Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pyrenes”

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.

At least 793 records · Page 44Linked to original sources
PubMed2000

Effect of sediment-chemical contact time on availability of sediment-associated pyrene and benzo

Hydrophobic organic chemicals achieve equilibrium in sediments and soils by adsorption and desorption processes driven by diffusion into organic material of particle aggregates. Exposure of benthic animals to contaminated sediments results in bioaccumulation and, in theory, a steady state is established between sediment organic carbon and the organism lipids. The purpose of this study was to test the importance of sediment-chemical contact time in bioaccumulation of pyrene and benzo[a]pyrene to the freshwater oligochaete, Lumbriculus variegatus. Also, the applicability of semi-permeable membrane devices (SPMDs) in mimicking accumulation of sediment-associated chemicals by benthic invertebrates was evaluated. Feeding and nonfeeding animals were exposed to dual spiked lake sediment in five consecutive 144 h accumulation tests. SPMDs were exposed in five consecutive single point 12 h exposures to test the effect of aging of sediment on accumulation. SPMDs were also exposed in a 28 day accumulation test to determine uptake rate coefficients. Increase in sediment-chemical contact time decreased pyrene and benzo[a]pyrene uptake clearance coefficients of successive exposures for both feeding and nonfeeding animals. This decrease in bioavailability was strongest at the start of contact and slowed down with time. Ingestion of sediment considerably increased accumulation of both compounds indicating the importance of feeding behavior in bioaccumulation of sediment-associated chemicals. The significance of ingested sediment as uptake route for pyrene varied between exposures. This was probably due to combined effect of variable ingestion rate and decreasing bioavailable fraction of chemical. Availability of PAHs decreased also for SPMDs with increasing sediment chemical contact time. SPMDs reached curvilinear portion of overall uptake curve in 28 days and calculated uptake clearance constants (k(s), g sediment/g SPMD per hour) corresponded to constants calculated for nonfeeding organisms. The results of this work emphasize the significance of sediment-chemical contact time in bioaccumulation and the importance of feeding behavior of deposit feeders in bioaccumulation of sediment-associated contaminants. Both should be taken into account when performing and modeling bioaccumulation of sedimented contaminants. Furthermore, uptake of sediment-associated PAHs by SPMDs appeared to mimic uptake by nonfeeding organisms. However, more research is needed to compare the uptake of artificial devices to sediment-dwelling species in sediment exposures.

Journal Article↗
PubMed1979

The binding to mouse skin DNA of benzo[a]pyrene, its 7,8-diol and 7,8-diol-9,10-epoxides in relation to the tumorigenicity of these compounds.

Tritium labelled and carbon-14 labelled benzo[a]pyrene (PB), (+/-)trans 7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (PB-7,8-diol), (+/-)-7 alpha,8 beta-dihydroxy-9 beta,10 beta-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene and (+/-)-7 alpha, 8 beta-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]-pyrene were applied to the shaved backs of mice. After 24 h the DNA was isolated from the treated skin and the extent of hydrocarbon binding was determined. The level of DNA binding is considered in relation to the previously reported carcinogenicity of the various benzo[a]pyrene derivatives.

Animals↗
PubMed2000

High-performance liquid chromatographic method with fluorescence detection for the determination of 3-hydroxybenzo[a]pyrene and 3-hydroxybenz[a]anthracene in the urine of polycyclic aromatic hydrocarbon-exposed workers.

The described high-performance liquid chromatographic method with fluorescence detection (HPLC-FD) permits the simultaneous determination of 3-hydroxybenzo[a]pyrene and 3-hydroxybenz[a]anthracene as the most important metabolites of the carcinogenic polycyclic aromatic hydrocarbons (PAHs) benzo[a]pyrene and benz[a]anthracene in human urine. After enzymatic hydrolysis, to release the conjugated metabolites, the analytes are separated from the matrix by means of a liquid-solid extraction step which is followed by a coupled column HPLC procedure using an enriching precolumn consisting of silica modified with copper phthalocyanine. This special precolumn selectively adsorbs PAHs with at least three condensed rings and thus separates them from the urine matrix. The quantitative analysis was carried out using a switchable fluorescence detector. The detection limits were 6 ng/l urine (3-hydroxybenzo[a]pyrene) and 8 ng/l urine (3-hydroxybenz[a]anthracene). The relative standard deviations of the within-series imprecision ranged between 4.0% and 9.0%. The between-day imprecision was 7.7% (3-hydroxybenz[a]anthracene) and 12.9% (3-hydroxybenzo[a]pyrene). The recovery rates ranged between 102% and 124%. Using this analytical method we determined PAH metabolites in post shift urine samples from 19 workers engaged in the production of fire-proof materials. The urinary concentrations ranged from 3 to 198 ng 3-hydroxybenzo[a]pyrene per g creatinine and from 15 to 1871 ng 3-hydroxybenz[a]anthracene per g creatinine.

Adsorption↗
PubMedDate not supplied

Microfluorometric study of oxygen dependence of (1"-pyrene butyl)-2-rhodamine ester probe in mitochondria of living cells.

The access to oxygen concentration is of importance in various organelles of living cells, especially in mitochondria. A new probe, (1"-pyrene butyl)-2-rhodamine ester, was designed to target this organelle. We present here the properties of the probe in such an environment. Microspectrofluorometry confirms the localization of the probe in the mitochondrial environment at low doses (1 microM). At these doses, the cell toxicity experiments show no effect on the cell growth. The emission spectrum measured at an excitation wavelength of 340 nm (pyrene centered) indicates energy transfer from the pyrene to the rhodamine chromophore, as also observed in an ethanol solution. With excitation at 337 nm, the excited state decays biexponentially with lifetime decays of 6-9 ns and 90 ns. The first corresponds to the intrinsic fluorescence of the cell and the latter corresponds to the pyrene chromophore. In degassed conditions the pyrene lifetime decay increases up to 130 ns. Under an oxygen atmosphere the lifetime decays decrease to 62 ns. The lifetime changes with the oxygen concentration were compared with the range obtained during our previous study in ethanol solution (5-220 ns). The observed differences were interpreted by studying the lifetime of the probe in simplified environments, liposome suspensions and protein solutions. In this paper we show that the new probe can be used to measure the fluctuation of oxygen concentration in the surroundings of mitochondria.

3T3 Cells↗
PubMed2005

Direct determination of dibenzo[a,l]pyrene and its four dibenzopyrene isomers in water samples by solid-liquid extraction and laser-excited time-resolved Shpol'skii spectrometry.

Dibenzo[a,l]pyrene is considered the most potent carcinogen of all polycyclic aromatic hydrocarbons ever tested. Its four isomers, which include dibenzo[a,e]pyrene, dibenzo[a,h]pyrene, dibenzo[a,i]pyrene, and dibenzo[e,l]pyrene, are also carcinogenic and, therefore, a potential threat to humans. The method presented here provides a direct way for their determination in water samples. The entire procedure--from water extraction to LETRSS analysis--takes less than 15 min/sample and it consumes only 100 microL of organic solvent. This fact makes our approach environmentally friendly and cost-effective. Unambiguous isomer determination is accomplished via multidimensional data formats, namely, wavelength time matrixes, excitation-emission matrixes, and time-resolved excitation-emission matrixes. The analytical figures of merit demonstrate precise and accurate analysis at the sub-parts-per-billion level. Limits of detection are at the parts-per-trillion level. The potential of this approach for real-world analysis is illustrated with a heavily contaminated water samples.

Journal Article↗
PubMed1985

Fluorescence studies of the conformation of pyrene-labeled tropomyosin: effects of F-actin and myosin subfragment 1.

The fluorescence of pyrene-TM [rabbit skeletal tropomyosin (TM) labeled at Cys with N-(1-pyrenyl)maleimide] consists of monomer and excimer bands [Betcher-Lange, S., & Lehrer, S.S. (1978) J. Biol. Chem. 253, 3757-3760]; an increase in excimer fluorescence with temperature is due to a shift in equilibrium from a chain-closed state (N) to a chain-open state (X) associated with a helix pretransition [Graceffa, P., & Lehrer, S.S. (1980) J. Biol. Chem. 255, 11296-11300]. In this study, we show that the presence of appreciable excimer fluorescence at temperatures below the N----X pretransition (initial excimer) is due to perturbation of the TM chain-chain interaction by the pyrenes at Cys-190. Fluorescence and ATPase titrations indicated that the label caused a decrease in TM binding to F-actin primarily due to reduced end to end TM interactions on the actin filament. Under conditions where pyrene-TM was bound to F-actin, however, the excimer fluorescence did not increase with temperature, indicating that F-actin stabilizes tropomyosin by inhibiting the N----X transition. The binding of myosin subfragment 1 (S1) to pyrene-TM-F-actin at low ratios to actin caused time-dependent changes in fluorescence. After equilibrium was reached, the initial excimer fluorescence was markedly reduced and remained constant over the pretransition temperature range. Further stabilization of tropomyosin conformation on F-actin is therefore associated with S1 binding. Effects of the binding of S1 to the F-actin-tropomyosin thin filament on the state of tropomyosin were studied by monitoring the monomer fluorescence of pyrene-TM.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed2005

Pyrene-assisted synthesis of size-controlled gold nanoparticles in sodium dodecyl sulfate micelles.

Gold nanoparticles prepared by chemical reduction in sodium dodecyl sulfate (SDS) solution are size-controlled with the addition of pyrene. Micellar electrokinetic capillary chromatography (MEKC) is applied to the system to examine the size and polydispersity of gold nanoparticles and to show that pyrene has the extraordinary effect in decreasing the size and narrowing the dispersity of gold nanoparticles. The MEKC electropherograms further suggest that pyrene could be oxidized by the aqueous Au(III) complexes first. All the reduced Au complexes were then solubilized in the pyrene-SDS micelles. The growth of gold nanoparticles beyond the embryonic stage was subsequently inhibited by the encapsulating SDS and electrophilic pyrene.

Journal Article↗
PubMed2007

Color-tunable fluorescent organogels: columnar self-assembly of pyrene-containing oligo(glutamic acid)s.

New fluorescent gelators containing pyrene moieties and dendritic oligopeptides have been developed. These molecules self-assemble into 1D helical columnar structures that lead to the formation of 3D fibrous random networks. The resulting gel materials show monomer emission of pyrenes because the hydrogen-bonded array of the oligopeptide moieties greatly suppresses the formation of pyrene excimers. In contrast, in the sol states green excimer emission of the pyrenes is observed because of the dissociation of intermolecular hydrogen bonds. This is the first example of the reverse-mode color switching of fluorescence for supramolecular pyrene assemblies.

Journal Article↗
PubMed1971

X-irradiation enhancement of transformation by benzo(a)pyrene in hamster embryo cells.

The addition of benzo(a)pyrene to cells obtained from Syrian hamster embryo cultures that had been plated to produce discrete colonies resulted in transformation. Altered colonies were not seen in controls. Prior irradiation of hamster embryo cells increased the transformation by benzo(a)pyrene, both per cell and per total colony. Maximum enhancement occurred when benzo(a)pyrene was added 48 hr after irradiation. Enhancement was greatest after 250-500 R, and decreased with higher doses of radiation. The addition of benzo(a)pyrene 72 hr after irradiation resulted in very little enhancement. Although transformation increased with benzo(a)pyrene concentration, enhancement was independent of concentration within the range used. No colony with transformed morphology was recognized among the colonies of normal cells that survived irradiation.

Animals↗
PubMed1975

Position-specific oxygenation of benzo(a)pyrene by different forms of purified cytochrome P-450 from rabbit liver.

High-pressure liquid chromatography was used to detect oxygenated products of benzo[a]pyrene formed in a reconstituted microsomal mixed-function oxidase system containing cytochrome P-450 (P-450LM), phospholipid, and NADPH-cytochrome P-450 reductase (NADPH: ferricytochrome oxidoreductase, EC 1.6.2.4). Three cytochrome fractions purified from a single source, hepatic microsomes from phenobarbital-treated rabbits, were studied; the various forms of the cytochrome are designated by their relative electrophoretic mobilities. The total benzo[a]pyrene oxygenation rate was greatest for P-450LM1,7, intermediate for P-450LM2, and least for P-450LM4. The phenolic products were eluted in two peaks, A and B, that contained primarily 9-hydroxy- and 3-hydroxybenzo[a]pyrene, respectively. The ratio of peak A to peak B phenols was 0.11 for P-450LM2 and 0.45 for P-450LM4. Thus, the relative amounts of the various phenols formed by these two cytochrome fractions differ markedly. The positional specificity of the hydroxylation is also indicated by large differences in the fluorescence spectra of the phenolic products formed by the two cytochromes. P-450LM2 and P-450LM4 did not form benzo[a]pyrene dihydrodiols, thereby showing that benzo[a]pyrene oxide hydratase activity was absent from these purified preparations. Ninety percent of the phenols formed by P-450LM1,7 were eluted in peak B; the metabolites produced by this preparation also included dihydrodiols, thus indicating the presence of hydratase activity. The positional specificities of different forms of cytochrome P-450 may channel polycyclic aromatic hydrocarbon metabolism into the various activation and detoxification pathways and thereby help determine the cytotoxic and carcinogenic activity of these compounds.

Animals↗
PubMed1979

Differences in mutagenicity and cytotoxicity of (+)- and (-)-benzo[a]pyrene 4,5-oxide: a synergistic interaction of enantiomers.

In order to study the biological effects of (+)- and (-)-benzo[a]pyrene 4,5-oxide, a synthesis of these molecules has been developed based on the resolution of (+/-)-cis-4,5-dihydroxy-4,5-dihydrobenzo[a]pyrene. The (-) enantiomer of benzo[a]pyrene 4,5-oxide was 1.5- to 5.5-fold more mutagenic than the (+) enantiomer in strains TA 98, TA 100, TA 1537, and TA 1538 of Salmonella typhimurium and in Chinese hamster V79 cells. In studies with V79 Cells, the (-) enantiomer of benzo[a]pyrene 4,5-oxide was also more cytotoxic than the (+) enantiomer. When mixtures of the enantiomers were studied in V79 cells, synergistic cytotoxic and mutagenic responses were observed. The greatest cytotoxic and mutagenic effects occurred with a 3:1 mixture of the (-) and (+) enantiomers of benzo[a]pyrene 4,5-oxide, respectively.

Animals↗
PubMed1980

Cultured mouse embryos metabolize benzo[a]pyrene during early gestation: genetic differences detectable by sister chromatid exchange.

Mouse embryos explanted at 7 1/2 or 8 1/2 days of gestation were cultured in medium containing benzo[a]pyrene and supplemented with 5-bromodeoxyuridine to allow detection of sister chromatid exchanges. The murine Ah locus regulates the inducible metabolism of polycyclic hydrocarbons such as benzo[a]pyrene. A high frequency of sister chromatid exchange was induced by benzo[a]pyrene in embryos from three Ah-"responsive" inbred strains (BALB/cDub, C3H/AnfCum, and C57BL/6N); there was little or no increase in two Ah-"nonresponsive" inbred strains (AKR/J and DBA/2J). Benzo[a]pyrene also induced sister chromatid exchanges in the Ah-responsive recombinant inbred line B6NXAKN-12 but not in the Ah-nonresponsive recombinant inbred line B6NXAKN-3. Sister chromatid exchange in cultured Ah-responsive mouse embryos was thus shown to be a sensitive assay. These data provide direct evidence that genetically responsive mouse embryos (early postimplantation stage) possess the subcellular processes necessary for induction of enzymes that metabolize benzo[a]pyrene to its chemically active forms(s). Both the Ah regulatory gene product (a cytoslic receptor) and the structural gene product (inducible cytochrome P1-450) therefore appear to be functional at an early embryonic age. Furthermore, this metabolic capacity may play an important role in the damage to embryonic cells by polycyclic hydracarbons.

Animals↗
PubMed1994

Inhibitory effect of vitamin C on the mutagenicity and covalent DNA binding of the electrophilic and carcinogenic metabolite, 6-sulfooxymethylbenzo[a]pyrene.

6-Sulfooxymethylbenzo[a]pyrene has recently been shown to be a strong hepatocarcinogen in infant male B6C3F1 mice (Y.-J.Surh et al., Biochem. Biophys. Res. Commun., 172, 85-91, 1990) and appears to be an ultimate carcinogenic metabolite of 6-hydroxymethylbenzo[a]pyrene and possibly of benzo[a]pyrene. It produced high levels of aralkyl DNA adducts in the livers of B6C3F1 mice and also exhibited strong direct mutagenicity toward Salmonella typhimurium TA98 without metabolic activation. In the present study we found that ascorbic acid significantly reduced the bacterial mutagenicity and in vitro covalent DNA binding of 6-sulfooxymethylbenzo[a]pyrene. Ascorbic acid forms a mutagenically inactive covalent adduct with 6-sulfooxymethylbenzo[a]pyrene, which appears to account for its novel protective mechanism against this reactive sulfuric acid ester. It seems likely that the formation of this adduct involves aralkylation of an ascorbic acid anion by a presumed carbo cation derived from the electrophilic sulfuric acid ester.

Animals↗
PubMed1983

Benzo[e]pyrene metabolism in rat liver microsomes: dependence of the metabolite profile on the pretreatment of rats with various monooxygenase inducers.

Benzo[r]pyrene (B[e]P) is metabolized by liver microsomes of untreated rats to trans-4,5-dihydroxy-4,5-dihydrobenzo(e)pyrene and 1- as well as 3-hydroxybenzo[e]pyrene as shown by g.l.c. and mass spectrometry of their trimethylsilyl ethers. After pretreatment of the rats with various monooxygenase inducers oxidation at the 9/10-position was also observed. In addition, secondary oxidation to dihydrodiolepoxides and the formation of a tetrol, tentatively identified as 4,5,9,10-tetrahydroxy-4,5,9,10-tetrahydrobenzo[e]pyrene was detected after incubation of B[e]P with liver microsomes of rats treated with polycyclic aromatic hydrocarbons. However, no formation of the supposed ultimate carcinogen, the 9,10-dihydroxy-11,12-epoxy-9,10,11,12-tetrahydrobenzo[e]pyrene could be observed after any of the pretreatments.

Animals↗
PubMed1977

Inhibition by CO of hepatic benzo[a]pyrene hydroxylation and its reversal by monochromatic light.

Inhibition by CO of benzo[a]pyrene hydroxylation was studied in hepatic microsomes from rats pretreated with phenobarbital, 3-methylcholanthrene or 2,3,7,8-tetrachlorodibenzo-p-dioxin, from animals treated with vehicle (saline or corn oil, respectively), and in a reconstituted microsomal cytochrome P-448 system prepared from rats treated with 3-methylcholanthrene. In all preparations the hydroxylation was inhibited by CO, and this inhibition was most effectively reversed by irradiation with monochromatic light of 450 nm wavelength. These observations provide direct evidence that the oxygen-activating component of all the examined benzo[a]pyrene hydroxylase systems is a P-450-type heme protein. The only striking difference observed in these systems was the low CO sensitivity of the benzo[a]pyrene hydroxylase reaction in microsomes from animals treated with 3-methylcholanthrene or 2,3,7,8-tetrachlorodibenzo-p-dioxin. Half-maximal inhibition occurred at CO/O2 ratios of 9--12, rather than at 1--2, which is the usual range for P-450-linked mixed-function oxidase reactions. In contrast, the reconstituted benzo[a]pyrene hydroxylase system, with purified cytochrome P-448 from 3-methylcholanthrene-induced rats, exhibited a considerably higher sensitivity towards CO (CO/O2 ratio approximately 1), well within the range for mixed-function oxidase reactions. It is concluded that the observed diminished CO sensitivity of microsomal benzo[a]pyrene hydroxylase in 3-methylcholanthrene- or 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated rats results from alterations in the composition and/or structural organization of the microenvironment of cytochrome P-448 in the endoplasmic reticulum in response to the inducing action of polycyclic aromatic hydrocarbons and related agents, and is not related to changes in the heme protein P-448 per se. The detailed nature of these changes is the subject of ongoing studies.

Animals↗
PubMed1977

Benzo[a]pyrene diol epoxides: mechanism of enzymatic formation and optically active intermediates.

Studies of the mechanism of benzo[a]pyrene metabolism to reactive diol epoxides and of their disposition indicate that the metabolic intermediates of the activation pathways, 7,8-epoxide and trans-7,8-diol, as well as the two stereoisomeric diol epoxides are all optically active. Benzo[a]pyrene is converted to optically active 9,10-epoxides of (-)trans-7,8-diol by three enzymatic steps: (i) stereospecific oxygenation at the 7,8 double bond of benzo[a]pyrene by the mixed-function oxidases to essentially a single enantiomer of 7,8-epoxide, (ii) hydration of the 7,8-epoxide by epoxide hydratase to an optically pure (-)trans-7,8-diol, and (iii) stereoselective oxygenation by the mixed-function oxidases at the 9,10 double bond of the (-) trans-7,8-diol to optically active r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene and optically active r-7,t-8-dihydroxy-c-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene in a ratio of approximately 10 to 1.

Animals↗
PubMed1994

Pyrene Metabolism in Crinipellis stipitaria: Identification of trans-4,5-Dihydro-4,5-Dihydroxypyrene and 1-Pyrenylsulfate in Strain JK364.

The isolation and identification of two novel metabolites in the fungal metabolism of pyrene are described. The plant-inhabiting basidiomycete Crinipellis stipitaria JK364 metabolized pyrene, a polycyclic aromatic hydrocarbon containing four rings, when grown in submerged cultures in a medium containing malt extract, glucose, and yeast extract. In experiments with [C] pyrene, after 7 days of incubation 40% of the labeled substrate was converted into organic solvent-extractable metabolites. Metabolites isolated from cultures grown with pyrene were identified as 1-pyrenylsulfate and trans-4,5-dihydro-4,5-dihydroxypyrene. 1-Hydroxypyrene, the precursor of 1-pyrenylsulfate, was also detected. 1-Pyrenylsulfate was isolated from mycelial extracts, whereas trans-4,5-dihydro-4,5-dihydroxypyrene was recovered from the culture filtrate. Identification of the compounds was based on their UV spectra, mass spectra, and nuclear magnetic resonance spectra. This is the first report on the detoxification of a polycyclic aromatic hydrocarbon by a plant-inhabiting basidiomycete. The occurrence of 1-pyrenylsulfate and trans-4,5-dihydro-4,5-dihydroxypyrene among fungal metabolites of pyrene is also new.

Journal Article↗
PubMed1996

Oxidation of Anthracene and Benzo[a]pyrene by Laccases from Trametes versicolor.

The in vitro oxidation of the two polycyclic aromatic hydrocarbons anthracene and benzo[a]pyrene, which have ionization potentials of <=7.45 eV, is catalyzed by laccases from Trametes versicolor. Crude laccase preparations were able to oxidize both anthracene and the potent carcinogen benzo[a]pyrene. Oxidation of benzo[a]pyrene was enhanced by the addition of the cooxidant 2,2(prm1)-azinobis(3-ethylbenzthiazoline-6-sulfonate) (ABTS), while an increased anthracene oxidizing ability was observed in the presence of the low-molecular-weight culture fluid ultrafiltrate. Two purified laccase isozymes from T. versicolor were found to have similar oxidative activities towards anthracene and benzo[a]pyrene. Oxidation of anthracene by the purified isozymes was enhanced in the presence of ABTS, while ABTS was essential for the oxidation of benzo[a]pyrene. In all cases anthraquinone was identified as the major end product of anthracene oxidation. These findings indicate that laccases may have a role in the oxidation of polycyclic aromatic hydrocarbons by white rot fungi.

Journal Article↗