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PubMed1990

Molecular dosimetry of DNA adducts in Chinese hamster ovary cells and C3H10T1/2 mouse embryo fibroblast cells treated with benzo[a]pyrene.

Chromatographic profiles of DNA adducts formed following treatment of Chinese hamster ovary (CHO) cells or C3H10T1/2 mouse embryo fibroblast cells with benzo[a]pyrene (BP), in the presence or absence of rat liver S9 fraction, have been obtained by both direct labelling ([3H]BP) and 32P-post-labelling methods. The principal adduct formed in both cell lines was (+)-N2-(7R,8S,9R-trihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene- 10S-yl) 2'-deoxyguanosine (detected as its 3',5'-bisphosphate by 32P-post-labelling). In both cell lines significantly higher levels of adducts were observed in the presence of S9 fraction. The results of these studies provide useful reference data on the genotoxic metabolism of BP in these widely used cell culture systems and allow comparisons with data obtained in other experimental mammalian systems. Valid comparisons of metabolism in experimental systems used as extrapolative models for man are particularly important where multiple bioactivation pathways are possible, such as in the case of polycyclic aromatic hydrocarbons.

Animals↗
PubMed1994

Detection of nitro-azabenzo[a]pyrene derivatives in the semivolatile phase originating from airborne particulate matter, diesel and gasoline vehicles.

Mutagens in the semivolatile phase of airborne particulate matter, diesel and gasoline engine emissions were investigated using chemical and biological assays. The previously unknown mutagens, 1-(3-)nitro-6-azabenzo[a]pyrenes (1-N-6-ABP and 3-N-6-ABP) and 1-(3-)nitro-6-azabenzo[a]pyrene-N-oxides (1-N-6-ABPO and 3-N-6-ABPO), were detected in the semivolatile phase, which was adsorbed onto XAD-4 resin combined with a Teflon-coated fibre filter. Dichloromethane extracts of materials adsorbed onto XAD-4 resin were divided into acidic, neutral and basic by liquid-liquid separation. These chemicals in the basic fraction were the major mutagens in the semivolatile phase when they were bioassayed using Salmonella typhimurium TA98 in the absence of S9 mix; the mutagenicity of the basic fraction contributed at the rate of 42.9-68.8% of that of crude extracts for airborne, diesel and gasoline emission materials. As the mutagens were found to be difficult to analyse by gas chromatography (because of their probable absorption onto the packing) they were purified by HPLC and analysed by mass spectrometry. The concentrations of 1-N-6-ABP, 3-N-6-ABP, 1-N-6-ABPO and 3-N-6-ABPO detected were 1.1, 1.2, 0.8 and 0.3 ng/g, respectively, of materials in the airborne sample, and 4.9, 7.7, 2.2 and 3.8 ng/g, respectively, of materials in the diesel emission. Only 1-N-6-ABP (3.4 ng/g) and 3-N-6-ABP (4.9 ng/g) were detected in the semivolatile phase of the gasoline engine emission.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants↗
PubMed1995

Stereochemistry-dependent bending in oligonucleotide duplexes induced by site-specific covalent benzo[a]pyrene diol epoxide-guanine lesions.

The apparent persistence length of enzymatically linearized pIBI30 plasmid DNA molecules approximately 2300 bp long, as measured by a hydrodynamic linear flow dichroism method, is markedly decreased after covalent binding of the highly tumorigenic benzo[a]pyrene metabolite 7R,8S-dihydroxy-9S,10R-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene [(+)-anti-BPDE]. In striking contrast, the binding of the non-tumorigenic, mirror-image 7S,8R,9R,10S enantiomer [(-)-anti-BPDE] to DNA has no measurable effect on its alignment in hydrodynamic flow gradients (< or = 2.2% of the DNA bases modified). In order to relate this effect to BPDE-nucleotide lesions of defined stereochemistry, the bending induced by site-specifically placed and stereochemically defined (+)- and (-)-anti-BPDE-N2-dG lesions in an 11mer deoxyoligonucleotide duplex was studied by ligation and gel electrophoresis methods. Out of the four stereochemically isomeric anti-BPDE-N2-deoxyguanosyl (dG) adducts with either (+)-trans, (-)-trans, (+)-cis, and (-)-cis adduct stereochemistry, only the (+)-trans adduct gives rise to prominent bends or flexible hinge joints in the modified oligonucleotide duplexes. Since both anti-BPDE enantiomers are known to bind preferentially to dG (> or = 85%), these observations can account for the differences in persistence lengths of DNA modified with either (+)-anti-BPDE or the chiral (-)-anti-BPDE isomer.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1981

The distribution of benzo(a)pyrene DNA adducts in mammalian chromatin.

This paper describes the distribution of DNA-lesions generated by the potent carcinogen benzo(a)pyrene (BP) or its ultimate metabolic derivative 7 alpha, 8 8 beta, di-hydroxy-9 beta, 10 beta-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDE) within mammalian chromatin using the enzymic probe micrococcal nuclease. We have shown that the progress of the nuclease on naked DNA is unaffected by the presence of the hydrocarbon lesion at moderate extents of digestion. Digestion of nuclei isolated from murine erythroleukaemic cells immediately following BPDE treatment, and analysis of micrococcal nuclease resistant DNA by TCA precipitation, hydroxyapatite chromatography and gel electrophoresis demonstrates a non-random distribution of lesions. Approximately three times more binding occurs on the linker DNA regions between nucleosome cores than on the nucleosome core DNA itself. A similar result was obtained with BPDE treated primary mouse embryo cells; however nuclei isolated from these cells after prolonged treatment with BP (to allow metabolic activation) showed no such preferential binding. Post-treatment incubation of BPDE-treated cells shows that this difference can be accounted for by the loss of preferential localisation with time.

Animals↗
PubMed1999

Study on RNA structure by pyrene-labeled 2'-O-methyloligoribonucleotides.

Properties of 2'-O-methyloligoribonucleotides containing 2'-O-(1-pyrenylmethyl)uridine were investigated as the fluorescent probe to search the single strand regions on RNA secondary and tertiary structure. The pyrene-labeled 2'-O-methyloligoribonucleotide (OMUpy) showed remarkable increase of fluorescence intensity to 333-fold at 375 nm when hybridized with the complementary oligoribonucleotide. When OMUpy, complementary to loop or stem regions, was applied to E. coli 5S-rRNA, the fluorescence intensities were increased in a sequence specific manner. The difference of the fluorescence intensities corresponds to the higher-order structure of 5S-rRNA, suggesting that pyrene-labled 2'-O-methyloligoribonucleotide can be applicable to search single strand regions of RNA.

Base Sequence↗
PubMed2000

Characterization of RNA structure by bis-pyrene-labeled 2'-O-methyloligonucleotides.

Properties of 2'-O-methyloligoribonucleotides containing two consecutive 2'-O-(1-pyrenylmethyl)uridine were investigated as a fluorescent probe to search the single strand regions of RNA. The bis-pyrene-labeled 2'-O-methyloligoribonucleotide (OMUpy2) induced the formation of pyrene dimer upon hybridization with the complementary oligoribonucleotides and showed remarkable appearance of broad structureless fluorescence at 480 nm. Contrarily, when OMUpy2 was hybridized with the complementary oligodeoxyribonucleotides, such enhancement of fluorescence was scarcely observed. When various OMUpy2 were applied to E. coli 5S-rRNA, the fluorescence intensity at 480 nm was varied in a sequence specific manner.

Base Sequence↗
PubMed2006

Photoelectrochemical properties of pyrene modified DNA immobilized on gold electrode.

Self-assembled monolayers (SAMs) of pyrene-modified DNA were prepared on gold electrode and their photoelectrochemical properties were investigated. The cathodic photocurrent was generated by photoirradiation of the SAM in the presence of methyl viologen as an electron carrier. The photocurrent efficiency increased with increasing the distance between the pyrene and the gold substrate.

DNA↗
PubMed2003

Dietary fibers reduce the urinary excretion of 1-hydroxypyrene following intravenous administration of pyrene.

During biological monitoring of exposure to a chemical, a possible source of interindividual variability in the measurement of a urinary metabolite that undergoes enterohepatic cycling is the presence of dietary fiber in the gastrointestinal tract. This study examined the effect of diets containing either the insoluble fiber Alphacel (nonnutritive bulk cellulose) or the soluble pectin (from citrus fruit, MW 20,000-40,000). Five groups of male Sprague-Dawley rats received one of the following diets: poor (5% w/w) or rich (15% w/w) in Alphacel, poor (5% w/w) or rich (15% w/w) in pectin, or no fiber (NF). Five micromol/kg of pyrene was administered by iv injection immediately after feeding the animals with their respective diet, and urine and feces collections started for the determination of 1-hydroxypyrene (1-OHP), a metabolite of pyrene. The type of fiber had no influence on the results. The rats receiving diets both poor and rich in fiber excreted less 1-OHP (18 +/- 8 and 15 +/- 7 pmol per g of rat, respectively) in the 24-h urine samples than the NF group (28 +/- 6 pmol/g). There was a nonstatistically significant trend towards increased fecal and total (urinary + fecal) 1-OHP excretion with increasing amount of fiber in the diet. An in vitro experiment showed an inverse correlation (r(2) = 0.98) between the amount of Alphacel in suspension in a 1-OHP aqueous solution and the recovery of 1-OHP from the soluble fraction. The reduction in urinary output of the metabolite due to fiber reaching approximately 40% may contribute to its interindividual variability observed in occupational and environmental studies.

Adsorption↗
PubMed1995

4,5-Dihydrobenzo[a]pyrene-4,5-trans-(e,e)-diol.

The title compound, C20H14O2, is a metabolite of the chemical carcinogen benzo[a]pyrene. The crystal structure consists of groups of molecules in each of which both hydroxy groups donate and accept hydrogen bonds. Stacking of dihydrobenzo[a]pyrene ring systems occurs along the crystallographic c axis.

Benzo(a)pyrene↗
PubMed1984

Aryl hydrocarbon hydroxylase, epoxide hydrolase, and benzo[a]-pyrene metabolism in human epidermis: comparative studies in normal subjects and patients with psoriasis.

Prior studies have shown that human skin possesses a cytochrome P-450-dependent microsomal enzyme that is capable of metabolizing drugs and polycyclic aromatic hydrocarbon (PAH) carcinogens. This study characterized benzo[a]pyrene (BP) metabolism in human epidermis of normal and psoriatic individuals. The basal level of the cytochrome P-450-dependent microsomal enzyme aryl hydrocarbon hydroxylase (AHH) and epoxide hydrolase (EH) were measured in freshly keratomed epidermis from 12 normal individuals and from uninvolved skin sites of 12 patients with psoriasis. The induction response of AHH following the in vitro addition of the PAH benz[a]anthracene (BA) was also assessed. The basal activity (mean +/- SE) of AHH in normal epidermis was 62.1 +/- 5.6 units (fmol 3-hydroxybenzo[a]pyrene, 3-OH-BP/min/mg protein) whereas the activity in uninvolved skin of psoriatic individuals was 62.9 +/- 5.1 units (NS), Epoxide hydrolase activity was 25.1 +/- 1.1 (pmol BP 4,5-diol/min/mg protein) unites in normal epidermis and 24.8 +/- 2.1 units in epidermis from patients with psoriasis (NS). Following addition of BA (100 microM), in vitro, AHH activity in normal epidermis increased by a mean value of 165% whereas activity in nonlesional epidermis of psoriatic individuals increased 320%. Kinetic studies in normal epidermis revealed that AHH reaction was linear up to 60 min and to 50 micrograms protein, had a pH optimum of 7.4, and the Km for BP was 0.62 microM. High-performance liquid chromatography (HPLC) confirmed that the pattern of metabolism of BP was quite similar in epidermal microsomes prepared from normal and psoriatic individuals, insofar as the formation of diols, phenols, and quinones was concerned. These studies indicate that human epidermis is capable of metabolizing BP and that there is no significant difference between normal individuals and patients with psoriasis insofar as basal AHH activity or total BP metabolism is concerned. Furthermore, the epidermal enzyme system in patients with psoriasis has a greater responsiveness to environmental PAH than does that of normal individuals.

Aryl Hydrocarbon Hydroxylases↗
PubMed1982

Interindividual variation in benzo(a)pyrene metabolism and composition of isoenzymes of cytochrome P-450 as revealed by SDS-gel electrophoresis of human liver microsomal fractions.

Human liver microsomal fractions from 13 different individuals were characterized with respect to SDS-polyacrylamide gel electrophoretic profiles and regiospecificity in the metabolism of the polyaromatic hydrocarbon benzo(a)pyrene. Pronounced interindividual differences in the composition of microsomal proteins in the molecular weight region of Mr=49,000-60,000 were found. Furthermore, gel electrophoresis combined with staining for peroxidase activity indicated most of the variations among the profiles of microsomal proteins being attributed to interindividual differences in the composition of isoenzymes of cytochrome P-450. One type of human liver microsomal fraction was selectively induced in specimens obtained from patients with known regular drug intake before death and correlated well in molecular weight to the phenobarbital-inducible form of cytochrome P-450 in the rabbit. Large variations among the human liver microsomal samples were also seen in the benzo(a)pyrene metabolism. The results indicate the presence of 7-8 different froms of cytochrome P-450 in human liver microsomes and that the interindividual variations seen in drug metabolism may at least in part be explained by interindividual variations in the distribution of these isoenzymes.

Adolescent↗
PubMed1986

Metabolism of benzo(a)pyrene in the nuclear and microsomal fractions from rhesus monkey liver.

The metabolism of benzo(a)pyrene was studied in the nuclear and microsomal fractions from four rhesus monkey livers. The nuclear fraction was obtained by differential centrifugation, including a step in 2.3 M sucrose. The metabolites from 3H-benzo(a)pyrene were separated by high performance liquid chromatography (HPLC) and the radioactivity was measured. The nuclear fraction catalyzed the formation of 4,5- and 7,8-dihydrodiols and that of 9-OH and 3-OH phenols. The ratio between the nuclear and microsomal rate of formation of the metabolites ranged between 0.02 and 0.03. The nuclear fraction did not catalyze the formation of 9,10-dihydrodiol or quinones at a detectable rate. In the microsomal fraction there was a preferential formation of 4,5-dihydrodiol and 3-OH phenol. Nuclei differ from the microsomes for the lack of formation of quinones.

Animals↗
PubMed1996

Demonstration of benzo(a)pyrene-induced DNA damage in mice by alkaline single cell gel electrophoresis: evidence for strand breaks in liver but not in lymphocytes and bone marrow.

Alkaline single cell gel electrophoresis (also known as the 'comet assay') was used to measure DNA strand breaks and alkali-labile sites in peripheral lymphocytes, bone marrow and liver cells of C57BL/6 mice orally exposed to benzo(a)pyrene. Although this polycyclic aromatic hydrocarbon is a well-known genotoxic agent, little is known about to what extent it actually induces DNA strand breaks in peripheral lymphocytes and other tissues after in vivo exposure. Significant and dose-related damage was observed in liver cells after three days of exposure (lowest observed effect level being 3 x 100 mg benzo(a)pyrene/kg b.wt. No such damage could be observed in the lymphocytes and bone marrow cells even after administration of 3 x 150 mg benzo(a)pyrene/kg b.wt. The reference substance cyclophosphamide produced pronounced DNA damage in lymphocytes and bone marrow cells already in a single dose of 100 mg/kg b.wt. The present mouse study questions the usability of DNA strand breaks in peripheral lymphocytes as an indicator of benzo(a)pyrene-induced genotoxicity.

Animals↗
PubMed1995

The use of lipid headgroup charge to enhance photoinduced electron transfer in vesicles: reactions of functionalized pyrene with a two component viologen system.

Kinetics of photoinduced electron transfer from a lipid functionalized pyrene, 1-(10-(6(8)-octadecylpyrenyl) decanoyl)-2-hexanoyl-sn-glycero-3-phosphorycholine (OPyPC), to a two component viologen acceptor system have been measured by laser flash photolysis. N,N'-tetramethylene-2,2' -bipyridinium ion (DQ2+) and N,N'-dipropyl-4,4'-bipyridinium sulfonate (PVS), have been utilized as the primary and secondary acceptors. It has been shown that utilization of a lipid with a net negatively charged phosphatidylglycerol headgroup provides a driving force for localizing high concentrations of primary acceptor (DQ2+) in the region of donor. Subsequently, the charged interface can act to maintain long-term separation between the oxidized pyrene donor (OPyPC+) and the reduced secondary acceptor, PVS-. When a dioleoyl lipid is used, reaction of (OPypc+) with the double bond competes significantly with back reaction. However, substitution of diphytylphosphatidylglycerol for the dioleoyl analog results in a cation lifetime of about 0.5 ms and a continued very long-lived reduced species (approximately 4 h). Quantum yields of approximately 0.15 may be obtained in this system.

Electron Transport↗
PubMed1998

Overexpression of stably transfected human glutathione S-transferase P1-1 protects against DNA damage by benzo[a]pyrene diol-epoxide in human T47D cells.

The (+)-anti enantiomer of benzo[a]pyrene-7,8-dihydrodiol-9, 10-epoxide (BPDE) is a potent mutagenic and carcinogenic metabolite of benzo[a]pyrene (BP), and a major fraction is conjugated with glutathione in vivo. The chemopreventive role of glutathione S-transferases (GSTs) in protecting against covalent modification of DNA and other cellular macromolecules by BPDE was modeled in human T47D and MCF-7 cell lines previously stably transfected with human GSTpi1 (hGSTP1). Cells were exposed to [3H]BPDE (30-600 nM). Dose-response experiments indicated that the high level of expression of hGSTP1-1 in the T47Dpi cell line (4411 +/- 183 milliunits/mg of cytosolic protein, using 1-Cl-2,4-dinitrobenzene as substrate), resulted in 70-90% reduction in the covalent 3H-adduct formation in DNA or RNA isolated from the GSTP1-transfected T47Dpi cell line. The lower level of hGSTP1-1 expression in the transfected MCF-7 cell line (91 milliunits/mg) provided only marginal protection against [3H]BPDE adduct formation and did not affect sensitivity to BPDE-induced cytotoxicity. Protection against BPDE-induced cytotoxicity was observed only in the T47Dpi cell line, which had an IC50 value 5.8-fold greater than that of the T47Dneo control cell line. Measurement of glutathione conjugates of BPDE indicated that the total conjugation was 5-fold higher in the GSTpi-transfected T47D line, most of which was exported into the culture medium over the 20-min exposure period. These results indicate that hGSTP1-1 protects effectively against DNA and RNA modification by BPDE, but moderate to high level expression may be required for strong protection against BPDE-induced genotoxicity and cytotoxicity.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1996

Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in P53.

Cigarette smoke carcinogens such as benzo[a]pyrene are implicated in the development of lung cancer. The distribution of benzo[a]pyrene diol epoxide (BPDE) adducts along exons of the P53 gene in BPDE-treated HeLa cells and bronchial epithelial cells was mapped at nucleotide resolution. Strong and selective adduct formation occurred at guanine positions in codons 157, 248, and 273. These same positions are the major mutational hotspots in human lung cancers. Thus, targeted adduct formation rather than phenotypic selection appears to shape the P53 mutational spectrum in lung cancer. These results provide a direct etiological link between a defined chemical carcinogen and human cancer.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1980

Mitochondrial DNA is a major cellular target for a dihydrodiol-epoxide derivative of benzo[a]pyrene.

When mammalian cell cultures are exposed for 2 hours to (+/-)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene, a mutagenic and carcinogenic derivative of benzo[a]pyrene, the extent of covalent modificationof mitochondrial DNA is 40 to 90 times greater than that of nuclear DNA. Evidence is presented that this reflects the lipophilic character of the derivative and the very high ratio of lipid to DNA in mitochondria. These results suggest that mitochondrial DNA may be an important cellular target of chemical carcinogens.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1993

Degradation of phenanthrene, fluorene, fluoranthene, and pyrene by a Mycobacterium sp.

Mycobacterium sp. strain BB1 was isolated from a former coal gasification site. It was able to utilize phenanthrene, pyrene, and fluoranthene as sole sources of carbon and energy and to degrade fluorene cometabolically. Exponential growth with solid phenanthrene, pyrene, and fluoranthene was obtained in fermentor cultures. The growth rates were 0.069, 0.056, and 0.040 h-1, respectively. Several metabolites of phenanthrene and fluorene metabolism were identified.

Bacteriological Techniques↗