Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Polycyclic Compounds”

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 865 records · Page 48Linked to original sources
PubMed1976

Particle size distribution and chemical composition of coal-tar fumes.

The study was intended to characterize the chemical and physical nature of coal-tar fumes emitted from spreading applications of coal tar. Two separate experiments were performed. The first resulted in the determination of a coal-tar fume particle size distribution. The second experiment resulted in the identification of the primary compounds found in collected tar fumes and a determination of their relative concentration.

Air Pollutants↗
PubMed2003

[Tetracyclic derivatives of diltiazem from aurones and thioaurones].

Tetracyclic derivatives of diltiazem from aurones and thioaurones Heating the aurones 1a, b and the thioaurones 1c, d with 2-aminothiophenol in polyphosphoric acid (PPA) under nitrogen yields the 6,12-dihydrobenzofuro[2,3-c][1,5]benzothiazepines 3a,b and the sulfur analogues 3c, d, respectively. Reaction of the annulated benzofuranes 3a,b with 2-chloroethyl-N,N-dimethylammonium chloride and potassium carbonate leads to S-alkylation and ring opening forming the 3-imino-aurones 5. The tetracycles 3 react with sodium hydride in DMF under ring contraction to afford the benzofuro- and benzothieno[3,2-b]quinolines 6. The stability of the partially saturated tetracycles 3 is investigated by anodic oxidation using the rotating platinum electrode by means of differential pulse voltammetry. The measured half wave potentials of the 1,4-dihydropyridine partial structure in compounds 3 are compared with that of nifedipine.

Alkylation↗
PubMed1995

Loss of adenosine-induced negative inotropic effect in hyperexcited rabbit hearts: relationship to PKC.

Adenosine produced a negative inotropic effect in hearts isolated from calm rabbits but not from those exhibiting alarm behavior during handling. This study was conducted to determine whether protein kinase C (PKC) activation is responsible for the loss of adenosine-induced negative inotropism in the hearts of hyperexcited rabbits. Adenosine (10 microM) decreased myocardial contractility (dP/dtmax) in the hearts of calm, but not hyperexcited, rabbits but decreased heart rate (HR) and coronary perfusion pressure (PP) in the hearts of both calm and hyperexcited animals. During infusion of calphostin C (200 nM), a PKC inhibitor, adenosine also decreased dP/dtmax in the hearts of hyperexcited rabbits. Calphostin C did not alter the actions of adenosine in the hearts of calm rabbits. Agents that stimulate PKC directly [phorbol 12,13-dibutyrate (PDBu), 1 nM] or indirectly [norepinephrine (NE), 3 nM; angiotensin II (ANG II), 5 nM] abolished the adenosine-induced decrease in dP/dtmax but not HR or PP in the hearts of calm rabbits. During calphostin C, infusion of PDBu, NE, and ANG II failed to prevent the adenosine-induced decrease in dP/dtmax. These data suggest that the lack of a negative inotropic effect of adenosine in hyperexcited rabbits is due to an increase in PKC activity.

Acetylcholine↗
PubMed1987

Mutagenicity testing of some medicinal herbs.

Extracts of four brands of a Pakistani local medicine called naswar and six indigenous herbs commonly used as medicine in children were tested for their ability to induce mutations to prototrophy in Salmonella typhimurium tester strains TA98, TA100, TA1535, and TA1537. Petroleum ether extracts of one brand of naswar, namely green naswar of Peshawar, exhibited mutagenicity in all of the four tester strains. Organic extracts of three herbs, Saussurea lappa, Swertia chiraita, and Skimmia laureola, exhibited mutagenic activity in tester strain TA98. Green naswar of Bannu, grey naswar, red naswar, and the remaining three herbs, namely, Acorous calamus, Azadarachta indica, and Zanthozylum alatum, exhibited no mutagenic activity under the present experimental conditions. The abilities of green naswar of Peshawar and Saussurea lappa to induce mutations was shown to be related to the presence of cyclic aromatic compounds with molecular formulas C34 H44 O9 and C15 H18 O2, respectively. The experimental data are discussed as they relate to the potential hazards of such naturally occurring compounds and to synthetic compounds in excessive and uncontrolled use by the general public in villages in Pakistan.

Animals↗
PubMed1994

Human bioassays to assess environmental genotoxicity: development of a DNA repair assay in HepG2 cells.

A direct assessment of the effects of environmental chemicals on human health has been hampered by the lack of suitable experimental systems. We have recently employed a human liver cell line (HepG2) to assess the biological effects of pollutants at both cellular and DNA levels. A Neutral Red dye uptake assay was used to assess potential cytotoxic effects of xenobiotics. DNA damage was quantified using an unscheduled DNA synthesis assay that measures repair that is induced following exposure to genotoxic compounds. HepG2 cells responded to the known mutagens, 4-nitroquinoline N-oxide and methylmethane sulfonate, both in the Neutral Red assay for cytotoxicity and two DNA repair assays for genotoxicity (monitored autoradiographically or by liquid scintillation counting). The HepG2 DNA repair and cytotoxicity assays also responded to an extract (containing polycyclic aromatic hydrocarbons) of sediment obtained from a polluted site in the Great Lakes. Results indicate that this system can be deployed further to assess potential cyto- and genotoxicity of pollutants. The development of human cell culture assays is a critical step towards a full assessment of the risk that such pollutants pose to human health.

4-Nitroquinoline-1-oxide↗
PubMed1993

Reversed-phase liquid chromatography with microspherical octadecyl-zirconia bonded stationary phases.

Microspherical zirconia particles were synthesized and surface modified with octadecylsilane compounds for reversed-phase high-performance liquid chromatography. Monomeric and "polymeric" octadecyl-zirconia bonded stationary phases were obtained by reacting the support with octadecyldimethylchlorosilane or octadecyltrichlorosilane, respectively. The surface coverage of the zirconia-based stationary phases with octadecyl functions was approximately the same as that of octadecyl-silica sorbents. These phases were evaluated in terms of reversed-phase chromatographic properties with non-polar, slightly polar and ionic species over a wide range of mobile phase composition and pH. Monomeric octadecyl-zirconia with end-capping exhibited some metallic interactions with both basic and acidic solutes, but these interactions were greatly reduced in the presence of competing agents (e.g., tartrate ions) in the mobile phase. The "polymeric" octadecyl-zirconia sorbents exhibited higher retention than the monomeric ones with the various solutes investigated, and their residual absorptivities toward acidic solutes were much lower. The retention of non-polar and slightly polar aromatic compounds was quasi-homoenergetic on both types of octadecyl-zirconia stationary phases. Stability studies conducted at extreme pH conditions (pH 2.0 and pH 12.0), have shown that "polymeric" octadecyl-zirconia sorbents are more stable than their monomeric counterparts. These stationary phases were quite useful in the separation of polycyclic aromatic hydrocarbons, alkylbenzene and phenyl alkylalcohol homologous series, oligosaccharides, dansyl-amino acids, peptides and proteins.

Amino Acid Sequence↗
PubMed2004

Genotoxic and mutagenic activity of environmental air samples in Flanders, Belgium.

Atmospheric pollution is assumed to play a role in the incidence of respiratory diseases and cancers. Airborne particles are able to penetrate deep into the lung and are composed of complex chemical mixtures, including mutagens and carcinogens such as polycyclic aromatic compounds (PACs). The present study reports mutagenic and genotoxic activities associated with ambient air collected near a busy street in Borgerhout, at an industrial site in Hoboken and in Peer, a rural community 70 km east of Antwerp in Flanders, Belgium. Airborne particulates (PM10) and semi-volatile organic compounds were sampled during winter and summer. Samples were collected with a high-volume sampler using quartz filters (QF) and polyurethane foam (PUF) cartridges. The mutagenic and genotoxic activity of the organic extracts was determined using the Salmonella test/standard plate-incorporation assay and the Vitotox assay. Concentrations of 16 polycyclic aromatic hydrocarbons (PAHs) in the extracts were determined by reversed-phase high-performance liquid chromatography (HPLC). The mutagenicity assay, using Salmonella typhimurium strain TA98, demonstrated direct mutagenicity of up to 58 revertants/m3 for the QF extracts and low or no mutagenic activity in the PUF extracts. Metabolic activation of the samples resulted in high indirect mutagenicity for both QF and PUF extracts: up to 96 revertants/m3 were found in QF samples and 62 revertants/m3 in PUF samples. Genotoxic effects of the filter extracts were assessed with the Vitotox assay: some direct genotoxic effects were noted, i.e. without metabolic activation, but almost no effects were observed after metabolic activation. Without activation, most PUF extracts were bacteriotoxic. With metabolic activation this toxicity disappeared, but genotoxic effects were not observed. Statistical analysis showed that the observed biological effects correlated well with the PAH concentrations.

Air Pollutants↗
PubMed1994

On cancer risk estimation of urban air pollution.

The usefulness of data from various sources for a cancer risk estimation of urban air pollution is discussed. Considering the irreversibility of initiations, a multiplicative model is preferred for solid tumors. As has been concluded for exposure to ionizing radiation, the multiplicative model, in comparison with the additive model, predicts a relatively larger number of cases at high ages, with enhanced underestimation of risks by short follow-up times in disease-epidemiological studies. For related reasons, the extrapolation of risk from animal tests on the basis of daily absorbed dose per kilogram body weight or per square meter surface area without considering differences in life span may lead to an underestimation, and agreements with epidemiologically determined values may be fortuitous. Considering these possibilities, the most likely lifetime risks of cancer death at the average exposure levels in Sweden were estimated for certain pollution fractions or indicator compounds in urban air. The risks amount to approximately 50 deaths per 100,000 for inhaled particulate organic material (POM), with a contribution from ingested POM about three times larger, and alkenes, and butadiene cause 20 deaths, respectively, per 100,000 individuals. Also, benzene and formaldehyde are expected to be associated with considerable risk increments. Comparative potency methods were applied for POM and alkenes. Due to incompleteness of the list of compounds considered and the uncertainties of the above estimates, the total risk calculation from urban air has not been attempted here.

Air Pollution↗
PubMed1994

Characterization of cytochrome P4501A induction in medaka (Oryzias latipes) by samples generated from the extraction and processing of coal.

The objective of this study was to characterize cytochrome P4501A induction in medaka liver as a biomarker for detecting polyaromatic hydrocarbon (PAH)-type compounds in samples of processed coal or petroleum. Ethoxyresorufin-O-deethylase (EROD) activity in individual medaka livers was used to asses induction of P4501A following the addition of various samples to aquaria water. Samples included a known P4501A inducer, beta-naphthoflavone, and various processed coal samples, as well as a petroleum-pitch. The sensitivity of detecting significant EROD induction by adding samples to aquaria water was approximately 0.1 mg/L for most samples; however, a coal-tar pitch significantly increased EROD activity at 0.01 mg/L. Different samples induced EROD activity to different extents. All samples elicited a concentration-dependent increase in EROD activity, with maximum EROD induction 2 days after a single administration of xenobiotics to aquaria water. Western blot studies established that induction of EROD activity by all xenobiotics tested was associated with corresponding increased amounts of immunoreactive P4501A. EROD induction was not influenced by gender, by single or multiple xenobiotic exposures, nor by feeding or fasting animals during the course of xenobiotic exposure. The ability of xenobiotics to induce EROD activity in medaka liver did not always correlate with their genotoxic potential determined by bacterial mutagenesis assays. Induction of P4501A in medaka liver appears to provide a convenient, economical, reliable and sensitive indicator for the presence of PAH-type compounds in coal- or petroleum-derived samples.

Animals↗
PubMed1990

Interaction of hydrophobic organic compounds with mercury adsorbed dioleoylphosphatidylcholine monolayers.

The interaction of hydrophobic organic compounds with biological membranes is an important factor in their biological activity. A fundamental insight into the mechanisms can be obtained by examining the influence of these substances on model membrane systems. The effect of four groups of hydrophobic aromatic compounds on a mercury-adsorbed dioleoylphosphatidylcholine (DOPC) monolayer is described in this paper. The compounds studied were: (1) polynuclear aromatic hydrocarbons (PAH), (2) polychlorinated biphenyls (PCB), (3) neurotoxic pesticides, and (4) phenothiazines. The monolayer properties were measured using phase-sensitive a.c. voltammetry and cyclic voltammetry. The response of the monolayer to these compounds is recorded as a change in the form of the capacity-potential curve especially with respect to two capacity peaks which correspond to two well-defined phase transitions. Planar aromatic molecules cause a negative shift of the capacity peaks, however, as the molecule becomes more globular the response becomes less and the peaks become suppressed. It is shown that planar aromatic molecules exert their effect by penetrating the hydrocarbon region of the monolayer and that there is a molecular size cut-off for higher membered PAH molecules. In addition, the monolayer is not so sensitive to the bulky PCB which have a more disruptive effect on the phase transitions and thus on the mechanisms of self-assembly of the monolayer. A direct correlation is shown between the biological membrane activity of the phenothiazines and their effect on the monolayer at submicromolar levels. A molecular selectivity of phospholipid monolayers to these compounds is indicated which has implications for their effect on biological membranes.

Adsorption↗
PubMed1995

CYP1 induction, binding to the hepatic aromatic hydrocarbon receptor and mutagenicity of a series of 11-alkoxy cyclopenta[a]phenanthren-17-ones: a structure activity relationship.

A series of four 11-alkoxy cyclopenta[a]phenanthren-17-ones, ranging from the methoxy to the butoxy derivative, has been synthesised in order to investigate the effect of the size of the 11-substituent on the mutagenicity and ability of these compounds to induce hepatic CYP1 activity in rats. The latter was monitored by using as diagnostic probes methoxy and ethoxy-resorufin, and immunologically in Western blots employing anti-CYP1A1 antibodies. All four members of the series induced both CYP1A1 and CYP1A2 activities and apoprotein levels, but the methoxy- and ethoxy-CPP-17-ones were clearly the most potent. Of the four isomers, only 11-methoxy-CPP-17-one displaced 3H-TCDD from the cytosolic Ah receptor. Similarly only 11-methoxy-CPP-17-one elicited a positive mutagenic response in the Ames test in the presence of an Aroclor 1254-induced activation system. The relevance of these findings to the carcinogenicity of these compounds in the mouse skin painting model is discussed.

Animals↗
PubMed1976

Dimethylnitrosamine-demethylase: molecular size-dependence of repression by polynuclear hydrocarbons. Nonhydrocarbon repressors.

Studies with 58 polynuclear aromatic hydrocarbons have shown that to repress demethylation of dimethylnitrosamine (DMN) in rat liver, the hydrocarbons must satisfy specific requirements of molecular geometry regarding size, shape, and coplanarity. Expressing the molecular size of these planar compounds by the two-dimensional area occupied, the size for maximal repressor activity ranges between about 85 and 150 A2. In addition to being within the correct molecular size range the hydrocarbons must have an elongated-rather than compact-molecular shape; circularly shaped and/or highly symmetrical hydrocarbons, such as coronene, triphenylene, ovalene, and tetrabenzonaphthalene, have very low activity or are inactive, in spite of being in the optimum size range. Coplanarity of the molecule is a critical requirement; thus, the potent carcinogen, 9,10-dimethyl-1,2-benzanthracene, is inactive as repressor of DMN-demethylase synthesis. Two exceptions, fluoranthene and benzol[ghi] fluoranthene, showed significant induction of DMN-demethylase. The molecular size distribution of hydrocarbons that repress the DMN-demethylase shows a mirror-image relationship with respect to the earlier reported molecular size requirement for indcution of azo dye N-demethylase. Compounds other than hydrocarbons also show the mirror-image relationship in the sense that pregnenolene-16alpha-carbonitrile, alpha- and beta-naphthoflavone, and Aroclor 1254 (known to be inducers of various mixed-function oxidases) are strong repressors of DMN-demethylase. Aminoacetonitrile, a strong inhibitor of carcinogenesis by DMN, is also a potent repressor of DMN-demethylase. The enzyme is inhibited by pretreatment of the animals with cobaltous chloride, an inhibitor of the synthesis of cytochrome P-450. Pregnenolone-16alpha-carbonitrile and 3-methylcholanthrene, despite their similarity of action on DMN-demethylase, have different effects on azo reductase, which is repressed by the former and induced by the latter compound.

Animals↗
PubMed1991

Proline is required for transcriptional control of the aromatic hydrocarbon-inducible P(1)450 gene in C57BL/6 mouse monolayer-cultured hepatocytes.

Expression of aryl hydrocarbon hydroxylase (AHH) and the corresponding gene, Cyp1A1, or P(1)450 in mice, in C57BL/6 mouse hepatocytes in primary culture was investigated after exposure to benz[a]-anthracene with respect to proline-related metabolic regulation. When the cells were cultivated in complete Waymouth MB752/1 (Way), prominent induction of AHH by benz[a]anthracene was observed, whereas the induction was inefficient in the same but proline-deficient medium [Way-(-pro)]. Constitutive AHH activities decreased with increasing culture period. P(1)450 gene transcripts were slightly expressed when the medium was changed, independently of whether the cells were cultivated in either Way or Way(-pro), followed by decreased within 24 h and no apparent induction of AHH. However, treatment with delta 1-pyrroline-5-carboxylic acid (P5C), a biosynthetic precursor for proline, dose-dependently increased basal AHH activities in the cells cultivated in Way-(-pro). Benz[a]anthracene induction of AHH in cells cultivated in Way(-pro) was additively increased in the presence of P5C as much as with proline. Treatment with o-aminobenzaldehyde, which inactivates P5C, drastically reduced the induced AHH activities in hepatocytes cultivated in either P5C-added Way(-pro) or Way medium. Benz[a]anthracene induced both P(1)450 and P(3)450 mRNAs. Neither proline nor P5C increased the induced transcripts within 12 h after the start of benz[a]-anthracene treatment, but the two compounds increased the amounts of P(1)450 mRNA found at later time points. After treatment with actinomycin D, the half-life of the induced P(1)450 mRNA was approximately 12 h, being independent of the presence of either proline or P5C. Our observations suggest that induction of AHH after treatment with polycyclic aromatic hydrocarbon is dependent on proline-related metabolism which influences the transcriptional process of P(1)450 gene expression.

Animals↗
PubMed1986

The influence of bile on the bioavailability of polynuclear aromatic hydrocarbons from the rat intestine.

The mechanisms governing absorption of polynuclear aromatic hydrocarbons (PAHs) are important since these carcinogenic compounds occur as solutes in dietary lipids. These highly lipophilic compounds are well absorbed in the intestine. Bile salt micellar solubilization probably facilitates their transport across the unstirred water layer to the enterocytes. To study the role of bile in the intestinal absorption of PAHs, conscious rats with bile duct and duodenal catheters were given isotopically labelled 2,6-dimethylnaphthalene (DMN), phenanthrene, anthracene, 7,12-dimethylbenzanthracene (DMBA), and benzo[alpha]pyrene (BP); the recovery of radioactivity in bile and urine was measured. The PAHs were given intraduodenally in corn oil with or without exogenous bile. Cumulative recovery of radiolabel in bile and urine over 24 h was used to assess the efficiency of absorption of the hydrocarbons with and without bile. The following values for absorption without bile (as percentage of absorption with bile) were obtained: DMN, 91.6%; phenanthrene, 96.7%; anthracene, 70.8%; DMBA, 43.4%; BP, 22.9%. The values for anthracene, DMBA, and BP were significantly less than 100% (P less than 0.05); the values for DMN and phenanthrene were not significantly different from 100%. The dependence of the tricyclic compound anthracene (a structural isomer of phenanthrene) on bile for its absorption correlates with its lower water solubility. These results are consistent with the concept that the unstirred water layer presents a significant barrier to the absorption of this group of compounds and that micellar solubilization facilitates the uptake process.

9,10-Dimethyl-1,2-benzanthracene↗