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At least 73 records · Page 4Linked to original sources
PubMed1983

Effect of polycyclic aromatic compounds and phorbol esters on ornithine decarboxylase and aryl hydrocarbon hydroxylase activities in mouse liver.

Single i.p. injections of 3-methylcholanthrene (MC; 50 mg/kg) administered to inbred C57BL/6 mice or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 100 micrograms/kg) to DBA/2 mice gave an increase in the hepatic activities of ornithine decarboxylase (ODC) and aryl hydrocarbon hydroxylase (AHH) with peaks occurring by 12 and 48 hr, respectively. A single i.p. dose of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA; 100 micrograms/kg) enhanced the activity of ODC about 70-fold within 12 hr in C57BL/6 mice and 18-fold within 24 hr in DBA/2 mice without affecting AHH activity markedly. 4-O-Methyl-12-O-tetradecanoylphorbol-13-acetate (100 micrograms/kg) raised ODC activity to about 25% of the TPA-treated value in C57BL/6 mice; in DBA/2 mice, TPA and 4-O-methyl-12-O-tetradecanoylphorbol-13-acetate induced ODC activity to roughly the same level. Benzo(e)pyrene (50 mg/kg) failed to affect ODC and AHH activities significantly in either strain. The inducing effect of TPA on ODC activity was potentiated by a simultaneous administration of MC to C57BL/6 mice; combined TPA and TCDD to DBA/2 mice exerted an additive effect on hepatic ODC activity. Difluoromethylornithine administered i.p. effectively inhibited the induction of ODC activity elicited by TPA, MC, or TCDD either alone or in various combinations but did not interfere with AHH induction. These data indicate that different regulatory factors are involved in the ODC induction process elicited by TPA and polycyclic aromatic compounds and that MC and TCDD may induce ODC activity by different mechanisms. The results also confirm our earlier findings in rat skin and cells in culture which suggest that the ODC and AHH induction processes can occur independently of each other. Additionally, there is a strain-related difference in sensitivity with regard to ODC-inducing activity of TPA in the livers of C57BL/6 and DBA/2 mice.

Animals↗
PubMed1986

Polycyclic aromatic compounds (PAC) in leaf lettuce.

Twenty-three samples of leaf lettuce (Lactuca sativa var. crispa) cultivated in private gardens in southern Finland were analyzed for polycyclic aromatic hydrocarbons (PAH) and derivatives. The total PAH concentrations varied from 4.8 to 94 micrograms/kg fresh weight. Nitro derivatives of PAH were detected in only five samples. One lettuce sample was also analyzed for PAH oxy-derivatives. 9H-Fluoren-9-one (1.3 microgram/kg) and 6 H-benzo[cd]pyren-6-one (0.3 microgram/kg) were found. The profiles of PAH in lettuce were compared with those in ambient air. It was concluded that PAH in lettuce originate from deposition of PAH-containing particles present in ambient air.

Finland↗
PubMed1988

Determination of polycyclic aromatic compounds in fish tissue.

A method is presented for the analysis of polycyclic aromatic hydrocarbons (PAHs), polycyclic aromatic sulfur heterocycles (PASHs), and basic polycyclic aromatic nitrogen heterocycles (PANHs) in fish. The analytical procedure includes Soxhlet extraction of prepared fish tissue with methylene chloride followed by gel permeation chromatography (GPC) using Bio-beads SX-3. For PAHs/PASHs, further cleanup is performed using adsorption chromatography on Florisil (5% water deactivated) and elution with hexane. For basic PANHs further cleanup of the fish extracts after GPC is achieved using liquid-liquid partitioning with 6 M hydrochloric acid and chloroform and then basifying the aqueous phase and extracting it with chloroform. Analysis of fortified fish samples was performed using capillary gas chromatography with flame ionization detection and capillary gas chromatography-mass spectrometry. Good agreement was observed for both methods of analysis when applied to fish samples fortified with PAHs, PASHs and basic PANHs at 0.1 to 1 microgram/g, suggesting that the method is effective at removing interfering biogenic compounds prior to analysis. Average recovery of PAHs/PASHs from fortified fish tissue was 87% and 70% for fish tissue fortified at 0.24-1.1 and 0.024-0.11 microgram/g, respectively. Average recovery for basic PANHs was 97% for fish fortified at 1.2-1.4 micrograms/g.

Animals↗
PubMed1995

Actions of a versatile fluorene-degrading bacterial isolate on polycyclic aromatic compounds.

Pseudomonas cepacia F297 grew with fluorene as a sole source of carbon and energy; its growth yield corresponded to an assimilation of about 40% of fluorene carbon. The accumulation of a ring meta-cleavage product during growth and the identification of 1-indanone in growth media and washed-cell suspensions suggest that strain F297 metabolizes fluorene by mechanisms analogous to those of naphthalene degradation. In addition to fluorene, strain F297 utilized for growth a wide variety of polycyclic aromatic compounds (PACs), including naphthalene, 2,3-dimethylnaphthalene, phenanthrene, anthracene, and dibenzothiophene. Fluorene-induced cells of the strain also transformed 2,6-dimethylnaphthalene, biphenyl, dibenzofuran, acenaphthene, and acenaphthylene. The identification of products formed from those substrates (by gas chromatography-mass spectrometry) in washed-cell suspensions indicates that P. cepacia F297 carries out the following reactions: (i) aromatic ring oxidation and cleavage, apparently using the pyruvate released for growth, (ii) methyl group oxidations, (iii) methylenic oxidations, and (iv) S oxidations of aromatic sulfur heterocycles. Strain F297 grew with a creosote-PAC mixture, producing an almost complete removal of all aromatic compounds containing 2 to 3 rings in 14 days, as demonstrated by gas chromatography analysis of the remaining PACs recovered from cultures. The identification of key chemicals confirmed that not only are certain compounds depleted but also the anticipated reaction products are found.

Biodegradation, Environmental↗
PubMed1984

Polycyclic aromatic compounds in curing smoke.

The curing smoke, generated by the smouldering of alder chips, from a commercial food smoking plant was investigated with respect to polynuclear aromatic compounds (PAC). Samples were taken from inside the ovens and in the working zone immediately outside them. Analysis showed that considerable amounts of methyl phenanthrenes were present in the smoke as a major part of the PAC content.

Chromatography, Gas↗
PubMed1987

Polycyclic aromatic compounds as phototoxic mosquito larvicides.

The phototoxicity of 2-acetylnaphthalene, 1-acetylnaphthalene, 1-naphthalenecarboxaldehyde, 9-xanthenone, 9-thioxanthenone, 9-methylanthracene, anthracene, alpha-terthienyl, pyrene and fluoranthene was tested with larvae of Aedes aegypti, Ae. taeniorhynchus and Culex quinquefasciatus. The larvae were exposed to the chemicals in the presence of sunlight for intervals from 1 to 6 hr and the corresponding LC50 values calculated. The LC50 values determined when the 6-hr exposure was followed by 18 hr in the dark range from over 10 ppm to below 0.001 ppm. Naphthalene derivatives were the least active while alpha-terthienyl, anthracene, 9-methylanthracene, pyrene and fluoranthene were the most phototoxic.

Animals↗
PubMed1983

Experimental studies on the carcinogenicity of five nitrogen containing polycyclic aromatic compounds directly injected into rat lungs.

Using a beeswax/tricaprylin mixture as vehicle, three doses each of acridine, benz[a]acridine (BaAC), benz[c]acridine (BcAC), dibenz[a,h]-acridine (DBa,hAC) and dibenz[a,j]acridine (DBa,jAC) were injected into the lungs of 35 female Osborne-Mendel rats per group. To compare the carcinogenic potency of the heterocycles, benzo[a]pyrene (BaP) was taken as reference substance. Dose-response relationships were obtained for DBa,hAC as well as for BaP. DBa,jAC and BcAC exhibited no carcinogenic effects in the dose range from 0.1 mg to 1 mg tested in the lung implantation model. From the results presented here, it cannot be excluded that tumor development may occur when testing higher doses. BaP, however, must be considered much more potent since it revealed, by far, higher tumor incidences and diminished life times.

Acridines↗
PubMed1992

The formation of proximate carcinogens from three polycyclic aromatic compounds by human liver microsomes.

1. The metabolism of 3H-benzo[a]pyrene (BP), 3H-7-methylbenz[c]acridine (7MBAC) and 3H-dibenz[a,j]acridine (DBAJAC) have been studied in human liver microsomes from 13 subjects. 2. When the metabolism of these carcinogens to more polar ethyl acetate-soluble metabolites were compared, the activities towards the nitrogenous carcinogens were twice that determined for BP. 3. The specific rates of formation of the three proximate carcinogens, BP-7,8-dihydrodiol, 7MBAC-3,4-dihydrodiol and DBAJAC-3,4-dihydrodiol per nmol cytochrome P-450 for 12 subjects were positively correlated. 4. These dihydrodiols constituted 5.9 +/- 0.7% (mean +/- SEM), 57.8 +/- 2.6% and 3.0 +/- 0.4% of the total metabolites identified by cochromatography with standards, 7MBAC, DBAJAC and BP respectively.

Acridines↗
PubMed1983

Mixtures of polycyclic aromatic compounds inhibit mutagenesis in the Salmonella/microsome assay by inhibition of metabolic activation.

We observed that complex mixtures of aromatic compounds isolated from a coal-derived oil suppressed the mutagenic activity of the indirect mutagens benzo[a]pyrene, 7,12-dimethylbenz[a]anthracene, 2-aminofluorene, and 2-acetylaminofluorene as measured in the Salmonella/microsome mutagenicity assay, using strain TA98 and metabolic activation with Aroclor-induced rat-liver S9 or microsomes. The mixture also inhibited S9-dependent benzo[a]pyrene metabolism and covalent binding to DNA in a cell-free system. The mixture did not suppress the activity of either the direct acting mutagens 2-nitrofluorene and benzo[a]pyrene diol-epoxide, or of the indirect mutagen N-hydroxy-2-acetylaminofluorene which requires a microsomal deacetylase for metabolic activation. Spectrophotometric measurements showed that components of the mixture bound to microsomal cytochrome P-450. The mixture did not inhibit microsomal NADPH-cytochrome c (P-450) reductase. These observations show that the mixtures inhibited metabolic activation by the microsomal monooxygenase system, probably by binding of unidentified components to cytochrome P-450. The resulting inhibition of mutagenesis may have implications for risk estimates for the mixtures we examined as well as for other types of complex mixtures for which similar inhibitory effects have been observed.

Animals↗