Metabolism of pentachlorophenol by an axenic bacterial culture.
A bacterial isolate obtained from a continuous-flow enrichment culture has been shown to metabolize pentachlorophenol as a sole source of organic carbon and energy.
Bacteria↗
SEARCH · Search PubMed
Results for “Pentachlorophenol”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Enzymatic dehalogenation of pentachlorophenol by extracts from Arthrobacter sp. strain ATCC 33790.
Arthrobacter sp. strain ATCC 33790 was grown with pentachlorophenol (PCP) as the sole source of carbon and energy. Crude extracts, which were prepared by disruption of the bacteria with a French pressure cell, showed no dehalogenating activity with PCP as the substrate. After sucrose density ultracentrifugation of the crude extract at 145,000 x g, various layers were found in the gradient. One yellow layer showed enzymatic conversion of PCP. One chloride ion was released per molecule of PCP. The product of the enzymatic conversion was tetrachlorohydroquinone. NADPH and oxygen were essential for this reaction. EDTA stimulated the enzymatic activity by 67%. The optimum pH for the enzyme activity was 7.5, and the temperature optimum was 25 degrees C. Enzymatic activity was also detected with 2,4,5-trichlorophenol, 2,3,4-trichlorophenol, 2,4,6-trichlorophenol, and 2,3,4,5-tetrachlorophenol as substrates, whereas 3,4,5-trichlorophenol, 2,4-dichlorophenol, 3,4-dichlorophenol, and 4-chlorophenol did not serve as substrates.
Arthrobacter↗
Mechanism of enzymatic dehalogenation of pentachlorophenol by Arthrobacter sp. strain ATCC 33790.
Pentachlorophenol (PCP) dehalogenase from Arthrobacter sp. strain ATCC 33790 converts PCP to tetrachlorohydroquinone. In labeling experiments with H(2)18O or 18O2, only with H(2)18O was labeled product found. However, unlabeled tetrachlorohydroquinone became labeled after incubation with the enzyme in H(2)18O. Therefore, distinction between an oxygenolytic or a hydrolytic dehalogenation mechanism for the PCP dehalogenase is not possible.
Arthrobacter↗
Purification of a Flavobacterium pentachlorophenol-induced periplasmic protein (PcpA) and nucleotide sequence of the corresponding gene (pcpA).
A pentachlorophenol (PCP)-induced periplasmic protein (PcpA) with a molecular weight of 30,000 has been identified and purified from Flavobacterium sp. strain ATCC 39723. Results suggest that PcpA may be involved in PCP mineralization. The induction of PcpA correlated with the induction of PCP-degrading activity. When PcpA was released from the periplasmic space by EDTA or osmotic shock treatment, PCP-degrading activity was arrested. Two PCP- mutants of ATCC 39723, which do not degrade PCP, did not produce PcpA following induction with PCP. The N terminus of PcpA was sequenced, and two degenerate primers were synthesized for use in DNA amplification of a 68-bp probe which hybridized to a genomic library clone containing pcpA. The nucleotide sequence of pcpA was determined and found to encode an open reading frame of 816 bp. pcpA was found to be part of a 1.35-kb transcript with a transcriptional start site 67 bp upstream of the translational start site. Data base search comparisons yielded no sequences of high similarity to pcpA or its protein product.
Amino Acid Sequence↗
Organization and regulation of pentachlorophenol-degrading genes in Sphingobium chlorophenolicum ATCC 39723.
The first three enzymes of the pentachlorophenol (PCP) degradation pathway in Sphingobium chlorophenolicum (formerly Sphingomonas chlorophenolica) ATCC 39723 have been characterized, and the corresponding genes, pcpA, pcpB, and pcpC, have been individually cloned and sequenced. To search for new genes involved in PCP degradation and map the physical locations of the pcp genes, a 24-kb fragment containing pcpA and pcpC was completely sequenced. A putative LysR-type transcriptional regulator gene, pcpM, and a maleylacetate reductase gene, pcpE, were identified upstream of pcpA. pcpE was found to play a role in PCP degradation. pcpB was not found on the 24-kb fragment. The four gene products PcpB, PcpC, PcpA, and PcpE were responsible for the metabolism of PCP to 3-oxoadipate in ATCC 39723, and inactivational mutation of each gene disrupted the degradation pathway. The organization of the pcp genes is unusual because the four PCP-degrading genes, pcpA, pcpB, pcpC, and pcpE, were found to be located at four discrete locations. Two hypothetical LysR-type regulator genes, pcpM and pcpR, have been identified; pcpM was not required, but pcpR was essential for the induction of pcpB, pcpA, and pcpE. The coinducers of PcpR were PCP and other polychlorinated phenols. The expression of pcpC was constitutive. Thus, the organization and regulation of the genes involved in PCP degradation to 3-oxoadipate were documented.
Base Sequence↗
A previously unrecognized step in pentachlorophenol degradation in Sphingobium chlorophenolicum is catalyzed by tetrachlorobenzoquinone reductase (PcpD).
The first step in the pentachlorophenol (PCP) degradation pathway in Sphingobium chlorophenolicum has been believed for more than a decade to be conversion of PCP to tetrachlorohydroquinone. We show here that PCP is actually converted to tetrachlorobenzoquinone, which is subsequently reduced to tetrachlorohydroquinone by PcpD, a protein that had previously been suggested to be a PCP hydroxylase reductase. pcpD is immediately downstream of pcpB, the gene encoding PCP hydroxylase (PCP monooxygenase). Expression of PcpD is induced in the presence of PCP. A mutant strain lacking functional PcpD has an impaired ability to remove PCP from the medium. In contrast, the mutant strain removes tetrachlorophenol from the medium at the same rate as does the wild-type strain. These data suggest that PcpD catalyzes a step necessary for degradation of PCP, but not for degradation of tetrachlorophenol. Based upon the known mechanisms of flavin monooxygenases such as PCP hydroxylase, hydroxylation of PCP should produce tetrachlorobenzoquinone, while hydroxylation of tetrachlorophenol should produce tetrachlorohydroquinone. Thus, we proposed and verified experimentally that PcpD is a tetrachlorobenzoquinone reductase that catalyzes the NADPH-dependent reduction of tetrachlorobenzoquinone to tetrachlorohydroquinone.
Alphaproteobacteria↗
Pentachlorophenol and the peripheral nervous system: a longitudinal study in exposed workers.
A longitudinal study was performed to examine whether chronic occupational exposure to pentachlorophenol (PCP) or its compounds causes measurable alterations in the conduction velocity in peripheral nerves as an "adverse effect." In total, the results of nerve conduction velocity (NCV) determinations in 1980 and 1984 in 10 subjects (7 men, 3 women) who had been exposed for an average of 16 years (range 4-24) were available. The concentrations of PCP in the air at the workplace varied between 0.3 and 180 micrograms/m3 and were thus below the maximum allowed concentration (MAK value) of 500 micrograms/m3. The biological monitoring carried out showed the following results: PCP in the serum: 38-1270 micrograms/l; PCP in the urine: 8-1224 micrograms/l. Compared with the upper normal limits (PCP in the serum 150 micrograms/l, PCP in the urine 60 micrograms/l), distinct internal exposure to PCP has resulted in some of the employees. Determinations of the NCV of motor and sensory nerve fibres (ulnar, median, peroneal, and sural nerve) were always in the normal range. A significant difference in the NCV for the period 1980-4 could not be detected. In addition, the correlation analyses did not show any hints of "dose-effect relations." It is concluded that occupational exposure to PCP over several years in the concentrations observed probably do not lead to any adverse effects on the peripheral nervous system.
Adult↗
Biodegradation of pentachlorophenol in soil: the response to physical, chemical, and biological treatments.
The effects of physical, chemical, and biological treatments on biodegradation of pentachlorophenol (PCP) were studied in a silt-loam soil contaminated with 175 mg PCP/kg and uniformly 14C-labelled PCP. Biodegradation of 14C-labelled PCP and technical-grade PCP were monitored over 210 days incubation. Mineralization of labelled PCP was significantly (p=0.05) influenced by soil treatments. Negligible biodegradation occurred in either the sterile control soil or the uninoculated control soil, with less than 1% of added 14C recovered as 14 CO2. Inoculation of unamended soil with a strain of Flavobacterium (ATCC 39723) known to degrade PCP increased biodegradation of PCP; approximately 60% of the [14C]PCP was recovered as 14CO2. Increased soil water content (60% versus 30% w/w) enhanced biodegradation (67% recovery of 14C as CO2), while increased chloride ion concentration and anoxic conditions were inhibitory (20 and 1% recoveries, respectively). Residual soil PCP concentrations were also influenced by various treatments. In the sterile control soil and noninoculated control, after 210 days incubation, concentrations of PCP were 143 and 1223 mg/kg, respectively, while the PCP concentration in the inoculated soil was 21 mg/kg. When soil organic matter was increased by adding finely ground red clover leaf and stem material, the residual PCP concentration was reduced to 6 mg/kg after 210 days. Increased soil water content resulted in a residual PCP concentration of 5 mg/kg. High-pressure liquid chromatography of soil extracts revealed no accumulation of partial PCP degradation products. The results indicated that biodegradation of PCP in soil was significantly influenced by various soil amendments.
Biodegradation, Environmental↗
Study of the reductive dechlorination of pentachlorophenol by a methanogenic consortium.
Pentachlorophenol (PCP) dechlorination by a methanogenic consortium was observed when glucose, formate, lactate, or yeast extract was present in the mineral medium as a secondary carbon source. Acetate was not a good substrate to sustain dechlorination. The consortium was able to dechlorinate the different monochlorophenols, although the chlorine in position ortho and meta was removed more readily than in para position. Dechlorination was most efficient at 37 degrees C. At 45 degrees C, the first PCP dechlorination steps were very rapid, but 3,5-dichlorophenol (3,5-DCP) was not further dechlorinated. At 15 and 4 degrees C, dechlorination was very slow. The dechlorination of PCP to 3-chlorophenol (3-CP) was still observed after the consortium had been subjected to heat treatment (80 degrees C, 60 min), suggesting that spore-forming bacteria were responsible. The dechlorinating activity of the consortium was significantly reduced by the presence of hydrogen, 2-bromoethanosulfonic acid (BESA), or sulfate but not of nitrate. The dechlorination of 3-CP was completely inhibited by heat treatment or the presence of BESA, suggesting that a syntrophic microorganism would be involved. Vigorous agitation of the consortium stopped the dechlorination, but the presence of DEAE-Sephacel acting as a support was very efficient in restoring the activity, suggesting that association between certain members of the consortium was important.
Alkanesulfonic Acids↗
Non-occupational exposure to pentachlorophenol: clinical findings and plasma-PCP-concentrations in three families.
1 The clinical findings are reported of 15 members of three families living in houses where relatively large amounts of pentachlorophenol (PCP) solutions had been applied. To be able to interpret the plasma concentrations in the patients, plasma-PCP-concentrations in 99 draftees were measured. The clinical and toxicological-analytical results are discussed. 2 Signs of a systemic PCP-intoxication were not found in any patient. 3 Symptoms and objective changes of the uncovered skin were present in three patients (a burning painful sensation, erythema, dryness and scaling) possibly caused by a direct influence of PCP in the air. 4 The plasma-PCP-concentrations in the patients ranged from 25-660 micrograms 1(-1). The mean plasma-PCP-concentrations in the draftees was 128.6 +/- 134.9 micrograms 1(-1) (mean +/- s.d.); the median was 88 micrograms 1(-1), the 95% range was 330 micrograms 1(-1). 5 There was an association between patients' plasma-PCP-concentrations and their staying in the affected house.
Adolescent↗
Absorption study of pentachlorophenol in persons working with wood preservatives.
Plasma and urinary pentachlorophenol (PCP) was measured in 209 workers who had occupational exposure to wood preservatives containing this compound and 101 workers not exposed occupationally to PCP. Workers were examined for chloracne and blood concentrations of bilirubin, gamma-glutamyltransferase (GGT), cholesterol and high-density lipoproteins (HDL) were determined. All the occupationally exposed groups showed evidence of PCP absorption; highest mean concentrations were found in remedial timber-treatment operatives (6.0 mmol/l for plasma and 274 nmol/mmol of creatinine for urine). Timber-yard workers also showed substantial evidence of absorption (mean plasma concentration 4.8 mmol/l). Persons formulating PCP-containing wood preservatives had the lowest concentrations of any exposed group sampled (mean plasma concentration 1.3 mmol/l, mean urinary concentration 39.6 nmol/mmol of creatinine). The occupational groups studied were not standardized for factors known to affect bilirubin, GGT, cholesterol and HDL. The inference that can be drawn from the results of these measurements is therefore limited. There was, however, no evidence of any disadvantageous effect of PCP on health as measured by these parameters. No overt case of chloracne was found.
Acne Vulgaris↗
Assessment of pentachlorophenol exposure in humans using the clearance concept.
1. Pentachlorophenol (PeCP), a widely-used wood preservative, is a ubiquitous compound which has been found to be carcinogenic in mice. The objective of this study is to assess the average net daily intake of PeCP in cohorts of individuals who are: (1) not specifically exposed to PeCP, (2) residents of homes made of PeCP-treated logs and (3) occupationally exposed to PeCP. 2. The average net daily intake was calculated using a basic pharmacokinetic principle, the clearance (CL) concept: net daily intake equals CL (in 1 d-1) times the average steady-state concentration of PeCP in plasma (Css). Css values reported in the literature were used for the calculations. 3. Because the two definitive studies on PeCP toxicokinetics in humans have given conflicting results, kinetic information from human exposure to PeCP was reviewed. Plasma clearance was estimated from retrospective analysis of urine and plasma concentrations measured in people after long-term exposure to PeCP. An overall clearance of 0.425 l d-1 was obtained. 4. In groups of individuals who are not specifically exposed to PeCP, net daily intake estimated in eight countries varied from 5 micrograms (Nigeria) to 37 micrograms (The Netherlands). Net intake was between 51 micrograms d-1 and 157 micrograms d-1 in residents of homes made of PeCP-treated logs. In individuals occupationally exposed to PeCP, net daily intake varied widely (from 35 micrograms to about 24,000 micrograms) depending on the type of work.
Adult↗
Pentachlorophenol carcinogenicity: extrapolation of risk from mice to humans.
1. Pentachlorophenol (PCP) has been found to be carcinogenic in mice. The objective of this study was to extrapolate to humans the risk of cancer from data obtained in mice using information on disposition, serum protein binding and metabolism of PCP across species. 2. A review of the literature indicates that neither PCP nor a mutagenic metabolite, tetrachlorohydroquinone (TCHQ), has been specifically identified as responsible for the carcinogenicity. In addition, the occurrence of TCHQ as a metabolite of PCP in humans is still questionable. Therefore, cancer risk assessment is performed on the assumption that PCP itself is responsible for the carcinogenicity. 3. For interspecies extrapolation, a new method in which interspecies differences in clearance and serum protein binding are taken into account is used. The method gives estimates of equivalent human doses of PCP which are up to 4 times smaller than those obtained using body surface area. For both interspecies extrapolation methods, the estimated virtually-safe doses of PCP are smaller than the average daily intakes reported in groups of subjects nonspecifically exposed to PCP. Corresponding extra risks of cancer for lifetime exposure are from 20 to 140 times greater than the acceptable extra risk (10(-6)). The results obtained with this approach indicate that PCP is a possible public health hazard.
Animals↗
Human pentachlorophenol poisoning.
Pentachlorophenol (PCP) was, and still is, one of the most frequently used fungicides and pesticides. Its toxicity is due to interference with oxidative phosphorylation. Acute and chronic poisoning may occur by dermal absorption, inhalation or ingestion. Chronic poisoning occurs mainly in sawmill workers or people living in log homes treated with PCP-containing wood protecting formulations. Quantitative determination of PCP in urine and serum is useful to detect occupational or subclinical exposure. The clinical features of acute and chronic PCP poisoning can be classified systematically into effects on the skin, metabolism (fever), the haematopoietic tissue, the respiratory system, the central and peripheral nervous system, the kidney and the gastrointestinal tract. Although PCP is not classified as a human carcinogen, some epidemiological observations suggest that exposure to chlorophenols in general and PCP solutions in particular may result in an increased risk for certain malignant disorders such as nasal carcinoma and soft tissue sarcoma. There is concern that contamination of PCP-solutions with products such as chlorodibenzo-p-dioxins is the real cause of this suspected carcinogenicity. No specific antidote exists for the treatment of (acute) PCP poisoning. The basis of the treatment of acute poisoning is intensive supportive care with prevention of dangerous rise in temperature. Use of PCP-based products as indoor wood preservatives poses an unacceptable risk to human health.
Carcinogenicity Tests↗
Assessment of pentachlorophenol-exposed timber workers using a test-of-poisoning model.
Sixty-two former New Zealand timber workers who were exposed to pentachlorophenol (PCP) at work were interviewed, examined, and assessed both by laboratory investigations and psychometrically for clinical syndromes that could be related to PCP exposure. Three such syndromes were identified: an acute complex of fever, headaches, upper and lower respiratory tract and eye irritation, skin disease, and foul smelling and discolored sweat; a chronic fatigue syndrome, beginning while still at work and frequently persisting; and a delayed encephalopathy. Neither of the sustained syndromes was considered characteristic of PCP poisoning, and many confounders were identified. An exposure index and a test-of-poisoning score had a statistically insignificant correlation.
Adult↗
Effects of pentachlorophenol and tetrachlorohydroquinone on mitogen-activated protein kinase pathways in Jurkat T cells.
When Jurkat human T cells were incubated with 20 microM of pentachlorophenol (PCP) or its metabolite, tetrachlorohydroquinone (TCHQ), for 10 hr, flow cytometric analyses revealed marked increase in the number of apoptotic cells. DNA fragmentation was also observed in these cells. TCHQ was more potent than PCP in causing apoptosis. After incubation with 20 microM TCHQ for 1 hr, all mitogen-activated protein kinases (MAPKs) examined [i.e., extracellular signal-regulated protein kinase (ERK), p38, and c-Jun NH(2)-terminal kinase (JNK)] were phosphorylated, whereas no clear phosphorylation was induced by PCP. TCHQ-induced apoptosis was markedly suppressed by treatment with a p38 inhibitor (SB203580) and mildly (but significantly) suppressed by treatment with a MAPK/ERK kinase inhibitor (U0126). When cells were treated with both inhibitors at the same time, TCHQ-induced apoptosis disappeared almost completely. PCP-induced apoptosis was also suppressed by SB203580 and/or U0126. Nevertheless, treatment with LL-Z1640-2, which inhibits JNK phosphorylation, did not suppress the apoptosis caused by either TCHQ or PCP. Thus, p38 and ERK appear to be important signal transduction pathways leading to apoptosis in a human T-cell line exposed to a ubiquitous pollutant or its metabolite in the general and occupational environment.
Apoptosis↗
Pentachlorophenol and hydroxylated polychlorinated biphenyl metabolites in umbilical cord plasma of neonates from coastal populations in Québec.
Concentrations of polychlorinated biphenyls (PCBs), hydroxylated metabolites of PCBs (HO-PCBs) and octachlorostyrene (4-HO-HpCS), and pentachlorophenol (PCP) were determined in umbilical cord plasma samples from three different regions of Québec. The regions studied included two coastal areas where exposure to PCBs is high because of marine-food-based diets--Nunavik (Inuit people) and the Lower North Shore of the Gulf of St. Lawrence (subsistence fishermen)--and a southern Québec urban center where PCB exposure is at background levels (Québec City). The main chlorinated phenolic compound in all regions was PCP. Concentrations of PCP were not significantly different among regions (geometric mean concentration 1,670 pg/g, range 628-7,680 pg/g wet weight in plasma). The ratio of PCP to polychlorinated biphenyl congener number 153 (CB153) concentration ranged from 0.72 to 42.3. Sum HO-PCB (sigma HO-PCBs) concentrations were different among regions, with geometric mean concentrations of 553 (range 238-1,750), 286 (103-788), and 234 (147-464) pg/g wet weight plasma for the Lower North Shore, Nunavik, and the southern Québec groups, respectively. Lower North Shore samples also had the highest geometric mean concentration of sum PCBs (sum of 49 congeners; sigma PCBs), 2,710 (525-7,720) pg/g wet weight plasma. sigma PCB concentrations for Nunavik samples and southern samples were 1,510 (309-6,230) and 843 (290-1,650) pg/g wet weight plasma. Concentrations (log transformed) of sigma HO-PCBs and sigma PCBs were significantly correlated (r = 0.62, p < 0.001), as were concentrations of all major individual HO-PCB congeners and individual PCB congeners. In Nunavik and Lower North Shore samples, free thyroxine (T4) concentrations (log transformed) were negatively correlated with the sum of quantitated chlorinated phenolic compounds (sum PCP and sigma HO-PCBs; r = -0.47, p = 0.01, n = 20) and were not correlated with any PCB congeners or sigma PCBs. This suggests that PCP and HO-PCBs are possibly altering thyroid hormone status in newborns, which could lead to neurodevelopmental effects in infants. Further studies are needed to examine the effects of chlorinated phenolic compounds on thyroid hormone status in newborns.
Diet↗
Human prenatal and postnatal exposure to polybrominated diphenyl ethers, polychlorinated biphenyls, polychlorobiphenylols, and pentachlorophenol.
The aim of this study was to determine human prenatal and postnatal exposures to polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), hydroxylated metabolites of PCBs (polychlorobiphenylols; OH-PCBs), and pentachlorophenol (PCP). The median PBDE fresh-weight concentrations in maternal and cord blood plasma and in breast milk were 24, 4.3, and 75 pg/g, respectively. The PCB concentrations were approximately 60 times higher in each compartment (1,560, 277, and 4,310 pg/g, respectively). Calculated on a lipid weight basis, the levels were comparable in maternal blood plasma and breast milk. In contrast to PCBs, differences were found between PBDE congener distribution in maternal and cord blood plasma. The OH-PCBs constituted up to 26% of the PCB levels in maternal blood plasma and 53% in cord blood plasma, with levels of 120 and 88 pg/g fresh weight, respectively, and in breast milk 3 pg/g. The corresponding concentrations for PCP were 2,830, 1,960, and 20 pg/g. The ratios of PCB to OH-PCB were 13, 3, and 1,400 in maternal, cord plasma, and breast milk, respectively. It is evident that prenatal exposures occur for all the analytes. Moreover, the exposure continues after birth via breast milk. However, levels of OH-PCBs and PCP in breast milk are low compared with levels in blood plasma. Exposures to both PCBs and PBDEs, and in particular to the endocrine-active halogenated phenolic compounds, are of concern and implicate a potential risk for developmental disturbances.
Adult↗