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PubMedDate not supplied

Characterization of (+/-)-7,8,10-trihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene-9-sulfonate.

The genotoxicity of certain benzo[a]pyrene (BP) derivatives is significantly enhanced in strains of Salmonella typhimurium following addition of sulfite to the incubations. The interaction between sulfite and those BP derivatives also results in the formation of isomeric BP sulfonates. As these trihydroxy sulfonates are formed in incubations of BP derivatives and sulfite in which a marked potentiation of bacterial mutagenicity occurs, we have investigated the properties of these novel intermediates. The compound (+/-)-7,8,10-trihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene-9-sulfonate (BPT-9-sulfonate) was isolated and characterized in terms of its chemical and biological activity. This BPT sulfonate isomer is formed by the addition of the sulfite anion radical to the 9,10-double bond of the known promutagen, (+/-)-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (BP-7,8-diol). Evidence for the free radical character of this addition includes the initiation of the reaction by either peroxidase-catalyzed or chemical one-electron oxidation of sulfite, the inhibition of the reaction by phenolic antioxidants, and the isolation and characterization of the chain termination product, 7,8-dihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene-9,10-disulfonate (BPD-disulfonate). Analysis of incubations of S. typhimurium strain TA98 with BP-7,8-diol and sulfite, which resulted in a 10-fold increase in revertant bacterial colonies above control levels, showed that BPT-9-sulfonate and BPD-disulfonate were the only isolable products derived from BP-7,8-diol. This prompted a further investigation of the chemistry of these products. BPT-9-sulfonate was found to be quite stable in aqueous media, being refractory to acid- or base-catalyzed hydrolysis over a pH range of 3-11.(ABSTRACT TRUNCATED AT 250 WORDS)

DNA↗
PubMedDate not supplied

Sulfotransferase-mediated activation of 7,8,9,10-tetrahydro-7-ol, 7,8-dihydrodiol, and 7,8,9,10-tetraol derivatives of benzo[a]pyrene.

Some hydroxymethyl-substituted polycyclic aromatic hydrocarbons have been shown to be converted to electrophilic, mutagenic, or tumorigenic sulfuric acid ester metabolites by cytosolic sulfotransferase activity in rodent liver. Likewise, certain types of aromatic compounds with a secondary alcoholic functional group at the benzylic position undergo metabolic activation through sulfonation. Enzymatic oxidation of benzo[a]pyrene produces such secondary alcohols as dihydrodiol and tetraol derivatives as primary metabolites. Sulfo conjugation of the benzylic hydroxy group of each of these metabolites is expected to generate an electrophilic sulfuric acid ester capable of covalently binding to DNA, which may contribute to mutagenesis and carcinogenesis by benzo[a]pyrene. Although the model benzo-ring secondary benzyl alcohol, 7-hydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene, covalently bound to DNA and also exerted mutagenicity in the presence of rodent hepatic cytosols and 3'-phosphoadenosine 5'-phosphosulfate, no such sulfotransferase-dependent activation was observed with dihydrodiol or tetraol derivatives of benzo[a]pyrene. Thus, it seems likely that appearance of the adjacent non-benzylic hydroxy functional group(s) in latter metabolites hinders the benzylic sulfonation in these molecules.

Animals↗
PubMed2002

Synthesis and characterization of site-specific and stereoisomeric fjord dibenzo[a,l]pyrene diol epoxide-N(6)-adenine adducts: unusual thermal stabilization of modified DNA duplexes.

The fjord polycyclic aromatic hydrocarbon compound dibenzo[a,l]pyrene (DB[a,l]P) is significantly more tumorigenic than the bay region benzo[a]pyrene in animal model systems. The molecular origins of the unusually strong genotoxic properties of DB[a,l]P and its fjord region diol epoxide metabolites are of great interest and are believed to be related to the structural characteristics of the DNA adducts formed. Site-specifically modified oligonucleotides were prepared by reacting the single adenine residue in 5'-d(CTCTCACTTCC) (I) with the racemic fjord diol epoxide r11,t12-dihydrodiol-t13,14-epoxide-11,12,13,14-tetrahydrodibenzo[a,l]pyrene (anti-DB[a,l]PDE) in aqueous solutions. Four different oligonucleotides I with the single adenosine residues involving a covalent bond between the C14 position of DB[a,l]PDE and N(6)-dA are identified and purified. The CD spectra of the mononucleotide adducts are similar to those of Li et al. [Li et al. (1999) Chem. Res. Toxicol. 12, 758] who characterized DB[a,l]PDE-N(6)-dA adducts by a combination of CD and NMR methods. The stereochemical properties of each of the four DB[a,l]PDE-modified oligonucleotides were assigned on the basis of a combination of empirical CD rules and other approaches and differ from those of Li et al. The thermal melting points, T(m), of the unmodified duplex of I with its complementary strand (IC), T(m) = 43.8 +/- 0.5 degrees C, were compared with the same duplexes containing stereoisomeric anti-DB[a,l]PDE-N(6)-dA lesions. The T(m) of duplexes I.IC containing lesions with R absolute configurations at C14 of the DB[a,l]PDE residues are greater by 6-8 degrees C, while those with S configuration are lower by 6-10 degrees C. Similar effects are observed with adducts in the same sequence context derived from the fjord PAH anti-diol epoxides of benzo[g]chrysene, while duplexes containing lesions derived from benzo[c]phenanthrene diol epoxides with 1R and 1S configurations exhibit unchanged T(m) values. In contrast, the T(m) values of duplexes with lesions derived from the bay region benzo[a]pyrene diol epoxides (B[a]PDE) in the same sequence are lower by 12 degrees (10R adducts) and by 19 degrees (10S adducts). The greater thermal stabilities of duplexes with fjord PAH-N(6)-dA lesions relative to those with bay region B[a]PDE-N(6)-dA adducts, are correlated with lower susceptibilities of excision by human nucleotide excision repair enzymes [Buterin et al. (2000) Cancer Res. 60, 1849]. The implications of these relationships are discussed in terms of present knowledge of the conformations of fjord and bay region PAH diol epoxide-N(6)-dA lesions in double stranded DNA.

Adenine↗
PubMed2003

Extraction and purification of depurinated benzo[a]pyrene-adducted DNA bases from human urine by immunoaffinity chromatography coupled with HPLC and analysis by LC/quadrupole ion-trap MS.

In this paper, we describe implementation and testing of an immunoaffinity (IA) column for rapid and selective extraction of 7-(benzo[a]pyren-6-yl)adenine (BP-6-N7Ade) and 7-(benzo[a]pyren-6-yl)guanine (BP-6-N7Gua) from urine, where BP is benzo[a]pyrene. The BP radical cation is a carcinogenic metabolite that reacts with double-stranded DNA, producing depurinated BP-adducted DNA bases excreted in urine. The expected modified nucleobases are BP-6-N7Gua, BP-6-N7Ade, and 8-(benzo[a]pyren-6-yl)guanine (BP-6-C8Gua), and they may serve as important biomarkers for DNA damage by PAHs. IA extracts of urine from a cigarette smoker and a nonsmoker contained less than 5% of contaminants present in Sep-Pak extracts and, unlike the latter, were suitable for analytical HPLC. IA extraction achieved 75-95% recovery of BP-6-N7Gua (10 fmol/mL) and BP-6-N7Ade (1 fmol/mL) added to urine samples. Tandem mass spectrometry of IA/HPLC fractions of urine from two coal smoke-exposed women at high risk for lung cancer demonstrated the presence of 20 and 50 fmol BP-6-N7Gua per mL of urine. Unexposed controls were negative. With proposed modifications, the IA-based protocol can achieve a detection limit of 0.1 fmol/mL urine, which is sufficient for routine quantification of BP-adducted bases in urine of cigarette smokers. This procedure may allow screening of persons at risk for lung cancer associated with exposure to PAH in cigarette and other forms of smoke.

Adenine↗
PubMed2006

Photophysical behaviour of 1-(4-N,N-dimethylaminophenylethynyl)pyrene (DMAPEPy) in homogeneous media.

The photophysical behaviour of a new pyrene derivative, 1-(4-N,N-dimethylaminophenylethynyl)pyrene (DMAPEPy), in various solvents has been studied. Due to the presence of an ethynyl link with a cylindrical pi cloud between the donor (N,N-dimethyl group) and the acceptor (pyrene), the molecule shows efficient intramolecular charge transfer, with a high extinction coefficient in all the solvents. There is significant solvatochromism in the fluorescence with a large increase in the Stokes' shift of around 125 nm between n-hexane and acetonitrile. The solvent-dependent spectral data show a good correlation with the Kamlet-Taft solvent polarity parameter (pi*). The plots of Stokes' shifts with E(T)(30) are linear for non-protic solvents and for protic solvents but with different slopes. The fluorescence quantum yields are high for non-polar solvents and decrease as the solvent polarity increases. Unlike the parent molecule pyrene, DMAPEPy shows a short lifetime, which is fairly insensitive to oxygen-induced quenching and is dependent on solvent polarity. The molecule shows high steady-state fluorescence anisotropy, which is very sensitive to the viscosity change of the medium.

Journal Article↗
PubMed2004

Electric field effects on photoinduced electron transfer processes of methylene-linked compounds of pyrene and N,N-dimethylaniline in a polymer film.

Time-resolved measurements of the electric-field-induced change in fluorescence intensity have been made for methylene-linked compounds of pyrene and N,N-dimethylaniline (DMA) doped in a polymer film. The lifetime of the fluorescence emitted from the locally excited state of pyrene chromophore becomes shorter in the presence of electric field (F), when the dopant concentration is high. The lifetime of the excipelx fluorescence resulting from the photoinduced electron transfer (PIET) from DMA to the excited state of pyrene chromophore between different molecules also becomes shorter in the presence of F. Based on the simulation of the electric field effect on fluorescence decay, the mechanism of intermolecular PIET between DMA and pyrene chromophore in a polymer film is discussed.

Journal Article↗
PubMed1979

Photoelectric properties and detection of the aromatic carcinogens benza[a]pyrene and dimethylbenzanthracene.

The absolute photoelectron quantum yield spectra for benzo[a]pyrene and dimethylbenzanthracene are presented in the wavelength range 180--230 nm. These polycyclic aromatic carcinogens have photoelectron quantum yields of approximately 2 x 10(-3) electrons per incident photon at 180 nm. The quantum yields fall off quickly and monotonically at wavelengths longer than 210 nm (5.9 eV). Threshold values for benzo[a]pyrene and dimethylbenzanthracene are 5.25 +/- 0.06 cV and 5.27 +/- 0.04 eV, respectively. The photoelectron quantum yields of benzo[a]pyrene and dimethylbenzanthracene are several orders of magnitude greater than typical components of biological membranes (amino acids, phospholipids, and polysaccharides). Preliminary micrographs of benzo[a]pyrene and dimethylbenzanthracene sublimed onto poly(L-lysine) and onto dimyristoyl phosphatidylcholine demonstrate the high contrast of small crystallites of carcinogens against a background of membrane components. These results and calculations involving relative contrast factors suggest that the distribution of these carcinogens in biological membranes can be determined by using photoelectron microscopy.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Reactive intermediates from 3-hydroxybenzo[a]pyrene and its glucuronide.

3-Hydroxybenzo[a]pyrene (3-OH-BaP) is oxidized by the horseradish peroxidase/H2O2 system to benzo[a]pyrene-3,6-quinone. In the presence of N-acetylcysteine one other product is also formed. This was identified by its chemical, and u.v., mass and n.m.r. spectral properties as 6-(H-acetyl-cystein-S-yl)-3-hydroxybenzo[a]pyrene (6-NAc-cys-3-OH-BaP). Replacement of the N-acetylcysteine by glutathione leads to the formation of a 3-OH-BaP-glutathione adduct. Enzymic hydrolysis of benzo[a]pyrene-3-glucuronide in the presence of N-acetylcysteine yields, in addition to 3-OH-BaP, a product which co-chromatographs with 6-NAc-cys-3-OH-BaP and has identical chemical and spectral characteristics.

Acetylcysteine↗
PubMed2000

Oral bioavailability and pharmacokinetics of elimination of 9-hydroxybenzo[a]pyrene and its glucoside and sulfate conjugates after administration to male and female American lobsters, Homarus americanus.

The pharmacokinetics of [(3)H]-9-hydroxybenzo[a]pyrene (9-OH-BaP), a highly lipophilic primary metabolite of benzo(a)pyrene, were examined after intrapericardial (iv) or oral doses of 50 or 200 microg/kg to intermolt American lobsters, Homarus americanus. Combining data for all lobsters, the average terminal elimination half-life of parent 9-OH-BaP was 97.3 h after iv and 56.5 h after oral administration, considerably less than found previously for benzo(a)pyrene (720 h). The oral bioavailability of parent 9-OH-BaP, calculated from the area under the hemolymph concentration curve, was 15.9%. The low bioavailability and variable elimination rates were attributed to extensive first-pass conjugation and sequestration in the hepatopancreas. BaP-9-sulfate was the major metabolite. Hemolymph concentrations of BaP-9-sulfate increased up to one day after the dose, and then decreased, with a terminal elimination half-life of 45 h. BaP 9-beta-D-glucoside was a minor metabolite in most hemolymph and tissue samples; an exception was hemolymph from the iv high-dose group. Concentrations of 9-OH-BaP and metabolites in the edible muscle tissue were similar to those in hemolymph, and 9-OH-BaP residues at 10 to 16 days after the dose were 3 to 12 ng/g muscle. Sulfotransferase and UDP-glucosyltransferase (UGT) activities with 9-OH-BaP were found in the antennal gland, intestinal mucosa, and hepatopancreas (UGT only). Sulfatase activity with BaP-9-sulfate, found in both the hepatopancreas and the antennal gland, was thought to contribute to metabolite cycling. These studies showed that 9-OH-BaP was readily conjugated to sulfate and glucose in the lobster, and that despite their high lipophilicity, 9-OH-BaP and conjugates were excreted from the lobster hemolymph and tissues much more rapidly than benzo[a]pyrene.

Administration, Oral↗
PubMed1994

Bovine inositol monophosphatase. Ligand binding to pyrene-maleimide-labelled enzyme.

Inositol monophosphatase can be modified at two sites by pyrene maleimide. These sites have been identified as Cys141 and Cys218. Stoichiometric addition of pyrene maleimide allows the sole modification of Cys218. The fluorescence of the pyrene moiety on the modified protein can be excited directly or by resonance energy transfer. The fluorescence properties of the pyrene group on Cys218 allows the interaction of ligands with the enzyme to be monitored. This feature has allowed dissociation constants for various metal ions to be determined and allowed the formation of various enzyme/ligand complexes to be observed. These studies have demonstrated that Mg2+ is required to support Pi binding and that Li+ interacts with a post-catalytic complex which is only formed in the forward reaction.

Amino Acid Sequence↗
PubMed1987

Phenobarbital depression of hepatic microsomal benzo[a]pyrene hydroxylation in rats starved and refed a diet containing menhaden fish oil: substrate and fat level dependency.

The influence of phenobarbital on the activity of hepatic mixed function oxidases responsible for benzo[a]pyrene hydroxylation was studied in rats fed diets containing menhaden fish oil (rich in n-3 fatty acids). Male rats were starved for 2 days and refed diet devoid of fat or containing 0.5, 10, or 20% menhaden oil for 4 days. Phenobarbital increased the apparent Km value as well as Vmax for benzo[a]pyrene hydroxylase in microsomes from rats fed the 20% menhaden oil diet. The increased Km was due to a progressive decrease in benzo[a]pyrene metabolism at the lower substrate concentrations, even in the presence of increased cytochrome P-450 content. The phenobarbital-induced increase in Km and the decreases in benzo[a]pyrene hydroxylation were not observed in rats fed 0.5% menhaden oil or a diet devoid of fat.

Animals↗
PubMed1988

Cell-catalyzed binding of 3H-(-)-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene to cellular and exogenous DNA and the role of purified human liver epoxide hydrolase.

Cultured human monocytes, lymphocytes, Fischer rat liver (TRL-2) cells, and Buffalo rat liver (BRL) cells catalyzed the conversion of 3H(-)-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene [3H(-)t-7,8-dihydrodiol BP] to r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (diol epoxide I) and r-7,t-7-8-dihydroxy-c-9,10-oxy-7,8,9,10- tetrahydrobenzo[a]pyrene (diol epoxide II; r-7 indicates that the substituent at the 7-position is the reference, and t and c indicate that the substituents trans and cis, respectively, to the reference substituent). These appear to be the most reactive metabolites of benzo[a]pyrene (BP) and were covalently bound to both exogenous and intact cellular DNA in tissue culture media. The cells induced by benzanthracene (BA) exhibited greater levels of DNA binding than the controls and this binding was linear with increasing cell content in human monocytes, in TRL-2 cells and in Buffalo rat liver cells. The binding to DNA was greater than controls in BA-preinduced lymphocytes, but was not linear. The DNA binding in control cells showed a nonlinear increase with increasing cell concentration in all experiments. The addition of human liver epoxide hydrolase (EC 3.3.2.3) to the incubation medium reduced the amount of reactive metabolites binding to DNA by 12-15% in control and by 23-41% in BA-induced monocytes. Thus, with whole cell systems of either human monocytes or lymphocytes, the addition of purified human liver epoxide hydrolase reduced the binding of 3H(-)t-7,8-dihydrodiol BP metabolites to DNA. Human monocytes and lymphocytes also catalyzed the covalent binding of 3H(-)t-7,8-dihydrodiol BP to intact cellular DNA. The addition of 3H(-)t-7,8-dihydrodiol BA to tissue culture media caused the inhibition of covalent DNA binding in BA-preinduced monocyte by 58% and lymphocytes by 25%. Previous work has shown that BA is metabolized and converted to BA-diol epoxides by microsomes. These results indicate that BA-diol epoxides and BP diol epoxides are competing for the same binding sites on DNA. On the other hand, the addition of 10 nmol of 3H(-)t-7,8-dihydrodiol BP to the incubation of control and BA-preinduced cell homogenate and further incubation at 37 degrees C for 25 min showed that the DNA binding in BA-preinduced cell homogenates was much greater than controls. Homogenates of cells induced by BA exhibited a greater level of DNA binding than controls.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Comparison of oxidant activities and the activation of benzo(a)pyrene-7,8-dihydrodiol by polymorphonuclear leucocytes from human, rat and mouse.

1. Polymorphonuclear leucocytes (PMNs) from human, mouse and rat were compared for their ability to activate benzo(a)pyrene-7,8-diol to a DNA-binding intermediate and a chemiluminescent dioxetane derivative. 2. Human PMNs activated benzo(a)pyrene-7,8-diol to the greatest extent, which correlated with their rate of superoxide anion generation and myeloperoxidase activity relative to these activities by PMNs from mice and rats. 3. Benzo(a)pyrene-7,8-diol chemiluminescence elicited by PMNs from all three species was significantly inhibited by azide, a myeloperoxidase inhibitor. On the other hand, superoxide dismutase (SOD) was very effective in inhibiting benzo(a)pyrene-7,8-diol chemiluminescence with mouse PMNs but not human or rat PMNs. Mouse PMNs exhibited a high rate of superoxide generation but low myeloperoxidase activity, whereas rat PMNs exhibited a low rate of superoxide generation but high myeloperoxidase activity.

Animals↗
PubMed1992

Inhibition of rat hepatic aryl sulphotransferase IV by dihydrodiol derivatives of benzo[a]pyrene and naphthalene.

1. Although neither the (+)- nor (-)-enantiomer of trans-benzo[a]pyrene-7,8-dihydrodiol was a substrate for aryl sulphotransferase IV from rat liver, both enantiomers inhibited the enzyme-catalysed sulphation of 1-naphthalene-methanol with Ki values of 3.7 +/- 0.4 microM for the (+)-enantiomer, and 4.4 +/- 0.3 microM for the (-)-enantiomer. 2. Based on the magnitude of the Ki values, the binding affinity of these dihydrodiols for the aryl sulphotransferase was significantly greater than that for the corresponding phenolic derivatives of benzo[a]pyrene. That is 7-hydroxybenzo[a]pyrene and 8-hydroxybenzo[a]pyrene were both substrates for aryl sulphotransferase IV, with apparent Km values of 280 +/- 41 microM and 370 +/- 72 microM, respectively. 3. Both (+)- and (-)-trans-naphthalene-1,2-dihydrodiols were also inhibitors of aryl sulphotransferase IV, but with higher Ki values than would be expected from previously determined apparent Km and Ki values for (R)-(-)- and (S)-(+)-1,2,3,4-tetrahydro-1-naphthols, respectively.

Animals↗
PubMed1976

Differences in benzo(a)pyrene metabolism between rodent liver microsomes and embryonic cells.

Differences in benzo(a)pyrene metabolite pattern have been shown by rodent liver microsomes (Sprague-Dawley) and rodent embryo cells from Syrian hamsters and NIH Swiss mice. Rodent liver induced by methylcholanthrene shows marked quantitative variation between species. Additional pattern changes were found in mouse and hamster embryo secondary cultures with a reduction of the K-region metabolites and a marked increase in 9-hydroxybenzo(a)-pyrene. These results are indicative of a region-specific attack on the carcinogen by the cell monooxygenases which is distinct from the liver attack of microsomal enzymes on benzo(a)pyrene. These results suggest that activation and detoxification of benzo(a)pyrene may be species and tissue variable, and susceptibility and resistence to malignant transformation may be predicted on induction of a fortuitous combination of intermediate metabolic steps.

Animals↗
PubMed1975

Production of respiratory tract tumors in hamsters by benzo(a)pyrene.

Respiratory tumor induction was tested for the tumorigenic activity of benzo[a]pyrene alone. A group of 32 male and 28 female Syrian golden hamsters were given weekly intratracheal instillation of 1 mg of benzo[a]pyrene suspended in isotonic saline, for 30 weeks. Squamous cell carcinoma, adenocarcinoma, anaplastic carcinoma, adenoma, papilloma, and polyps were induced in the respiratory tract of hamsters. Tumor incidences were 42.3% in males and 57.7% in females. Respiratory carcinomas were inducible in hamsters by simple instillation of a low dose of benzo[a]pyrene without using a surface-active agent or carrier-dust. These findings may be useful as a standard data for cocarcinogenesis studies when using other modality combined with benzo[a]pyrene in experimental studies.

Adenocarcinoma↗
PubMed1975

Conditions modifying development of tumors in mice at various sites by benzo(a)pyrene.

The modifying roles of age, sex, and strain of mice on the incidence, multiplicity, and spectrum of tumors induced by benzo(a)pyrene have been investigated. The first-generation (F1) hybrids of C57BL/6J X C3HeB/FeJ and C3HEB/Fej X A/J mice of both sexes were given single i.p. injections (75 or 150 mug/g) of benzo(a)pyrene at 1, 15, or 42 days of age. Experimental animals were allowed to live their life-spans, while animals in control groups were killed at 52, 90, 142, or 170 weeks of age. Animals treated with benzo(a)pyrene died, in general, by the 100th week of age due to development of liver, lung, stomach and lymphoreticular tumors. Few of the control animals died during that same observational period. The age of mice at the time of exposure to the carcinogen modified development of tumors at all the sites. The sex of animals influenced the development of liver and lymphoreticular tumors. The C3HeB/FeJ X A/J F1 hybrids developed lung tumors more readily than did the C57BL/6J X C3HeB/FeJ F1 mice, which had significantly more liver tumors and neoplasms of the lymphoreticular system than the former strain. No strain difference was observed in regard to tumors at other sites. Higher doses of benzo(a)pyrene were more effective in inducing lung, liver, and stomach tumors. In addition, 5 cases of pancreatic ductal adenoma and adenocarcinoma were observed in carcinogen-treated mice.

Age Factors↗
PubMed1976

High-pressure liquid chromatographic separation of 10 benzo(a)pyrene phenols and the identification of 1-phenol and 7-phenol as new metabolites.

The separation of ten isomeric benzo(a)pyrene phenols has been accomplished by the use of high-pressure liquid chromatography utilizing a newly developed recycling technique and new column and solvent systems. Using this new system and comparing the metabolites obtained with authentic standards, we have isolated 1-hydroxybenzo(a)pyrene and 7-hydroxybenzo(a)pyrene and identified them as metabolites formed by rat liver microsomes. In previously reported chromatography systems, the new metabolites migrated with another metabolite, 3-hydroxybenzo(a)pyrene.

Animals↗