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PubMed1984

Persistence of benzo(a)pyrene metabolite:DNA adducts in lung and liver of mice.

The persistence of benzo(a)pyrene (BP) metabolite:DNA adducts has been studied in lung and liver of A/HeJ and C57BL/6J mice after a dose of BP (6 mg/mouse) which induces pulmonary adenomas in A/HeJ mice but not in C57BL/6J mice. BP is not a hepatic carcinogen in either strain. Following p.o. administration of [3H]BP, animals were killed at times ranging from 10 hr to 28 days, and BP metabolite:DNA adducts were analyzed by high-pressure liquid chromatography. The major adduct identified in each tissue was the (+)-7 beta-8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene:deoxyguanosine adduct. A 7 beta, 8 alpha-dihydroxy-9 beta,10 beta,epoxy-7,8,9, 10-tetrahydrobenzo(a)pyrene:deoxyguanosine adduct, a (-)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene:deoxyguanosine adduct, and an unidentified adduct were also observed. The disappearance of (+)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydro-BP adduct in A/HeJ mice followed first-order kinetics over the time period examined, with a half-life of 18 and 9 days in lung and liver, respectively. The decay of this adduct in C57BL/6J mice was biphasic in both tissues. Our data on cell turnover suggest that there is active removal of adducts in liver, but that normal DNA turnover can account for the partial or possibly total observed disappearance of adducts in lung. These results suggest that the tissue specificity for BP-induced neoplasia in A/HeJ mice may be related to the relative persistence of adducts and high cell turnover rates in lung. In contrast, the results on formation and persistence of adducts and cell turnover do not provide an explanation for the strain difference in susceptibility to BP-induced pulmonary adenomas. It was also shown that the rates of removal of BP metabolite:DNA adducts in A/HeJ mice are not significantly different at a 500-fold lower BP dose.

Animals↗
PubMed1984

Modulatory effect of glucose-6-phosphate dehydrogenase deficiency on benzo(a)pyrene toxicity and transforming activity for in vitro-cultured human skin fibroblasts.

Human skin fibroblasts isolated in vitro from subjects carrying the Mediterranean variant of glucose-6-phosphate dehydrogenase exhibit an 85% decrease of this enzymatic activity. There is a 26% and a 94% decrease of the hexose monophosphate shunt and of the reduced nicotinamide adenine dinucleotide phosphate/nicotinamide adenine dinucleotide phosphate ratio, respectively. Incubation with 0.1 mM methylene blue activates the hexose monophosphate shunt 7 times that of normal fibroblasts and only 2.2 times that of glucose 6-phosphate-deficient cells. This behavior is coupled with an increase of the resistance to cell death induced by benzo(a)pyrene, a carcinogen, the activation of which proceeds through a reduced nicotinamide adenine dinucleotide phosphate-dependent arene oxide formation. In contrast, no difference between the normal and the deficient fibroblasts exists as regards the toxic effect of methylnitrosourea, a carcinogen that does not need metabolic activation. A growth-retarding effect of benzo(a)pyrene was observed in both normal and deficient cells during 9 days in vitro. This effect is lower in the fibroblasts carrying the Mediterranean glucose-6-phosphate dehydrogenase variant. Glucose-6-phosphate dehydrogenase deficiency protects human fibroblasts against the benzo(a)pyrene-induced in vitro transformation. This effect is mimicked by the incubation of normal fibroblasts with dehydroepiandrosterone, a strong inhibitor of glucose-6-phosphate dehydrogenase. The deficiency of this enzymatic activity, either genetically transmitted or induced by dehydroepiandrosterone, is coupled with a reduced rate of benzo(a)pyrene conversion to water-soluble metabolites by human skin fibroblasts.

Benzo(a)pyrene↗
PubMed1980

The excimer fluorescence of pyrene-labeled tropomyosin. A probe of conformational dynamics.

Rabbit skeletal and cardiac tropomyosin were specifically labeled at their cysteine side chains with N-(1-pyrene)-maleimide. A high degree of intramolecular excimer formation due to interaction between adjacent pyrenes on Cys 190 of each chain was observed by fluorescence techniques. This modification produced low values of specific viscosity at low salt, indicating an inhibition of the salt-dependent polymerizability. Despite the loss of polymerizability, the excimer fluorescence of pyrene-tropomyosin increased with a similar salt dependence as the decrease in viscosity of an unlabeled control. Transient and steady state fluorescence measurements on the labeled tropomyosin indicated the presence of two states of labeled tropomyosin, an excimer-forming state (State B) and a nonexcimer-forming state (State A), in equilibrium with each other. The increase in excimer with increasing temperature and salt concentration can be explained by a shift in equilibrium toward State B. Steric considerations suggest that, in order for the pyrenes to form an excimer, localized chain separation in State B is required.

Animals↗
PubMedDate not supplied

[The effect of benz(a)pyrene on the thermal characteristics of DNA in vivo and in vitro].

Thermal properties of DNA-benz(a)pyrene complex and chromatin within liver cells in BALB/c mice and Macaca fascicularis monkeys after benz(a)pyrene administration were studied using a highly sensitive differential scanning microcalorimeter designed for investigations of dilute biopolymer solutions and complex biological systems. It was shown that benz(a)pyrene (BP) had different efforts on DNA in vivo and in vitro. It was established that at a molar ratio r < 0.03 BP/DNA bp, benz(a)pyrene served as a stabilizing but at higher concentrations as a destabilizing factor of DNA. It was found that BP damaged liver DNA stronger than bone marrow and spleen DNA of a given animal in vivo. Based on analysis of heat redistribution at the heat absorption stages corresponding to denaturation of inactive and active chromatin, we concluded that BP is capable of causing specific breaks in the DNA chain of inactive chromatin and unfolding the whole domain-loop of chromatin, which should lead to uncontrolled genome activation and, therefore, to carcinogenesis.

Animals↗
PubMed1998

Elevated frequencies of benzo(a)pyrene-induced Hprt mutations in internal tissue of XPA-deficient mice.

Xeroderma pigmentosum (XP) patients are hypersensitive to sunlight and have a high predisposition to developing cancer. At the cellular level, XP patients are defective in nucleotide excision repair (NER). Recently, mice have been generated via gene targeting that are deficient in the expression of the XPA gene [A. de Vries et al., Nature (Lond.), 377: 169-173, 1995]. We have assessed the consequences of defective NER for mutagenesis in normal and XPA mice exposed to benzo(a)pyrene and 2-acetylaminofluorene. To study mutagenesis, mature T lymphocytes were isolated from the spleen and stimulated to proliferate in vitro to select for mutants at the endogenous Hprt locus. Background mutant frequencies in normal and XPA mice were very similar and not influenced by age. Single doses of benzo(a)pyrene administered i.p. resulted in a dose-dependent increase of the Hprt mutant frequency in normal mice. In addition, after chronic exposure to benzo(a)pyrene, Hprt mutants were readily detectable in XPA mice at an early onset of treatment but only at a later stage in normal mice. In contrast, chronic treatment of either normal or XPA mice with 2-acetylaminofluorene did not increase Hprt mutant frequency above the background frequency. This absence of significant induction of Hprt mutants can be entirely attributed to the low frequency of 2-acetylaminofluorene-induced DNA adducts in lymphoid tissue. These results provide the first direct evidence in mammals that deficient NER leads to enhanced mutagenesis in endogenous genes in internal tissue after exposure to relevant environmental mutagens, such as benzo(a)pyrene.

2-Acetylaminofluorene↗
PubMed1978

A human plasma component that binds benzo(a)pyrene.

A component capable of binding benzo(a)pyrene was measured in plasma from cigarette smokers and nonsmokers. This plasma fraction was found to have a high specificity of binding to benzo(a)pyrene, bound benzanthracene competitively with benzo(a)pyrene, and was positively correlated (r = 0.861, p less than 0.001) with the capacity of the individual subject's lymphocytes to be induced for AHH activity in culture. An inverse correlation (r = -0.957, p less than 0.001) between the presence of the plasma component in lung cancer patients and the capacity of lung cancer patients' lymphocytes to be induced in culture is unexplained at this time. A benzo(a)pyrene-binding fraction was not found in induced or uninduced cultured lymphocytes from smokers or nonsmokers, or in homogenates of lung excisional tissue from smokers with or without primary lung cancer.

Aryl Hydrocarbon Hydroxylases↗
PubMed2006

Pyrene as chromophore and electrophore: encapsulation in a rigid polyphenylene shell.

Starting from the fourfold ethynyl-substituted chromophore 1,3,6,8-tetraethynylpyrene as core, a series of polyphenylene dendrimers was prepared in high yield by combining divergent and convergent growth methods. The fluorescence quantum yields (Q(f)>0.92) of the encapsulated pyrene chromophore were independent of the size of the polyphenylene shell. Fluorescence quenching studies and temperature-dependent fluorescence spectroscopy were performed to investigate the site isolation of the core. They indicate that a second-generation dendrimer layer is needed to efficiently shield the encapsulated pyrene and prevent aggregate formation. Alkali-metal reduction of the encapsulated pyrene core was carried out to afford the corresponding pyrene radical anions, for which hampered electron transfer to the core was observed with increasing dendrimer generation, which is further proof of the site isolation due to the polyphenylene shell. To improve film formation and solubility of the material, solubilizing alkyl chains were introduced on the periphery of the spherical particles. Furthermore, highly transparent films obtained by a simple drop-casting method showed blue emission mainly from the unaggregated species. The materials presented herein combine high quantum efficiency, good solubility, and improved film-forming properties, which make them possible candidates for several applications in electronic devices.

Journal Article↗
PubMed1976

[Benzo(a)pyrene contents in smoked fish in dependence of smoking procedure (author's transl)].

A survey of benzo(a)pyrene contents in 32 samples of smoked fish is given, which had been hot or cold smoked in two different types of kilns. Benzo(a)pyrene contents in 14 smoked fish samples from cans also were determined. The analytical method includes extraction, column and thin layer chromatography and measuring of the fluorescence of the eluated benzo(a)-pyrene in solution. Smoked fishes from kilns with external smoke generation contained less than 1 ppb benzo(a)pyrene in their edible parts, whereas much more than 1 ppb has often been found in products from tradional kilns.

Benzopyrenes↗
PubMed1978

[A rapid method for the isolation and quantitative analysis of 3,4-benzpyrene [benzo(a)pyrene] in food (author's transl)].

A method for the isolation and the quantitative determination of benzo(a)pyrene in food is described. The material is suspended in petroleum-ether. Benzo(a)pyrene is extracted from the organic phase as a water-soluble caffeine-complex. After re-extracting and purifying by column chromatography on silica gel the quantitative evaluation of benzo(a)pyrene is carried out by thinlayer chromatography and fluorimetric scanning of the cellulose acetate plates. To test the method benzo(a)pyrene was added to several products in concentrations of 100 to 1000 ng. A recovery of about 80% was achieved. Each analysis takes a total of 5 h.

Benzopyrenes↗
PubMed1978

Preparation, isolation, analysis, and characterization of 3-benzo[a]pyrenyl-beta-D-glucopyranosiduronic acid: a metabolite of 3-hydroxybenzo[a]pyrene with potentially high carcinogenic activity.

The aglycone, 3-hydroxybenzo[a]pyrene, was metabolized to 3-benzo[a]pyrenyl-beta-D-glucopyranosiduronic acid in the presence of uridine 5'-diphosphoglucuronic acid and rabbit liver microsomes. The course of the biosynthetic reaction was followed by fluorimetry and reverse-phase, paired-ion high pressure liquid chromatography (HPLC). Also, the HPLC system was used to analyze for glucuronide and 3-hydroxybenzo[a]pyrene during the isolation procedure. The existence of a glucuronide of 3-hydroxybenzo[a]pyrene was determined by radiotracer and enzymic techniques, utilizing the HPLC system. Field desorption and direct inlet mass spectral techniques were used to characterize the 3-hydroxybenzo[a]pyrene glucuronide.

Animals↗
PubMed1978

Postreplication repair of DNA in human fibroblasts after UV irradiation or treatment with metabolites of benzo(a)pyrene.

We have examined the ability of normal fibroblasts and of excision-deficient xeroderma pigmentosum (XP) and XP variant fibroblasts to perform postreplication DNA repair after increasing doses of either ultraviolet (UV) irradiation or mutagenic benzo(a)pyrene derivatives. XP cells defective in the excision of both UV-induced pyrimidine dimers and guanine adducts induced by treatment with the 7,8-diol-9,10-epoxides of benzo(a)pyrene were partially defective in their ability to synthesize high molecular weight DNA after the induction of both classes of DNA lesions. This defect was more marked in XP variant cells, despite their ability to remove by excision repair both pyrimidine dimers and the diol epoxide-induced lesions to the same degree as observed in normal cells. The benzo(a)pyrene 9,10-oxide had no effect in any of the 3 cell lines. The response of the excision and postreplication DNA repair mechanisms operating in human fibroblasts treated with benzo(a)pyrene 7,8-diol-9,10-epoxides, therefore, appears to resemble closely that seen after the induction of pyrimidine dimers by UV irradiation.

Benzopyrenes↗
PubMed1979

Magnesium ions affect the quantitative but not the qualitative microsome mediated binding of benzo[alpha]-pyrene to DNA.

Five distinct hydrocarbon-deoxyribonucleoside adducts are separated by high pressure liquid chromatography after reaction of benzo[alpha]pyrene with calf thymus DNA in the presence of liver microsomes from 3-methylcholanthrene treated rats. The two major adducts co-chromatography with deoxyribonucleoside adducts obtained after hydrolysis of calf thymus DNA previously reacted with liver microsomal metabolically activated 9-hydroxy-benzo[alpha]pyrene or trans-7,8-dihydro-7,8-dihydroxybenzo[alpha]pyrene. High magnesium ion concentrations in the microsomal incubations cause a significant decrease in the covalent binding of the hydrocarbon to DNA but do not affect the qualitative distribution of the individual benzo[alpha]pyrene-deoxyribonucleoside adducts.

Animals↗
PubMedDate not supplied

Estimation of the equilibrium lateral pressure in 1-palmitoyl-2-[6(pyren-1-yl)]hexanoyl-glycerophospholipid liposomes.

Compression isotherms for 1-palmitoyl-2-[6(pyren-1-yl)] hexanoyl-sn-glycero-3-phosphocholine (PPHPC), -ethanolamine (PPHPE), -glycerol (PPHPG), -serine (PPHPS) and -phosphatidic acid monomethylester (PPHPM) were recorded at an argon/water interface. Thereafter, the ratios of pyrene excimer to monomer fluorescence emission intensities (Ie/Im) were determined for liposomes of these lipids and were found to be 20.15, 12.30, 11.80, 10.15 and 6.95 for the ethanolamine, choline, monomethylester, glycerol and serine derivatives, respectively. Assuming Ie/Im to depend on the reciprocal of the mean molecular area of the pyrenelipids in liposomes, equilibrium surface pressure to be the same in liposomes of these lipids regardless of the head group structure and neglecting any possible influence due to differences in the orientation of the pyrene moiety, we sought for that surface pressure value in the compression isotherms where the correlation of the reciprocal of mean molecular area in monolayers to Ie/Im values observed in liposomes was maximal. This treatment results in a value of approximately 12 mN m-1 for the equilibrium surface pressure in 1-palmitoyl-2-[6(pyren-1-yl)]hexanoyl-glycerophospholipid liposomes.

Liposomes↗
PubMed1980

Kinetics of benzo[a]pyrene induced mutagenesis in a highly sensitive salmonella/microsome assay.

The kinetics of benzo[a]pyrene induced mutagenesis in Salmonella typhimurium TA98 and TA100 were studied using a liquid-phase assay and were compared to kinetics of metabolism of benzo[a]pyrene in the same system. Mutagenesis was terminated by the addition of pyrene + menadione at selected times. Under conditions of the assay using hepatic microsomes from 3-methyl-cholanthrene pretreated rats, metabolism of benzo[a]pyrene was over 50% complete in 5 min, and metabolism of initial metabolites became appreciable after this time. The revertant frequency (revertants/10(8) survivors) and the production of tertiary metabolites increased sharply after 5 min and leveled off at 40 min.

Animals↗
PubMed1979

A comparison of the activities of aryl hydrocarbon monooxygenase in liver microsomes from mice of different strains during prolonged 3,4-benzo(a)pyrene administration.

The content and activity of the components of liver microsomal aryl hydrocarbon monooxygenase system change biphasically during long-term 3,4-benzo(a)pyrene administration of C57BL/6 mice as well as to (C57BL/6 X DBA/2)F1 hybrids. The first activity peak (4--14 days) is associated with the induction of aryl hydrocarbon monooxygenase by 3,4-benzo(a)pyrene; the second peak (70--84 days) is related to noninductive mechanism. In DBA/2 mice, the second peak is absent while the slight increase in aryl hydrocarbon monooxygenase activity observed on days 14--28 indicates the aberrant inductive capacity of 3,4-benzo(a)pyrene under its prolonged administration. It is suggested that the weak sensitivity to the blastogenesis caused by 3,4-benzo(a)pyrene observed in C57BL/6 mice and in (C57BL/6 X DBA/2)F1 hybrids is due to the high level of liver aryl hydrocarbon monooxygenase activity at the time of tumor appearance.

Animals↗
PubMed1979

The effects of weak or non-carcinogenic polycyclic hydrocarbons on 7,12-dimethylbenz[a]anthracene and benzo[a]pyrene skin tumor-initiation.

Benzo[e]pyrene (B[e]P) inhibited 7,12-dimethylbenz[a]anthracene (DMBA) skin tumor-initiation in mice by 84%, whereas pyrene and fluoranthene inhibited DMBA initiation by 50 and 34%, respectively. However, B[e]P, pyrene and fluoranthene had either no significant effect or a slight enhancing effect on benzo[a]pyrene (B[a]P) skin tumor-initiation. In addition, B[e]P had essentially no effect on the initiating ability of (+/-)B[a]P-7 beta,8 alpha-diol-9 alpha,10 alpha-epoxide. As a tumor-initiator, B[e]P was found to have very weak activity at a 252 microgram/level (0.4 papillomas/mouse at 40 weeks) and no activity at 100 microgram. When given at a dose of 100 microgram twice weekly, B[e]P induced 2.1 papillomas/mouse at 30 weeks, and 25% of the mice had carcinomas at 40 weeks. However, B[e]P carcinogenic activity is weak when compared to B[a]P, which can induce a comparable tumor response at a dose of 5 microgram twice weekly. When B[e]P was tested as a tumor promoter at a dose of 100 microgram twice weekly after DMBA initiation, it induced 4.5 papillomas/mouse at 30 weeks and a 45% carcinoma incidence at 40 weeks, which was approximately twice as effective as B[e]P alone. The data show that B[e]P is a very weak tumor initiator, a weak complete carcinogen, a moderate tumor promoter, possibly a weak co-tumor-initiator when given with B[a]P, and a potent anit-tumor-initiator when given with DMBA. The anti-tumor initiating and co-tumor-initiating effects of B[e]P appear to be related to its ability to modify the conversion of the tumor initiator into an electrophilic intermediate(s) which are capable of covalently binding to DNA. In addition, B[e]P induced epidermal cellular proliferation which may be related to its promoting ability.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2003

Nonplanar aromatic compounds. 8. Synthesis, crystal structures, and aromaticity investigations of the 1,n-dioxa[n](2,7)pyrenophanes. How does bending affect the cyclic pi-electron delocalization of the pyrene system?

A series of 1,n-dioxa[n](2,7)pyrenophanes (n = 7-12) with increasingly nonplanar pyrene moieties was synthesized by a 9-10 step sequence starting from 5-hydroxyisophthalic acid. The crystal structure of each member of this series was determined crystallographically. Several spectroscopic properties were found to vary with the extent of the nonplanarity of the pyrene unit. The way in which the distortion from planarity of the pyrene system influences its pi-electron delocalization was investigated by using two quantitative descriptors of aromaticity based on geometry (HOMA) and magnetism (magnetic susceptibility and NICS). Both methods suggest that the aromaticity of the pyrene moiety is diminished only slightly upon increasing the bend angle theta from 0 degrees to 109.2 degrees.

Journal Article↗
PubMedDate not supplied

Evidence of involvement of multiple sites of metabolism in the in vivo covalent binding of dibenzo[a,h]pyrene to DNA.

The in vivo formation of dibenzo[a,h]pyrene-DNA adducts in mouse skin was assessed by laser-excited fluorescence spectroscopy at 77 and 4.2 K. Two adducts were identified with fluorescence origin bands at approximately 383.5 and 407.2 nm, and these were shown to possess pyrene and benzo[a]pyrene (B[a]P) chromophores, respectively. Both DNA-bound chromophores displayed considerable electron-phonon coupling and likely assume a highly base-stacked or quasi-intercalated configuration within DNA duplexes. The presence of B[a]P and pyrene aromatic systems indicates that two-electron or monooxygenation metabolism occurred on either the a or h benzo moieties (which are equivalent) in the former case, and on both these rings in the latter case. The presence of two adduct species agrees with 32P-postlabeling analysis of the DNA, which showed the presence of two major adducts in both thin-layer and high-performance liquid chromatographic separations.

Animals↗