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PubMed1982

Comparative tumor initiating activity on mouse skin of 6-nitrobenzo[a]pyrene, 6-nitrochrysene, 3-nitroperylene, 1-nitropyrene and their parent hydrocarbons.

6-Nitrobenzo[a]pyrene, 6-nitrochrysene, 3-nitroperylene, 1-nitropyrene, and the corresponding parent hydrocarbons were tested for tumor initiating activity on mouse skin with promotion by tetradecanoylphorbol acetate. The initiating doses of 6-nitrobenzo[a]pyrene and benzo[a]pyrene were 0.05 mg each; for all other compounds the initiating doses were 1.0 mg. 6-Nitrochrysene induced tumors in 60% of the mice (2.1 tumors per mouse), but was significantly less tumorigenic than chrysene. 3-Nitroperylene induced tumors in 42% of the mice (0.5 tumors per mouse) and was significantly more active than perylene. Neither 1-nitropyrene nor 6-nitrobenzo[a]pyrene exhibited significant tumorigenic activity in the concentrations tested.

Animals↗
PubMed1989

Effect of tannic acid on rat liver S9 mediated mutagenesis, metabolism and DNA binding of benzo[a]pyrene.

Tannic acid, a naturally occurring plant phenol, inhibited rat liver S9 mediated mutagenesis of benzo[a]pyrene in Salmonella typhimurium by 32-77% at concentrations of 5-50 micrograms/mutagenesis plate. Tannic acid (10-40 microM) had no affect on the formation of organosoluble metabolites of benzo[a]pyrene or of its water-soluble conjugates. It did, however, inhibit benzo[a]pyrene (B[a]P) metabolite binding to calf thymus DNA by 40% at a concentration of 40 microM and inhibited benzo[a]pyrene 7,8-dihydrodiol-9,10-epoxide (BPDE): deoxyguanosine adduct formation in calf thymus DNA by 12-54% at concentrations of 10-40 microM. These results suggest that the antimutagenic effect of tannic acid and inhibition of B[a]P metabolite binding to DNA is by a previously described scavenging mechanism and/or by a DNA-affinity binding mechanism that prevents BPDE interaction with DNA as previously described for ellagic acid.

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

Inhibition of covalent DNA binding and mutagenicity of benzo[a]pyrene by isopropyl-2-(1,3-dithietane-2-ylidene)-2-[N-(4-methylthiazol-2-yl) carbamoyl]acetate (YH439), a novel hepatoprotective agent.

Isopropyl-2-(1,3-dithietane-2-ylidene)-2[N-(4-methyl-2-thiazol+ ++-2-yl) carbamoyl]acetate (YH439) was synthesized as a hepatoprotective drug for the treatment of chronic hepatitis and liver cirrhosis. In the present investigation, we have tested YH439 for its chemoprotective activity against the carcinogen benzo[a]pyrene. The drug exhibited dose-dependent protection against bacterial mutagenesis induced by benzo[a]pyrene its covalent binding to DNA in vitro mediated by rat hepatic postmitochondrial supernatant enriched with NADPH. The direct mutagenicity of benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide, the ultimate electrophilic and carcinogenic metabolite of benzo[a]pyrene, was also ameliorated by YH439 in a dose-dependent manner. The results of this study suggest that YH439 has a potential as a chemopreventive agent.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMedDate not supplied

Benzo[a]pyrene bay-region sulfonates, a novel class of reactive intermediates.

The mutagenicity of 7r,8t-dihydroxy-9t,10t-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE) toward Salmonella typhimurium strain TA98 is enhanced by over 1.5-fold by the addition of 1-10 mM sulfite to the incubations. Sulfite itself is neither mutagenic nor toxic to the bacteria under these conditions. Analysis of anti-BPDE-derived products from these bacterial incubations demonstrates that, in addition to the expected hydrolysis products of the epoxide, novel more polar metabolites are produced. These same more polar compounds are produced by the addition of anti-BPDE to buffered aqueous solutions of sulfite. The major product of this reaction has been characterized by UV/visible and fluorescence spectroscopy, NI-FAB mass spectrometry, and proton NMR spectroscopy and is identified as 7,8,9-trihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene-10-sulfonate (BPT-10-sulfonate). This derivative is formed by the nucleophilic addition of sulfite to the 9,10-oxirane ring of anti-BPDE. This product is easily differentiated both spectrally and chromatographically from the isomeric 7,8,10-trihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene-9-sulfonate reported from the attack of the sulfite anion radical on the activated aliphatic double bond of 7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (BP-7,8-diol) [Curtis et al. (1988) Carcinogenesis 9, 2015]. The nucleophilic trapping of diol epoxides by water or thiols is assumed to represent a detoxication of this class of mutagen. In contrast, the extensive conversion of anti-BPDE to BPT-10-sulfonate in the bacterial incubations correlates with a marked enhancement of resultant mutagenicity. Further support for a key role of BPT-10 sulfonate in the enhancement of anti-BPDE mutagenicity is provided by our findings on the reactivity of this compounds.(ABSTRACT TRUNCATED AT 250 WORDS)

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1994

Photoinduced toxicity of three polycyclic aromatic hydrocarbons (fluoranthene, pyrene, and naphthalene) to the duckweed Lemna gibba L. G-3.

The authors recently demonstrated that light dramatically enhances the hazards of three polycyclic aromatic hydrocarbons (PAHs), anthracene, phenanthrene, and benzo[a]pyrene, to the duckweed Lemna gibba L. G-3 (X.-D. Huang, D. G. Dixon, and B. M. Greenberg, 1993, Environ. Toxicol. Chem., 12, 1067-1077). To extend this research, growth and chlorosis were used as end points to assess the photoinduced toxicity of three additional PAHs, fluoranthene, pyrene, and naphthalene, to L. gibba in the presence of simulated solar radiation (a light source with a UV-B: UV-A:visible light ratio equivalent to that of sunlight). The phytotoxicity of these three PAHs was photoactivated, with ultraviolet radiation being the only spectral region that enhanced the harmful effects of the chemicals. Dose-response curves based on chemical concentration and light intensity revealed that the order of phytotoxic strength was fluoranthene > pyrene > naphthalene. To explore whether photomodification (in addition to photosensitization) of fluoranthene, pyrene, and naphthalene could contribute to photoinduced toxicity, the chemicals were irradiated prior to (as opposed to simultaneously with) application to the plans. The rates of photomodification of the three PAHs were rapid enough for the photooxidized compounds to contribute to toxicity, and the photomodified PAHs were more toxic than the parent compounds. As well, toxicity could be correlated to photomodification; impacts increased in parallel with the extent of photomodification.

Fluorenes↗
PubMed2002

Joint toxicity of linear alkylbenzene sulfonates and pyrene on Folsomia fimetaria.

Surfactants may enhance the biodegradation of hydrophobic substances in soils. This has partly been attributed to an increase in the bioavailability, brought about by the presence of surfactants. The aim of this study was to examine the ecotoxicological effects of the detergent linear alkylbenzene sulfonate (LAS) and the polycyclic aromatic hydrocarbon pyrene, alone and in combination, using the survival and reproduction of the collembolan Folsomia fimetaria as endpoints. The EC(50) and EC(10) were 803 and 161 mg kg(-1) for LAS, and 23 and 15 mg kg(-1) for pyrene. If LAS was able to increase the bioavailability of pyrene to springtails, it was expected that the combined effect of the two substances would exceed the effect found for each of the compounds tested separately. However, the results showed no effect of LAS on the toxicity of pyrene in the concentration range tested (1-750 mg LAS kg(-1) dry weight). Both the toxic unit concept and the isobologram method indicated that an additive approach would be the most useful when assessing the risk of these two compounds.

Alkanesulfonic Acids↗
PubMed2004

Influence of diet and ration level on benzo[a]pyrene metabolism and excretion in rainbow trout (Oncorhynchus mykiss).

Juvenile rainbow trout (Oncorhynchus mykiss) were fasted or fed one of three isoenergetic diets varying in protein and lipid content at full satiation levels or half rations for up to 9 weeks. At 3, 6, and 9 weeks, fish in each treatment group were dosed intraperitoneally with 10 mg tritiated benzo[a]pyrene [3H]-B[a]P/kg (B[a]P) to examine the effects of diet composition and energy intake on xenobiotic biotransformation and excretion. The percent dose eliminated during the experiment did not differ among fish receiving the different diet compositions or rations (range 73% to 84%). However, it was significantly decreased (to 53%) in the group that was fasted for 9 weeks. Examination of fish fasted for 6 and 9 weeks showed a significant increase in the proportion of phase I metabolites and a concomitant decrease in the proportion of phase II metabolites found in bile compared with all other groups. Also, fish that were fasted for 9 weeks produced proportionately less 9,10-dihydroxy-benzo[a]pyrene-trans-9,10-diol, more 3-hydroxybenzo[a]pyrene and 9-hydroxybenzo[a]pyrene, and more glucuronic acid conjugates compared with all other groups. Thus, dietary protein and lipid concentration did not appear to affect either the rate of B[a]P metabolism or its excretion; however, prolonged fasting resulted in a shift in metabolite profiles and decreased excretion.

Animal Feed↗
PubMed1992

The effect of benzo(a)pyrene on murine ovarian and corpora lutea volumes.

OBJECTIVE: Women who smoke have impaired fertility and experience menopause at an earlier age. This experiment determined the effect of benzo(a)pyrene, a polycyclic aromatic hydrocarbon contained in cigarette smoke, on murine ovarian volume, total corpora lutea volume, individual corpora lutea volumes, and corpora lutea numbers. STUDY DESIGN: C57BL/6N mice were treated with intraperitoneal injections of 0 to 500 mg/kg benzo(a)pyrene in corn oil. The 20 mice at each dose were divided into four groups of five each and were killed at 1, 2, 3, or 4 weeks after treatment. Ovaries were serially sectioned and analyzed morphometrically. RESULTS: Benzo(a)pyrene produced a dose- and time-dependent decrease in ovarian volume, total corpora lutea volume, and number of corpora lutea per ovary. This effect was transitory at low doses with complete recovery of corpora lutea by 4 weeks. Compensatory hypertrophy of the individual corpora lutea occurred during the recovery phase. Ovarian function did not return in animals treated with the two highest doses. CONCLUSION: Benzo(a)pyrene is a murine ovarian toxicant that inhibits corpus luteum formation in a dose- and time-dependent fashion.

Animals↗
PubMed1988

Temperature, pressure and cholesterol effects on bilayer fluidity; a comparison of pyrene excimer/monomer ratios with the steady-state fluorescence polarization of diphenylhexatriene in liposomes and microsomes.

Pyrene excimer/monomer (E/M) ratios have been compared with the steady-state fluorescence polarization (P) of diphenylhexatriene (DPH) in multilamellar liposomes of dilaurylphosphatidylcholine and rat liver microsomes. The purpose was to use the well-understood properties of DPH to reveal the nature of bilayer fluidity which pyrene manifests as an E/M ratio. Reducing the temperature (from 37 degrees C to 8 degrees C), increasing the hydrostatic pressure (from 0.1 to 70 MPa), and, in liposomes, cholesterol enrichment (up to 0.30 mole fraction) separately decreased the E/M ratios and increased P. The pyrene membrane/buffer partition coefficient was affected by temperature but not by pressure, and in the case of cholesterol enrichment, it was assumed to be unaffected. Plots of P as a function of the E/M ratio showed the two to be closely correlated (r = 0.99 in liposomes and 0.96 in microsomes), independent of the treatment used to reduce fluidity. The apparent activation volume and enthalpy for excimer formation was calculated and compared with published data. Pyrene E/M ratios probably reflect the intermolecular volume (fluidity) of the outer region of the bilayer, which is reduced by a decrease in temperature and an increase in pressure and cholesterol. DPH reports the bilayer interior, which is similarly ordered by the experimental treatments. The regional distinction between the two probes, however, accounts for the divergence of E/M ratios and P, which has been reported in membranes enriched with fluidizing fatty acids.

Animals↗
PubMed1992

Transbilayer asymmetry of pyrene mobility in human spherocytic red cell membranes.

The diffusion-dependent formation of pyrene excimers (excited dimers) was studied in normal and spherocytic red cell membranes. Pyrene emission was alternatively quenched in either bilayer half by non radiative energy transfer to haemoglobin. Pyrene excimer to monomer fluorescence intensity ratio, I'/I, was 0.35 +/- 0.03 (S.E.) in washed red blood cells obtained from normal donors (n = 8) and 0.45 + 0.03 (n = 13) in the corresponding isolated, haemoglobin-free resealed membranes (P less than 0.02). In the spherocytic condition the respective values were 0.28 +/- 0.01 (n = 9) and 0.53 +/- 0.03 (n = 9), P less than 0.001. In contrast to the decrease of I'/I in red cells as compared to isolated membranes, being 22% in normal cells and 47% in spherocytic ones, haemoglobin added to the exofacial side of isolated membranes, respectively, reduced I'/I by 18% and 5%. In normal red cell membranes, pyrene mobility appears to be higher in the inner monolayer than in the outer one. In spherocytic membranes our results indicate an enhanced transmembrane asymmetry in lipid monolayer fluidity, probably due to a defect of the membrane protein skeleton organization.

Cholesterol↗
PubMed1983

Covalent binding of benzo[a]pyrene to rat liver cytosolic proteins and its effect on the binding to microsomal proteins.

Benzo[a]pyrene will bind covalently to rat liver cytosolic proteins when incubated with microsomes and NADPH. The binding is most extensive when microsomes from 3-methylcholanthrene-treated rather than phenobarbital-treated or control rats are used. The binding to cytosolic proteins increases when incubations are performed with increasing concentrations of cytosol. At the same time the covalent binding of benzo[a]pyrene to microsomal proteins decreases. Two cytosolic polypeptides are the main targets for benzo[a]pyrene. These have the same mobility in polyacrylamide gels as the subunits of purified glutathione S-transferase B. These subunits also react covalently with benzo[a]pyrene when the transferase is incubated with microsomes and NADPH.

Animals↗
PubMed1987

Evidence for distinct binding sites in the cumene hydroperoxide-dependent metabolism of benzo[a]pyrene catalyzed by cytochrome P-450.

A few constitutive cytochrome P-450 isozymes in male rat liver microsomes catalyzed the metabolism of benzo[a]pyrene (BP) in cumene hydroperoxide (CHP)-dependent reactions, which produced predominantly 3-hydroxyBP and BP quinones. This process varied with the concentration of CHP. At 0.05 mM CHP, 3-hydroxyBP was the major metabolite. An increase in CHP concentration reduced 3-hydroxyBP formation but increased the level of BP quinones. This change in metabolic profile was reversed by preincubation with pyrene. Pyrene selectively inhibited quinone formation and enhanced 3-hydroxyBP formation. Naphthalene, phenanthrene and benz[a]anthracene nonspecifically inhibited total metabolism. BP binding to microsomal protein correlated with quinone formation, suggesting a common precursor reactive intermediate. BP metabolism by female rat liver microsomes also depended on CHP concentration but was much less effective than that in the male. With females, quinones were the major metabolites at all CHP concentrations, and their formation was again modulated by pyrene. These data indicate that two distinct binding sites are responsible for the formation of 3-hydroxyBP and BP quinones.

Animals↗
PubMed1985

The homogeneity of rat liver microsomal cytochrome P-448 activity and its role in the activation of benzo[a]pyrene to mutagens.

The O-deethylation of ethoxyresorufin and the metabolic activation of benzo[a]pyrene to mutagens were determined in hepatic microsomal preparations from control and induced animals. An excellent direct correlation (r = 0.95) has been observed between ethoxyresorufin O-deethylase and the metabolic activation of benzo[a]pyrene to mutagens when the fraction of cytochromes P-450 present as cytochrome P-448 was altered by the administration of phenobarbitone and 3-methylcholanthrene alone or in combination with 9-hydroxyellipticine. The correlation between these activities was maintained following treatment of animals with Arochlor 1254, benzo[a]pyrene, benzo[e]pyrene, 7,12-dimethylbenzo[a]anthracene,2-anthramine and 2-naphthylamine.

Animals↗
PubMed1989

Effects of inhibition of NADPH: cytochrome P-450 reductase on benzo(a)pyrene metabolism in mouse liver microsomes.

1. Effects of antioxidants (butylated hydroxytoluene and nor-dihydroguaiaretic acid), vitamin K-related quinones (vitamin K1 and coenzyme Q10) and inorganic copper (CuSO4), in concentrations inhibiting NADPH: cytochrome P-450 reductase, were re-examined on benzo(a)pyrene metabolism in mouse liver uninduced microsomes. 2. It was found that all these compounds decrease production of the two-electron oxygenation products of benzo(a)pyrene (monophenoles, diols) and the amounts of glucuronides in a manner parallel to their inhibitory potency against NADPH: cytochrome P-450 reductase. 3. No correlation was found between amounts of one-electron oxidation products of benzo(a)pyrene and inhibition of NADPH: cytochrome P-450 reductase. 4. Without added UDPGA the compounds studied decreased protein associated benzo(a)pyrene metabolites in parallel to the decreased overall metabolism of this polyaromatic hydrocarbon. 5. The mode of action of the studied compounds is discussed.

Animals↗
PubMed1981

Use of nitrous acid-dependent decrease in mutagenicity as an indication of the presence of mutagenic primary aromatic amines. Non-specific reactions with phenols and benzo[alpha]pyrene.

Treatment of mutagenic primary aromatic amines with nitrous acid is known to decrease their mutagenicity. We examined some factors concerning the validity of using decreases in mutagenicity due to nitrous acid treatment as an indication of the presence of mutagenic primary aromatic amines in complex mixtures. We found that treatment of benzo[alpha]pyrene with nitrous acid for the extended periods of time previously employed leads to formation of three nitrobenzo[alpha]pyrene isomers. Some of the isomers are direct-acting mutagens for S. typhimurium with considerably greater mutagenicity than benzo[alpha]pyrene isomers. In attempts to minimize reaction of chemicals other than aromatic amines, we found that only very brief reaction periods are required for complete reaction of nitrous acid with representative aromatic amines, essentially eliminating their mutagenicity. During such brief reaction periods modification of benzo[alpha]pyrene is negligible, but phenols react readily. Chromatographic analysis indicated that reaction of nitrous acid with aromatic amines leads to the formation of families of products, thereby increasing the complexity of the mixtures in which the amines may occur. Thus, experiments examining the effects of nitrous acid on the mutagenic activity of complex mixtures must be carefully designed, and the results must be interpreted cautiously.

Amines↗
PubMed1983

Studies on oxidation of benzo [a] pyrene by sunlight and ozone.

The destruction of the carcinogen benzo[alpha]pyrene (BaP) by light is well known; laboratory workers are routinely advised to cover fluorescent lamps with yellow filters while treating samples containing BaP. However until recently the mechanism of oxidation by sunlight and ozone had not been studied in detail. Concentrations of benzo[a]pyrene in urban air are in the range of 5-10 micrograms/1000 m3. Oxidant concentrations (predominantly in the form of ozone) are reported to be in the range of 0.01 ppm (22 micrograms per m3). Thus a sampling system with a filter paper would filter about 22,000 micrograms of ozone passing through and collect about 5 micrograms of BaP for analysis. The effect of interactions of such large ozone concentrations with BaP deposited on the filter paper is reported; data for the oxidation rates for benzo[a]pyrene coated on quartz surface and exposed to ozone or sunlight are presented. The oxidation products were analysed by thin-layer chromatography and high-pressure liquid chromatography. From about eight products detected in these experiments, three have been identified as quinones based on UV-absorption spectrometry and mass spectrometry. Oxidation rates as high as 100% per hour of exposure are observed when less than 0.1 micrograms of BaP is coated inside the quartz tubes and exposed to ozone or sunlight. Oxidation rates for benzo[a]pyrene (using tritiated BaP) were determined for two types of experimental conditions. In the first set, tritiated BaP was spotted onto a glass fibre paper and sampling continued for 24 h; the loss of BaP was found to be 88%. In the second set tritiated BaP was spotted at intervals of one hour, for eight hours, while sampling is being carried out and the loss of BaP during the period was estimated to be 50%.

Benzo(a)pyrene↗
PubMed1995

Urinary excretion kinetics of 1-hydroxypyrene in volunteers exposed to pyrene by the oral and dermal route.

Two well-informed human volunteers were exposed to 500 micrograms pyrene by ingestion and by dermal application, in two separate experiments. Urinary measurements of 1-hydroxypyrene (1-OHP) were performed on all micturitions taken at intervals of 0.5-4 h for a total period of 48 h after dosing. Following the absorption phase, 1-OHP is excreted with a first order apparent half-life of approximately 12 h for both volunteers and both exposure routes. These results compare well with other previously published studies. A more refined analysis of the data was performed using a two-compartment toxicokinetic model for 'pyrene' (its fraction eventually excreted as 1-OHP). As it was found that a classical first-order system did not adequately fit the data, a non-linear term was introduced in the model for the elimination of urinary 1-OHP. Computer iteration performed on the oral absorption data allowed an estimation of various toxicokinetic parameter values. The mean intercompartmental exchange (k12 and k21) and elimination coefficients were 0.010, 0.006 and 0.012 min-1, respectively. The first two values compare well with those previously published for the rat, whereas the latter is smaller in humans. These values were used to satisfactorily simulate the experimental data for both routes of exposure, adjusting only for kabs which was estimated at 0.014 and 0.0029 min-1 for the oral and dermal exposure, respectively. The proposed model generates new hypotheses on the metabolism of pyrene. The information collected will contribute to the validation of the utilisation of 1-OHP as a biological indicator of exposure to pyrene.

Administration, Cutaneous↗
PubMed1995

Patterns of 1-hydroxypyrene excretion in volunteers exposed to pyrene by the dermal route.

The urinary excretion profiles following exposure to pyrene were established in one psoriasic patient under treatment with a coal tar-based shampoo and in two other volunteers exposed to a single dose of 100 microliters creosote and, in a separate experiment, to five consecutive daily dermal applications of 500 micrograms pyrene on 200 cm2 of the inner face of the forearms. Timed micturitions were collected for up to 48 h following exposure. Both in the psoriasic patient and in the volunteers exposed to creosote, the excretion peaks between 10 and 15 h after application and first-order apparent half lives of 11.5-15 h can be calculated for the elimination phase. Compatible with these observations, repeated exposure to pyrene in the volunteers causes an increase in peak and trough urinary 1-hydroxypyrene (1-OHP) values for the first few days following the first exposure. These results suggest that the difference between beginning-of-shift/beginning of work week and beginning-of-shift/end of work week 1-OHP excretions should reflect the average exposure of the week in workers having a constant exposure to pyrene. The difference between the beginning- and end-of-shift excretion values of a given day should reflect the exposure of that day but the maximum excretion would be attained a few hours after termination of exposure.

Administration, Cutaneous↗