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PubMed1990

Metabolism and bacterial mutagenicity of binary mixtures of benzo(a)pyrene and polychlorinated aromatic hydrocarbons.

The results of both the Salmonella/microsome mutagenicity assay and high-performance liquid chromatography (HPLC) analysis were used to evaluate the interactions of binary mixtures of benzo(a)pyrene (BAP) and several different polychlorinated aromatic hydrocarbons. Binary mixtures of either 2-nitro-3,7,8-trichlorodibenzo-p-dioxin (2NTCDD) or pentachlorophenol (PCP) with BAP produced synergism, whereas strictly additive effects were observed with mixtures of octa- or hepta-chlorodibenzo-p-dioxin and BAP. At a dose of 50 micrograms per plate, BAP induced 120 total revertants, whereas the binary mixture of BAP and PCP induced 303 total revertants. The binary mixture of BAP at 1 microgram per plate and 2NTCDD at 0.5 microgram per plate induced 261 net revertants, whereas BAP alone induced 42 net revertants. HPLC analysis of the mixtures indicated that preincubation of BAP with 2NTCDD increased the quantity of benzo(a)pyrene-7,8-dihydrodiol, and 9,10-dihydrodiol metabolites detected. The data suggest that nonmutagenic components of a complex mixture may alter the metabolism of promixate mutagens. Thus, in the present study, 2NTCDD appears to have inhibited the detoxication of BAP metabolites.

Benzo(a)pyrene↗
PubMed1975

[Identification of metabolites and metabolism of hexachlorobenzene in a mold culture].

Hexachlorobenzene is but slowly metabolized by a lindane-decomposing mould culture, only pentachlorobenzene being detected as a metabolite. The degradation of pentachlorobenzene yields the following metabolites: pentachlorophenol, 2,3,4,5-tetrachlorophenol, 2,3,4,6-tetrachlorophenol, 1,2,3,4-tetrachlorobenzene, 1,2,4,5- and/or 1,2,3,5-tetrachlorobenzene, 2,3,4-trichlorophenol, 2,4,6-trichlorophenol, 3,4,5-trichlorophenol, 1,3,5-trichlorobenzene. The establishment of a degradation pattern is under way.

Chlorine↗
PubMed1992

The Ca(2+)-transport-ATPase of human erythrocytes as an in vitro toxicity test system--acute effects of some chlorinated compounds.

Investigations to determine the inhibitory activity on the Ca(2+)-transport-ATPase of human erythrocyte membranes were performed with various compounds of toxicological significance, mostly chlorinated and mainly used as biocides, such as phenol, 4-chlorophenol, 2,4-dichlorophenol, 2,6-dichlorophenol, 3,4-dichlorophenol, 2,3,4-trichlorophenol, 2,3,4,5-tetrachlorophenol, pentachlorophenol (PCP), captan, folpet, captafol, (+)-camphene, toxaphene, dichlorodiphenyltrichloroethane (DDT), lindane, endrin, dieldrin, alpha-endosulfan, beta-endosulfan, paraquat, diallate, 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T). Some of the compounds investigated display an inhibitory effect on the Ca(2+)-transport-ATPase at very low concentrations. The in vitro results obtained in this enzyme assay can be correlated directly with the results of other in vitro assays and with the results of in vivo investigations in different species in which an inhibitory effect on various biological functions is observed. Therefore, an inhibitory effect on the Ca(2+)-transport-ATPase indicates a toxic effect of these compounds to cell functions. Since the inhibitory effect of these compounds can be measured rapidly and the enzyme is easy to handle, it might be a useful tool to screen the toxic effects of various compounds on cell function. The aim of the authors was to investigate the usefulness of this screening test system for the characterization of the cellular toxicity of various compounds.

Calcium-Transporting ATPases↗
PubMed1976

Effect of uncoupler on "downhill" substrate efflux of Escherichia coli is dependent on (Mg2+, Ca2+). Adenosine triphosphatase.

Previous studies have shown that mutations in the unc gene of Escherichia coli K12 cause defects in energy transduction as well as a membrane-bound (Mg2+, Ca2+)-adenosine triphosphatase. We studied the effect of this mutation on the "downhill" efflux of methyl-beta-D-galactopyranoside, a suboli K12 did not show significant differences in substrate influx of efflux, a differential effect of an uncoupler, 2,4-dinitrophenol was demonstrated. In contrast to the unc+, dinitrophenol failed to inhibit significantly the rate coefficient of efflux in the unc- strain. Analysis of spontaneous unc+ revertants of the unc- mutant provided additional evidence that a functional unc gene is necessary for dinitrophenol inhibition of efflux. Other uncouplers tested in the unc+ strain showed different effects on efflux. While arsenate, azide and carbonyl cyanide p-trifluoromethoxyphenulhydrazone caused little or no effect, 2,4-dibromophenol and pentachlorophenol increased efflux by a considerable factor.

Adenosine Triphosphatases↗
PubMed1999

Comparison of catalytic activity and inhibitors of quinone reactions of succinate dehydrogenase (Succinate-ubiquinone oxidoreductase) and fumarate reductase (Menaquinol-fumarate oxidoreductase) from Escherichia coli.

Escherichia coli succinate-ubiquinone oxidoreductase (SQR) and menaquinol-fumarate reductase (QFR) are excellent model systems to understand the function of eukaryotic Complex II. They have structural and catalytic properties similar to their eukaryotic counterpart. An exception is that potent inhibitors of mammalian Complex II, such as thenoyltrifluoroacetone and carboxanilides, only weakly inhibit their bacterial counterparts. This lack of good inhibitors of quinone reactions and the higher level of side reactions in the prokaryotic enzymes has hampered the elucidation of the mechanism of quinone oxidation/reduction in E. coli Complex II. In this communication DT-diaphorase and an appropriate quinone are used to measure quinol-fumarate reductase activity and E. coli bo-oxidase and quinones are used to determine succinate-quinone reductase activity. Simple Michaelis kinetics are observed for both enzymes with ubiquinones and menaquinones in the succinate oxidase (forward) and fumarate reductase (reverse) reactions. The comparison of E. coli SQR and QFR demonstrates that 2-n-heptyl 4-hydroxyquinoline-N-oxide (HQNO) is a potent inhibitor of QFR in both assays; however, SQR is not sensitive to HQNO. A series of 2-alkyl-4,6-dinitrophenols and pentachlorophenol were found to be potent competitive inhibitors of both SQR and QFR. In addition, the isolated E. coli SQR complex demonstrates a mixed-type inhibition with carboxanilides, whereas the QFR complex is resistant to this inhibitor. The kinetic properties of SQR and QFR suggest that either ubiquinone or menaquinone operates at a single exchangeable site working in forward or reverse reactions. The pH activity profiles for E. coli QFR and SQR are similar showing maximal activity between pH 7.4 and 7.8, suggesting the importance of similar catalytic groups in quinol deprotonation and oxidation.

Anilides↗
PubMed1993

Ecotoxicological studies with the freshwater rotifer Brachionus calyciflorus. III. The effects of chemicals on the feeding behavior.

The effect of short-term exposure to xenobiotics on the feeding behavior of the freshwater rotifer Brachionus calyciflorus was studied. The filtration and ingestion rates of this rotifer decreased after an exposure of 5 hr to sublethal concentrations of copper, pentachlorophenolate, 3,4-dichloroaniline, and lindane. The effective concentrations at which feeding rate was reduced to 50% of that in controls (EC50) for the respective chemicals are 0.032, 1.85, 41.2, and 8.5 mg/liter. The potential use of feeding behavior as test criterion for toxicity screening tests with aquatic invertebrates is discussed.

Aniline Compounds↗
PubMed1994

Statistical analysis of joint toxicity in biological growth experiments.

The authors formulate a model for the analysis of designed biological growth experiments where a mixture of toxicants is applied to biological target organisms. The purpose of such experiments is to assess the toxicity of the mixture in comparison with the toxicity observed when the toxicants are applied individually to the organisms. The analysis is based on a random differential equation describing the growth of the organisms. This model yields a natural measure of interaction between toxicants and the hypothesis of independent action from a mixture of toxicants can be tested. The proposed model is applied on data from an experiment where inhibition of the growth of the bacteria Pseudomonas fluorescens caused by different mixtures of pentachlorophenol and aniline was studied.

Aniline Compounds↗
PubMed2002

Repeatability of the submitochondrial particle assay.

A study assessing the intralaboratory precision of the in vitro submitochondrial particle (SMP) electron transfer (ETr) and reverse electron transfer (RET) assays was undertaken using the standard reference toxicants, pentachlorophenol (PCP), sodium dodecyl sulfate (SDS), and zinc sulfate 7-hydrate (ZnSO4 7H2O). One to three trials of each assay were manually conducted daily for at least 5 days with each toxicant using commercially available sources of particles and reagents. Composite coefficients of variation (CVs) for the ETr assay ranged from 20.6% for ZnSO4 to 29.3% for PCP (n > or = 15). Composite CVs for the RET assay ranged from 6.5% for SDS to 16.5% for PCP (n > or = 15). Comparison of intralaboratory results with in-house and published data demonstrates that the precision of both of these SMP assays is comparable to that of the more common in vivo, whole-organism bacterial, invertebrate, and fish toxicity tests.

Animals↗
PubMed1993

Modeling blood/plasma concentrations in dosed feed and dosed drinking water toxicology studies.

A computer model for predicting blood/plasma concentrations of test chemicals in dosed feed and dosed drinking water toxicology studies was developed. The model was constructed based on linear theory. The animal's feeding and drinking habits and the linear disposition kinetics of the test chemical obtained after a bolus gavage dose were built into the model. Blood/plasma concentrations of oxazepam and pentachlorophenol in dosed feed and dosed drinking water studies were predicted and compared with the experimentally determined data. The model proved highly reliable in predicting the blood/plasma concentrations of test chemical in dosed feed and dosed drinking water studies. The results suggest that if the kinetics of test chemicals fit a one-compartment model then bioaccumulation of the test chemical will occur in dosed feed or in dosed drinking water studies when absorption half-lives are less than 1.38 hr and elimination half-lives are longer than 5 hr. The extent of accumulation is mainly dependent on the elimination half-lives. For chemicals with absorption half-lives less than 1.38 hr and elimination half-lives less than 2 hr, the extent of bioaccumulation will be minimal. Blood/plasma concentrations of test chemicals in rats and mice will fluctuate daily and a quasi-steady state will be achieved after ad libitum exposure to dosed feed or dosed drinking water for approximately 4 days. If a daily 12-hr light cycle is used with the light cycle starting at 7:00 AM, the expected peak and trough blood concentrations in dosed feed studies will occur approximately in the early morning (5:00 AM) and in the late afternoon (4:00 PM), respectively. Similar results were obtained for dosed drinking water studies. The model should be applicable to dosed feed and dosed drinking water studies using other species.

Animals↗
PubMed2000

Induction of rat hepatic aryl sulfotransferase (SULT1A1) gene expression by triamcinolone acetonide: impact on minoxidil-mediated hypotension.

The hypotensive agent minoxidil (6-imino-1, 2-dihydro-1-hydroxy-2-imino-4-piperidinopyrimidine) depends upon aryl sulfotransferase (SULT1)-catalyzed sulfation for its bioactivation. Previous reports suggest that glucocorticoids induce class-specific SULT1 and isoform-specific SULT1A1 gene expression in rat liver. In the present study, rats were treated with the glucocorticoid triamcinolone acetonide (TA, 5 mg/kg/day i.p. x 3 days) or its vehicle, 2% Tween-20, prior to minoxidil, and subsequent effects on mean arterial pressure (MAP), heart rate (HR), and hepatic SULT1 gene expression were characterized. Minoxidil treatment (1.5 mg/kg) resulted in a steady decline in MAP values of 16.3 to 18.6% relative to basal control levels at 35 to 60 min following minoxidil injection. Pentachlorophenol (PCP, 40 micromol/kg i.p.), an inhibitor of SULT1 enzyme activity, effectively ablated the hypotensive effects of minoxidil. By contrast, pretreatment with TA significantly enhanced minoxidil-induced hypotension. Relative to vehicle-treated controls, TA-treated rats displayed a steeper rate of decline in MAP and more profound levels of hypotension with decreases in MAP following minoxidil administration of 27.8%. TA also produced significant increases in hepatic SULT1 mRNA expression (of 271%) and SULT1A1 immunoreactive protein levels (of 273%), relative to vehicle-treated controls. These results provide physiological evidence to support the biological relevance of SULT1A1 induction by glucocorticoids. The data indicate that steroid treatment induces SULT1A1 gene expression and, as a consequence, accentuates the hypotensive effects of minoxidil.

Animals↗
PubMed1984

Modulation of genotoxic and cytotoxic effects of aromatic amines in monolayers of rat hepatocytes.

Cultured rat hepatocytes exposed to 2-acetylaminofluorene (AAF), 2-aminofluorene (AF) or N-hydroxy-2-acetylaminofluorene (N-OH-AFF) for 3 hrs resulted in an increase in DNA repair measured as unscheduled DNA synthesis, with N-OH-AAF greater than AAF greater than AF. Cytotoxic effects were only seen with N-OH-AAF above 10(-6) M. alpha-Naphthoflavone increased the unscheduled DNA synthesis and cytotoxic effects of N-OH-AAF, whereas it decreased DNA repair and the covalent binding of AAF to cellular proteins. In contrast, very little effects of paraoxon were seen on the repair synthesis elicited by AAF, AF or N-OH-AAF. The addition of ascorbate reduced the covalent binding of AAF, the DNA repair synthesis caused by AAF and N-OH-AAF, and the cytotoxic effects of N-OH-AAF. The addition of pentachlorophenol or salicylamide all resulted in similar effects as ascorbate, through reduction of sulfation. Galactosamine, an inhibitor of glucuronidation, and the nucleophile GSH caused no or only minor effects of the activation of AAF, AF or N-OH-AAF as judged from the endpoints tested. These results are consistent with an arylnitrenium ion, a sulfate ester or a free radical as the arylamine metabolite causing cellular DNA damage, whereas the sulfate ester or a radical intermediate may be responsible for the cytotoxic effects of N-OH-AAF.

2-Acetylaminofluorene↗
PubMed1983

Mechanism of formation of mercapturic acids from aromatic aldehydes in vivo.

Male adult Wistar rats dosed i.p. with o-substituted benzaldehydes (o-F, o-Cl, and o-Br = V, VI, and VII) excreted mercapturic acids in urine. These acids were identified as N-acetyl-S-(ortho-substituted benzyl)cysteines (I, II, III). The total mercapturic acid excretion as % dose (2.0 mmol/kg, n = 4) was 1.2 +/- 0.4, 6.8 +/- 0.9, and 10.4 +/- 2.0 for V, VI, and VII. p-Cl-benzaldehyde administered in the same dose showed a non-significant urinary thioether excretion. The aim of the investigation was to prove in vivo a postulated metabolic pathway of substituted benzaldehydes via sulphate esters to mercapturic acids. After a single administration of the sodium salts of o- and p-Cl-benzylsulfuric acid a significant increase in mercapturic acid excretion of 21.2 +/- 1.8% and 14.5 +/- 1.2% of dose (2.0 mmol/kg, n = 4) was found. By pretreatment with pyrazole the mercapturic acid excretion increased after administration of o-Cl-benzyl alcohol (IX) whereas a significant decrease was found after administration of o-Cl-benzaldehyde (VI). After simultaneous administration of ethanol with IX and VI an increase in mercapturic acid excretion was observed. After previous administration of pentachlorophenol a significant decrease in urinary mercapturic acid excretion for IX and VI was found. These findings are in accordance with a metabolic pathway of substituted benzaldehydes via benzyl alcohols, subsequently sulphate esters to the corresponding benzylmercapturic acids.

Acetylcysteine↗
PubMed1996

Introduction of a de novo bioremediation activity into anaerobic granular sludge using the dechlorinating bacterium DCB-2.

The strictly anaerobic, pentachlorophenol (PCP) degrading bacterium DCB-2 was immobilized in an Upflow Anaerobic Sludge Blanket (UASB) reactor containing sterile granules. PCP and lactate were fed to the reactor and the concentration of chlorophenols in the effluent were monitored for 641 days. PCP was found to be degraded and transformed into 3,4,5-trichlorophenol in the reactor where DCB-2 introduced PPCP was still transformed to 3,4,5-trichlorophenol when the hydraulic retention time was decreased to six hours which was much lower than the generation time of DCB-2 insuring no free living cells in the reactor. This indicated that DCB-2 was immobilized in the granular layer. A control reactor that contained only sterile granules did not dechlorinate PCP indicating that the performance in the inoculated reactor was only due to the introduced bacteria. Immobilization of DCB-2 in the granules was further demonstrated by adding an antibody raised against DCB-2 to sliced granules. Bacteria thus visualized formed a net structure inside the granules. No DCB-2 bacteria could be found in granules from the control reactor. When lactate was omitted from the influent, the reactor still dechlorinated PCP in accordance with our findings that lactate was not used by DCB-2. This suggested that the reducing equivalents for reductive dechlorination were derived from the granules themselves. The reactor performance was 120 mumol.l reactor-1.day-1, comparable to the best described performance of a UASB-reactor and to aerobic reactors. Our study demonstrates that granules can be constructed which possess specific abilities such as a dechlorinating activity and at the same time be high performing. This result have implications for eco-engineering of granules for anaerobic treatment of contaminated waters.

Bacteria, Anaerobic↗
PubMed1982

Effect of sequence of exposure to chlorophenols in short-term bacterial bioassays.

A bioassay using Pseudomonas fluorescens was affected by the sequence of exposure to pentachlorophenol (PCP) and 2,3,4,5-tetrachlorophenol (TCP). Surviving cells from standardized cell suspensions initially treated with PCP at concentrations ranging from 10 to 75 micrograms/ml, followed by removal of the toxicant, were not affected by a second dose of PCP at the same concentration. However, if the second dose was TCP, the test organism was sensitive to the second exposure. The most toxic sequence was an initial exposure to TCP followed by a second exposure to PCP. The response of the test organism to PCP and TCP was clearly dependent upon both the toxicant concentrations used and the sequence of toxicant addition.

Bacteria↗
PubMed1980

The involvement of porphyrogenic steroids in the development of experimental porphyria.

Hexachlorobenzene alters the hepatic steroid metabolism, and it was suggested that a porphyria was induced by overproduction of 5 beta-H-steroids. Structurally similar chlorinated hydrocarbons (pentachlorobenzene, pentachlorophenol, 2,4,5-trichlorophenol) without porphyrogenic activity did not affect the steroid metabolism in rat liver.

3-Hydroxysteroid Dehydrogenases↗
PubMed1976

Some patterns of herbicide and growth regulator intake, persistence, and distribution in sugarcane.

Absorption of 14C-labeled herbicides from nutrient culture solution through the roots of sugarcane plants (Saccharum spp. hybrids) resulted in three major types of distribution. Labeled residues from atrazine, ametryne, and metribuzine moved easily through the xylem to the green leaves and were deposited mainly at the leaf margins and tip. Senescence and leaf abscission removed most of the deposit from the plant. Picloram translocated rapidly into the leaves, but appeared to recycle from older to younger leaves with only small portions remaining in the senescent leaves. Asulam and pentachlorophenol (PCP) were absorbed by the roots; residues did not pass into the xylem and remained fixed in the roots. Foliar additions of labeled herbicides and growth regulators generally showed only minor absorption and translocation within the leaf. Weathering processes and volatility during a 6- to 12-week period left variable amounts of residue, characteristic of individual compounds, absorbed at the treated sites.

Absorption↗
PubMed2002

[Genotoxic effect of PCP and lindane on human epithelial tonsil cells].

BACKGROUND AND OBJECTIVE: Experimental and epidemiological studies have provided evidence that pentachlorophenol (PCP) and gamma-hexachlorocyclohexane (lindane) may pose a potential carcinogenic risk for human epithelial cells of the upper aerodigestive tract. In the past, these two substances have been used for military and nonmilitary purposes, e.g., for impregnation of textiles and uniforms. In this study, we investigated the genotoxic effect of PCP and lindane on human mucosal tissue from the tonsils. METHODS: In epithelia obtained from the tonsillar mucosa removed during surgery, cell viability was evaluated by trypan blue staining. The specimens were incubated for 60 min with PCP (0.3, 0.75, and 1.2 mM) and lindane (0.5, 0.75, and 1.0 mM). The induction of DNA damage (single- and double-strand breaks) caused by PCP and lindane was measured using single-cell microgel electrophoresis. Evaluation was performed with an image analyzer enhanced by fluorescence microscopy. RESULTS: After exposure to PCP and lindane, strong genotoxic effects are apparent. The DNA migration rose from 26 micrometer in the control solution up to nearly 90 micrometer after incubation with PCP and lindane ( p<0.0001). CONCLUSIONS: This study could demonstrate for the first time genotoxic effects of PCP and lindane on human tonsillar epithelium. It has to be considered that chronic exposure to both agents might increase the risk for cancer of the upper aerodigestive tract.

Cell Transformation, Neoplastic↗
PubMed1996

DNA damage induced in mouse tissues by organic wood preserving waste extracts as assayed by 32P-postlabeling.

Numerous wood preserving waste (WPW) sites in the United States pose genotoxic hazards. WPWs consist of complex mixtures containing toxic, including genotoxic, compounds which are derived from the preservatives coal tar creosote and pentachlorophenol (PCP) and other polychlorinated aromatics. The genotoxicity of WPW extracts, which has not been tested in mammals, cannot be evaluated on the basis of data for individual components because of possible compound interactions. Therefore, whole extracts need to be assayed. 32P-postlabeling represents a powerful tool to determine DNA adduct formation by complex genotoxic mixtures, such as cigarette smoke, diesel exhaust, and coke oven and foundry emissions in experimental animals and humans. In the present study, a mouse bioassay was used in combination with 32P-postlabeling to determine DNA adduct formation induced by hexane/acetone extracts of two samples from a WPW site. Female ICR mice were treated dermally with extract corresponding to 3 mg residue or vehicle control once per day for 2 days and killed 24 h later. Skin, lung, liver, kidney, and heart DNA preparations were assayed by nuclease P1-enhanced postlabeling. Adduct profiles were tissue-specific and displayed a multitude of non-polar DNA adducts with levels amounting to one adduct in 1.6 x 10(6) DNA nucleotides in skin (both extracts) and one adduct in 3.2 x 10(7) or 1.2 x 10(7) DNA nucleotides in liver (extract 1 or extract 2). Based on their chromatographic properties, these adducts appeared largely derived from polycyclic aromatic hydrocarbons (PAHs) present in the extracts. One of the major adducts was identified as the 32P-labeled derivative of the reaction product of 7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7, 8,9,10-tetrahydrobenzo[a]pyrene (BPDE I) with N2 of deoxyguanosine. Total non-polar DNA adduct levels were highest in skin and lung, amounting to 17.4 and 24.0% of the skin values for extracts 1 and 2, respectively, in lung while the corresponding levels in liver were 5.0 and 12.6%. These results were in accord with the carcinogenic potencies of PAHs in these organs. Extract 2 induced higher adduct levels in internal organs, although its PAH concentrations were lower than those of extract 1, i.e. lung, liver, kidney, and heart had 1.4, 2.5, 1.9, and 1.7 times higher total adduct levels and 1.6, 3.3, 1.6, and 1.9 times higher benzo[a]pyrene adduct levels. With the exception of total adducts in lung, the differences between the two extracts were all significant, suggestive of compound interactions. The benzo[a]pyrene adduct levels in the five tissues correlated linearly with total adduct levels and thus represented a surrogate for the latter. Overall, the results suggest that DNA adducts in mouse tissues, as analyzed by 32P-postlabeling, are suitable biomarkers and dosimeters of the genotoxicity of WPW extracts.

Animals↗