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PubMed1987

Initiation of hepatocarcinogenesis in infant male B6C3F1 mice by N-hydroxy-2-aminofluorene or N-hydroxy-2-acetylaminofluorene depends primarily on metabolism to N-sulfooxy-2-aminofluorene and formation of DNA-(deoxyguanosin-8-yl)-2-aminofluorene adducts.

Previous work from this laboratory provided strong evidence that N-sulfooxy-2-aminofluorene is the major ultimate electrophilic and carcinogenic metabolite of N-hydroxy-2-acetylaminofluorene (N-hydroxy-AAF) in the livers of infant male B6C3F1 (C57BL/6J X C3H/HeJ F1) mice. Over 90% of the hepatic DNA adducts in these mice consisted of N-(deoxyguanosin-8-yl)-2-aminofluorene [N-(dGuo-8-yl)-AF] and less than 10% were deoxyguanosinyl adducts containing 2-acetylaminofluorene (AAF) residues. In the present study hepatic DNA adduct formation and tumor initiation by N-hydroxy-2-aminofluorene (N-hydroxy-AF) were examined in these mice. N-(dGuo-8-yl)-AF was the only adduct detected in the hepatic DNA; the level at 9 h after a single i.p. dose of 0.04 or 0.06 mumol/g body wt of [3H]N-hydroxy-AF was 1.0 or 1.7 pmol/mg DNA. Pretreatment with a single i.p. dose (0.04 mumol/g body wt) of the sulfotransferase inhibitor pentachlorophenol (PCP) decreased the DNA adduct level by greater than 80%. Similar levels of this adduct were found by 32P-postlabeling analysis of DNA from mice treated with unlabeled N-hydroxy-AF. The liver DNA of infant male brachymorphic B6C3F2 mice [deficient in 3'-phosphoadenosine-5'-phosphosulfate (PAPS)] contained only 0.3 pmol/mg DNA of N-(dGuo-8-yl)-AF after an i.p. dose of 0.06 mumol of N-hydroxy-AF/g body wt, while their phenotypically normal (PAPS-sufficient) male littermates had 1.9 pmol/mg DNA. A single i.p. dose of 0, 0.015, 0.03, 0.06 or 0.12 mumol/g body wt of N-hydroxy-AF in infant male B6C3F1 mice induced by 10 months an average of 0.2, 2.5, 7, 11 or 14 hepatomas/mouse. Pretreatment with PCP reduced the liver tumor multiplicity at each dose level by greater than 80%. Essentially the same average tumor multiplicities and inhibitions of tumor formation by PCP pretreatment were obtained following injections of N-hydroxy-AF or N-hydroxy-AAF at the three lower dose levels. Collectively these data strongly indicated that N-sulfooxy-2-aminofluorene is the major ultimate electrophilic and carcinogenic metabolite of N-hydroxy-AF in the livers of infant male B6C3F1 mice. Furthermore, since only N-(dGuo-8-yl)-AF adducts were found in the hepatic DNA these lesions appear to be critical in the initiation of hepatocarcinogenesis in these mice by N-hydroxy-AF.

2-Acetylaminofluorene↗

PubMed1988

The role of N-sulfation in the N-hydroxy-2-acetylaminofluorene-mediated outgrowth of diethylnitrosamine-initiated hepatocytes to gamma-glutamyltranspeptidase-positive foci in male rat liver.

The ability of N-hydroxy-2-acetylaminofluorene (N-OH-AAF) to promote the appearance of gamma-glutamyltranspeptidase-positive (GGT+) foci initiated by diethylnitrosamine (DEN) was studied in a slightly modified Solt and Farber protocol. This protocol consisted of the following treatments: initiation with a single dose of DEN followed by selection/promotion with several non-necrogenic doses of N-OH-AAF and partial hepatectomy. Treatment with N-OH-AAF resulted in a 25-fold increase of the liver volume occupied by GGT+ cells as compared to controls. The role of N-sulfation of N-OH-AAF in the GGT+ foci-selecting activity of N-OH-AAF was studied using the sulfotransferase inhibitor pentachlorophenol (PCP). Inhibition of the N-sulfation pathway with PCP during selection with N-OH-AAF resulted in a greater than 80% decrease in the volume occupied by GGT+ cells, without effects on the number of GGT+ foci generated with this protocol. Also, PCP reduced the number of so called oval and bile duct cells generated by the N-OH-AAF/partial hepatectomy treatment. It is concluded that N-sulfation of N-OH-AAF is responsible for the N-OH-AAF-mediated outgrowth of DEN-initiated hepatocytes to preneoplastic GGT+ foci.

2-Acetylaminofluorene↗

PubMed1988

Mutagenicity and in vitro covalent DNA binding of 2-hydroxyamino-3-methylimidazolo[4,5-f]quinoline.

The 2-hydroxyamino-3-methylimidazolo[4,5-f]quinoline (N-hydroxy-IQ), a metabolite of the food mutagen--carcinogen IQ, was mutagenic to Salmonella TA98 (nitroreductase deficient). When either rat hepatic cytosol, NADPH (1 mM) or ascorbate (0.5 mM) was added to the mutagenicity assay, mutagenicity increased up to 15-, 10- and 50-fold respectively. In light of the effects of ascorbate and NADPH, it appears likely that hepatic cytosol may contain factors that protect N-hydroxy-IQ from oxidative decomposition. In contrast, hepatic monooxygenase metabolism of N-hydroxy-IQ decreased mutagenicity. When pentachlorophenol, an inhibitor of O-acetyltransferase and sulfotransferase, was added to the mutagenicity assay, a dose-dependent inhibition of N-hydroxy-IQ mutagenicity was observed. 2,6-Dichloro-4-nitrophenol, a more specific inhibitor of sulfotransferase than O- acetyltransferase, did not inhibit the mutagenicity of N-hydroxy-IQ at concentrations which appear to selectively inhibit only bacterial sulfotransferase. The data suggest that bacterial O-acetyltransferase rather than sulfotransferase mutagenically activates N-hydroxy-IQ. N-hydroxy-IQ covalently bound to calf thymus DNA in vitro under non-enzymatic conditions at pH 7.4. Rat hepatic cytosolic O-acetyltransferase and sulfotransferase enhanced the covalent binding of N-hydroxy-IQ to DNA 30- and 5-fold respectively. The data suggest that the mutagenicity of N-hydroxy-IQ is due to the reactivity of N-hydroxy-IQ with DNA and the ability of N-hydroxy-IQ to be further activated by bacterial O-acetyltransferase.

Acetyltransferases↗

PubMed1979

Determination of chlorinated phenols in surface-treated lumber by HPLC.

A solution of internal standard in acetonitrile is used to extract samples of wood from lumber which had been commercially treated with chlorinated phenols. The tetrachlorophenol(TCP) and pentachlorophenol( PCP) were analytically separated from each other and from the other wood extractive compounds using a high performance liquid chromatograph (HPLC). The ultraviolet (UV) absorptions of the TCP, PCP, and internal standard were automatically measured as they eluted. The UV absorption peaks were integrated, and the amounts of TCP and PCP present were calculated with a dedicated microcomputer. Compared with the method previously used, this method is faster (up to 144 samples per 48 hours), has the same accuracy and precision, and it is linear over the concentration range used.

Chlorophenols↗

PubMedDate not supplied

Determination of hydroxylated polychlorinated biphenyls (HO-PCBs) in blood plasma by high-performance liquid chromatography-electrospray ionization-tandem quadrupole mass spectrometry.

Hydroxylated metabolites of polychlorinated biphenyls (HO-PCBs) and pentachlorophenol (PCP) are halogenated phenolic compounds, and they are increasingly common as environmental contaminants mainly in the blood of wildlife and humans. A methodology based on high-performance liquid chromatography (reversed-phase)-electrospray (negative) ionization-tandem quadrupole mass spectrometry (LC-ESI(-)-MS-MS) in the select ion monitoring or multiple reaction monitoring modes was developed for HO-PCB and PCP determination in blood plasma and serum. Among 11 environmentally relevant HO-PCB congeners and PCP spiked to fetal calf serum, quantitative assessments, including matrix effects on ESI(-) suppression/ enhancement, showed process (recovery) efficiencies of 73% to 89% without internal standard (IS) correction, and 88% to 103% with IS correction, and method limits of quantification ranging from 1 to 50 pg/g (wet weight). Using the developed LC-ESI(-)-MS methodology in comparison with GC-MS and GC-ECD based approaches, similar results were found for HO-PCB identification and quantification in the plasma of polar bear (Ursus maritimus) from the Canadian arctic. LC-ESI(-)-MS identified four HO-PCB congeners [4'-HO-2,2',4,6,6'-pentachlorobiphenyl (4'-HO-CB104), 4-HO-2,3,3',4',5-pentachlorobiphenyl (4-HO-CB107), 4-HO-2,3,3',5,5',6-hexachlorobiphenyl (4-HO-CB165) and 3'-HO-2,2',3,4,4',5,5'-heptachlorobiphenyl (3'-HO-CB180)], and 14 additional tetra- to hepta-chlorinated HO-PCBs isomers in the polar bear plasma.

Animals↗

PubMed1992

Hepatic triiodothyronine sulfation and its regulation by growth hormone and triiodothyronine in rats.

The regulatory mechanism of cytosolic sulfation of T3 has been studied in rat liver. Sulfation of T3 is sexually differentiated in adult rats of Sprague-Dawley (SD), Fisher 344, and ACI strains. In SD strain, the male animals showed 4 times higher sulfating activity than did the females. The specific activity was decreased by hypophysectomy of male adult rats, but was not affected in the females. Thus, the sex-difference was abolished in the hypophysectomized condition. Supplement of human GH intermittently twice daily for 7 days, to mimic the male secretory pattern, increased T3 sulfating activity in both sexes of hypophysectomized rats, whereas continuous infusion to mimic a female secretory pattern had no appreciable effect. Cytosolic sulfation of T3 was decreased by 25 to 30% by thyroidectomy or propylthiouracil treatment of male adult rats, and was restored by the supplementation of T3 (50 micrograms/kg daily for 7 days) to thyroidectomized rats. Administration of T3 in hypophysectomized rats almost completely restored the sulfating activity in the males and increased the activity in the females. Cytosolic T3 sulfation was inhibited by the addition of known inhibitors of phenol sulfotransferase, pentachlorophenol or 2,6-dichloro-4-nitrophenol. These results indicate a role of pituitary GH in hepatic sulfation of thyroid hormones in rats. The data obtained also raise the possibility that GH may modify the effect of thyroid hormones on the pituitary by a feed-back mechanism through changing the level of a sex-dominant phenol sulfotransferase(s) in rat livers. T3 was also sulfated in hepatic cytosols of mouse, hamster, rabbit, dog, monkey, and human.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

Pesticide application and increased dioxin body burden in male and female agricultural workers in China.

Large amounts of the powerful pesticide sodium pentachlorophenol (Na-PCP) salt have been sprayed over vast areas in central China to control schistosomiasis, a parasitic disease of epidemic proportions. Approximately 6000 tons of Na-PCP are produced in China annually. Dioxins, a class of toxic, persistent compounds, are found as impurities in commercial Na-PCP products. These contaminants are released into the environment and significantly contribute to human exposure to dioxins in China. This study was carried out to determine dioxin levels in environmental and human tissue samples from one schistosomiasis area to evaluate the health risks associated with exposure to Na-PCP. Na-PCP pesticide was applied in 1972, 1973, and again in 1978. A total of approximately 454 tons and 902 tons of 5-ppm Na-PCP in water were sprayed over large land and lake problem schistosomiasis areas, respectively. The groups studied were (1) sprayers or handlers of Na-PCP, (2) persons living in the sprayed areas, and (3) persons living in unsprayed areas 300 km north of the sprayed lake located in a city in the Jiangxi province. Individual whole-blood and breast-milk samples were collected and later pooled for dioxin analysis. Also, a sample of commercial Na-PCP was collected. In addition, sediment samples from the lake where Na-PCP was sprayed were collected from four different sites and one control sample was collected from a non-schistosomiasis area. All of the samples were analyzed by high-resolution gas chromatography/mass spectrometry. A sample of Na-PCP used in schistosomiasis regions was analyzed and levels of 2,3,7,8-substituted dibenzodioxin (PCDD) and dibenzofuran (PCDF) congeners were measured. In addition, the international dioxin toxic equivalent (I-TEQ) value of this sample was calculated. Total I-TEQ of 162 parts per billion (ppb) was found in the Chinese Na-PCP product. A pooled breast-milk sample from mothers, female agricultural workers who were born in the schistosomiasis areas where large amounts of Na-PCP were sprayed, had an I-TEQ of 5,4 parts per trillion (ppt), lipid, which was about double that of mothers from control regions, women born in areas not sprayed with Na-PCP (2.6 ppt, lipid). The dioxin I-TEQ values in human blood ranged from 9.0 (subjects 15 to 19 years of age) to 16.3 ppt, lipid (subjects 35 to 70 years of age) in the whole-blood samples from Na-PCP exposed persons, whereas the general population's whole-blood I-TEQs were 4.8 and 6.4 ppt, lipid, respectively. The PCDD/F congener distribution patterns in four sediment samples from schistosomiasis areas were similar to that of Na-PCP. By comparison of specific "fingerprint" congeners (higher chlorinated dioxins and the closely related dibenzofurans) in Na-PCP, human tissues, and sediment samples, we conclude that the chemical pesticide Na-PCP is a source of environmental and human dioxin exposure in the Chinese schistosomiasis area studied. Although human PCDD/F tissue levels in China are low compared with those in more industrialized countries, the elevated I-TEQ levels in exposed persons are cause for concern.

Adolescent↗

PubMed1993

Transient repression of the synthesis of OmpF and aspartate transcarbamoylase in Escherichia coli K12 as a response to pollutant stress.

The synthesis of total cellular proteins in Escherichia coli K12 was studied in batch culture following exposure of cells to low concentrations of monochlorophenol, pentachlorophenol and cadmium chloride. Changes in protein patterns were identified after pulse-chase labelling of proteins with [35S]methionine and subsequent two-dimensional gel electrophoresis (2D-PAGE). We demonstrated that besides the induction of some stress proteins, also a transient decrease in the rate of synthesis of other proteins occurred. Two of these proteins were identified as OmpF and aspartate transcarbamoylase (ATCase). Their transient repression appeared to be a general response to stress elicited by different pollutants and may therefore be used as a general and sensitive early warning system for pollutant stress.

Aspartate Carbamoyltransferase↗

PubMed2002

Rapid total destruction of chlorophenols by activated hydrogen peroxide.

A practical, inexpensive, green chemical process for degrading environmental pollutants is greatly needed, especially for persistent chlorinated pollutants. Here we describe the activation of hydrogen peroxide by tetraamidomacrocylic ligand (TAML) iron catalysts, to destroy the priority pollutants pentachlorophenol (PCP) and 2,4,6-trichlorophenol (TCP). In water, in minutes, under ambient conditions of temperature and pressure, PCP and TCP are completely destroyed at catalyst:substrate ratios of 1:715 and 1:2000, respectively. The fate of about 90% of the carbon and about 99% of the chlorine has been determined in each case. Neither dioxins nor any other toxic compounds are detectable products, and the catalysts themselves show low toxicity.

Catalysis↗

PubMed1982

Effects of kepone on growth and respiration of several estuarine bacteria.

The toxicity of Kepone to mixed populations of estuarine microorganisms was determined by standard plate assays on Zobell marine medium containing 0.02, 0.20, and 2.0 mg of Kepone per liter. Under aerobic conditions, Kepone reduced the number of colony-forming units at all concentrations tested, but had no effect on the number of anaerobic microorganisms. Gram-positive organisms were more sensitive to Kepone than were gram-negative organisms. Growth of gram-negative isolates was not inhibited in nutrient broth, but was significantly inhibited in a minimal salts broth. Oxygen uptake by most isolates was reduced 25 to 100% by 20 ppm (20 mg/ml) of Kepone. Oxygen evolution was observed when several gram-positive isolates were exposed to Kepone concentrations of 20 ppm. Pentachlorophenol at concentrations above 28 ppm produced effects similar to those produced by Kepone. Inhibition of electron transport by Kepone was demonstrated by a significant reduction in the specific activities of NADH oxidases and succinooxidase.

Bacteria↗

PubMed1983

Metabolism of Halophenols by 2,4,5-trichlorophenoxyacetic acid-degrading Pseudomonas cepacia.

Resting cells of 2,4,5-trichlorophenoxyacetic acid-grown Pseudomonas cepacia AC1100 were able to completely and rapidly dechlorinate several chlorine-substituted phenols, including 2,4,5-trichlorophenol, 2,3,4,6-tetrachlorophenol, and pentachlorophenol. Several other trichlorophenols were only partially dechlorinated. The evidence suggests that 2,4,5-trichlorophenol is an intermediate in the degradation of 2,4,5-trichlorophenoxyacetic acid by strain AC1100. Moreover, although strain AC1100 was isolated by selection for growth on a chlorinated aromatic compound, brominated and fluorinated analogs were efficiently dehalogenated by strain AC1100 resting cells, whereas an iodinated analog was poorly dehalogenated.

2,4,5-Trichlorophenoxyacetic Acid↗

PubMed1983

Regulation of 2,4,5-trichlorophenoxyacetic acid and chlorophenol metabolism in Pseudomonas cepacia AC1100.

The expression of the degradative genes encoding 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), 2,4,5-trichlorophenol (2,4,5-TCP), and pentachlorophenol (PCP) dechlorination in a 2,4,5-T-degrading strain of Pseudomonas cepacia was examined during growth on alternate carbon sources. The dechlorination mechanisms for all three compounds were expressed in 2,4,5-T- and 2,4,5-TCP-grown cells but were not expressed in cells grown on succinate, glucose, or lactate. The addition of 2,4,5-TCP or PCP to cells grown on succinate or lactate resulted in the expression of the 2,4,5-TCP dechlorination mechanism in resting cells after 1-h lag. This expression was prevented by the presence of chloramphenicol in the resting cell suspension. Succinate-plus-PCP-grown resting cells preincubated with 2,4,5-TCP fully induced the trichlorophenol dechlorination system and partially induced the PCP dechlorination system. Preincubation of succinate-plus-PCP-grown resting cells with PCP induced neither the 2,4,5-TCP nor the PCP dechlorinating system. Succinate-grown resting cells converted 2,4,5-T to 2,4,5-TCP even in the presence of chloramphenicol. Thus, the data indicate that the enzyme(s) which converts 2,4,5-T to 2,4,5-TCP is constitutively expressed, whereas those that convert 2,4,5-TCP to central intermediates are induced by 2,4,5-TCP but not by 2,4,5-T or PCP and are repressed in the presence of an alternate carbon source.

2,4,5-Trichlorophenoxyacetic Acid↗

PubMed1988

Microbial degradation of xenobiotic, aromatic pollutants in humic water.

The microbial degradation of a number of 14C-labeled, recalcitrant, aromatic pollutants, including trichloroguaiacol and di-, tri-, and pentachlorophenol, was investigated in aquatic model systems in the laboratory. Natural, mixed cultures of microorganisms in the water from a brown-water lake with a high content of humic compounds mineralized all of the tested substances to a higher degree than did microorganisms in the water from a clear-water lake. Dichlorophenol was the most rapidly degraded pollutant.

Biodegradation, Environmental↗

PubMed1973

Evidence for the direct action of colicin K on aerobic 32 P i uptake in Escherichia coli in vivo and in vitro.

Pentachlorophenol (PCP)-sensitive incorporation of (32)P-labeled orthophosphate ((32)P(i)) into nucleotides and nucleic acids by disrupted spheroplasts of Escherichia coli was inhibited by addition of colicin K. Incorporation by intact cells was also inhibited by a similar concentration of colicin K. Various colicin K-resistant mutants were isolated, and their ability to incorporate (32)P(i) was tested. When T6(r)-colK(r) mutants (T6 phage-resistant) and tol I mutants (T6-sensitive, colicin E-sensitive) were converted to disrupted spheroplasts, their (32)P(i)-incorporation became sensitive to colicin K. On the contrary, incorporation by disrupted spheroplasts from tol II mutants (T6-sensitive, colicin E-resistant) was fairly resistant to colicin K like that of intact cells. A modification of the cell surface of T6(r)-colK(r) mutants, caused by mutation to novobiocin-permeable, T4 phage-resistant cells, restored the sensitivity of the cells to colicin K. The modified T6(r)-colK(r) cells did not adsorb T6 phage or colicin K, indicating that the receptors for T6 phage or colicin K are not reactivated by this modification. Similar treatment of tol I mutants did not have this effect. These observations strongly suggest that colicin K can act on its target on the cell membrane if it can penetrate the cell surface to reach this target. The receptor for colicin K on the cell surface, which may be part of the T6 phage-receptor, may have some unknown function in relation to the action of colicin K in normal cells, but tends to become dispensable if the cells become permeable to colicin K.

Adsorption↗

PubMed1973

Manganese transport in Bacillus subtilis W23 during growth and sporulation.

Manganese is accumulated in Bacillus subtilis by a highly specific active transport system. This trace element "pump" is insensitive to added magnesium or calcium and preferentially accumulates manganese in the presence of cobalt, iron, and copper. Manganese uptake in B. subtilis is inhibited by cyanide, azide, pentachlorophenol, and m-chlorophenyl carbonylcyanide hydrazone. The uptake of manganese follows Michaelis-Menten kinetics, and the net accumulation of manganese is regulated by increasing the V(max) after exposure to manganese-starvation conditions and by decreasing the V(max) for manganese uptake during growth in excess manganese. The K(m) remains constant during these regulatory changes in V(max). Manganese accumulated during growth is exchangeable for exogenous manganese and can be released from the cells by toluene (which causes leakage but not lysis) or by lysis with lysozyme. Two stages can be distinguished with regard to intracellular manganese during the process of growth and sporulation. During logarithmic growth, B. subtilis maintains a relatively constant internal manganese content, which is a function of the external manganese concentration following approximately a Langmuir adsorption isotherm. At the end of log phase, net accumulation of manganese slows. A second phase of net manganese accumulation begins at about the same time during sporulation as the accumulation of calcium begins. The manganese accumulated during growth and early sporulation is exchangeable and therefore relatively "free"; intracellular manganese is converted later during sporulation into a bound form that cannot be released by toluene or lysozyme.

Azides↗

PubMed1974

Effect of uncoupling agents and respiratory inhibitors on the growth of Streptococcus agalactiae.

2,4-Dinitrophenol, dicoumarol, carbonylcyanide, m-chlorophenyl-hydrazone and pentachlorophenol all depressed aerobic molar growth yields of Streptococcus agalactiae to values equal to, or less than, those supported by substrate level phosphorylation. When the only source of energy was from substrate phosphorylation (anaerobic growth conditions), there was also a severe depression of the molar growth yield by the same four uncoupling agents. These results indicate that the effect of these agents is to uncouple both substrate and oxidative phosphorylation in S. agalactiae. Amytal inhibited glucose utilization, reduced the amount of O(2) used per mole of substrate and reduced the molar cell yield to that supported by substrate phosphorylation. Atebrin inhibited the respiration rate, but final O(2) consumed per mole of substrate was unchanged, and the respiration was coupled to biosynthesis. Rotenone had no effect on respiration, substrate utilization, or on molar growth yields.

Adenosine Triphosphate↗

PubMed1980

Adenosine 5'-triphosphate formation in Thiobacillus ferrooxidans vesicles by H+ ion gradients comparable to those of environmental conditions.

Vesicles prepared from iron-grown Thiobacillus ferrooxidans, and subsequently loaded with adenosine 5'-diphosphate and inorganic phosphate, produced adenosine 5'-triphosphate when subjected to H+ gradients comparable to those in the cells' normal environment (i.e., an internal pH in the range of 6.0 to 8.0 with an optimum of 7.0 to 7.8 and an external pH in the range of 2.1 to 4.1 with an optimum of 2.8). Nigericin, dicyclohexylcarbodiimide, and pentachlorophenol decreased adenosine 5'-triphosphate synthesis. Valinomycin at concentrations of 2.5 and 5.0 micrograms/ml increased adenosine 5'-triphosphate formation by 25 and 30%, respectively.

Adenosine Triphosphate↗

PubMed1995

Synergistic induction of the heat shock response in Escherichia coli by simultaneous treatment with chemical inducers.

Escherichia coli strains carrying transcriptional fusions of four sigma 32-controlled E. coli heat shock promoters to luxCDABE or lacZ reporter genes were stressed by chemicals added singly or in pairs. Much more than additive induction resulted from combinations of cadmium chloride, copper sulfate, ethanol, formamide, 4-nitrophenol, and pentachlorophenol.

Base Sequence↗