to be 74 mg . kg-1.

Animals↗
PubMed1982

Determination of total pentachlorophenol in the urine of workers. A method incorporating hydrolysis, an internal standard and measurement by liquid chromatography.

Free pentachlorophenol (PCP) represents a small and variable fraction of total PCP excreted in the urine of exposed workers. A method incorporating hydrolysis is essential to be able to relate PCP excretion to absorbed dose. 3,5-Dichloro-2,4,6-tribromophenol (DTP) is added as an internal standard to a urine sample which is then acidified and steam-distilled. The distillate is made alkaline and extracted with methylene chloride to remove interferences. The distillate is then acidified and the phenols extracted into methylene chloride. The extract is evaporated, redissolved in acetonitrile and the PCP is measured using high pressure liquid chromatography (HPLC) using a 15 X 0.46 cm Spherisob-ODS 5 microns column with isocratic elution (H2O:CH3CN:CH3CO2H, 45:55:0.3 v/v). Detection is by fixed wavelength detector at 313 nm and calculation by the method of internal standardization. The biological threshold value used to trigger action to reduce exposure is 7 mg/l (corrected to a specific gravity of 1.024).

Chlorophenols↗
PubMed1982

Pulmonary function after long-term exposure to trichlorophenol.

Symptoms and pulmonary function were evaluated in subjects exposed to trichlorophenol. Symptoms from upper airways and chest were more common among those exposed than in control subjects (60% and 10%, respectively) Significantly reduced forced expired flow at 75% of vital capacity [exposed: 5.721/s (5.08-6.85), mean and range; reference: 6.451/s (5.77-8.40), P less than 0.05] and increased closing volume [exposed: 25.2% (19.5-36.0), reference: 17.1% (12.0-23.5), P less than 0.01] were measured while other spirometric variables and the transfer factor of the lung for CO were normal. Increased elastic recoil pressure of the lung and signs of lung tissue engagement in X ray were noticed in two subjects. Blood and liver tests were normal. The findings suggest an irritating effect on the lung by trichlorophenol, and it cannot be excluded that long-term exposure may produce pulmonary fibrosis.

Adult↗
PubMed1992

Internal exposure to organic substances in a municipal waste incinerator.

Fifty-three persons occupied in a municipal waste incinerator were examined with respect to their internal exposure to organic substances which may be produced during pyrolysis of organic matter. For this purpose the levels of benzene in blood, polychlorinated biphenyls (PCBs) and hexachlorobenzene (HCB) in plasma, and mono- (MCPs), di- (DCPs), tri- (TCPs), tetra- (TCEPs) and pentachlorophenol (PCP) and hydroxypyrene in urine were determined. For control purposes, 431 men and women were examined. Significantly higher values for the workers were found for the excretion of hydroxypyrene [median (m): 0.24 vs 0.11 microgram/l; non-smokers], 2,4/2,5-DCP (m: 10.5 vs 3.9 micrograms/l) and 2,4,5-TCP (m: 1.2 vs 0.8 micrograms/l) and for the HCB level in plasma (m: 4.4 vs 2.8 micrograms/l). For the concentrations of 4-MCP and 2,3,4,6/2,3,5,6-TECP, the controls had significantly higher concentrations in urine than did the workers in the incineration plant (m: 4-MCP 1.7 vs 1.2; 2,3,4,6/2,3,5,6-TECP: 1.2 vs 0.3 micrograms/l). No significant differences between workers and controls were detected with respect to benzene in blood (m: 0.20 vs 0.28 microgram/l; non-smokers), 2,4,6-TCP and PCPs in urine (m: 0.85 vs 0.60 and 2.2 vs 2.2 micrograms/l) or the levels of PCB congeners in plasma (m: sigma 138, 153, 180: 5.6 vs 4.1 micrograms/l). The elevated levels of hydroxypyrene, 2,4/2,5-DCP, 2,4,5-TCP and HCB in biological material may be related to the incineration of the waste. These elevations, however, are very small and are of interest more from the environmental than from the occupational point of view.

Adult↗