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PubMed1985

Beta-carotene as an inhibitor of benzo(a)pyrene and mitomycin C induced chromosomal breaks in the bone marrow of mice.

Female mice of hybrid strain B6C3F1, 8-10 weeks old, were fed on powdered food with or without beta-carotene (100 mg/kg food). After 1 week of these diets, some of each group of mice were injected i.p. with either benzo(a)pyrene (150 mg/kg) in dimethyl sulfoxide, or mitomycin C (1 mg/kg) in distilled water. In the course of separate experiments, bone marrow samples were collected at various intervals after injection for analysis in the in vivo bone marrow micronucleus assay. At the time at which the maximum induction was observed, which coincided between experiments, the frequency of micronuclei induced by benzo(a)pyrene was reduced by 41-61% and that induced by mitomycin C was reduced by 44-71% in the presence of beta-carotene. Beta-carotene is widely distributed in plant material such as carrots and green leafy vegetables and, as such, is a component of the human diet. Our results suggest that beta-carotene provides significant protection against the genotoxicity of benzo(a)pyrene and mitomycin C.

Animals↗

PubMed2004

Correlation between the UDP-glucuronosyltransferase (UGT1A1) TATAA box polymorphism and carcinogen detoxification phenotype: significantly decreased glucuronidating activity against benzo(a)pyrene-7,8-dihydrodiol(-) in liver microsomes from subjects with the UGT1A1*28 variant.

Of the hepatic UDP-glucuronosyltransferases (UGTs), only UGT1A1 and UGT1A9 exhibit activity against benzo(a)pyrene-trans-7R,8R-dihydrodiol [BPD(-)], precursor to the highly mutagenic anti-(+)-benzo(a)pyrene-7R,8S-dihydrodiol-9S,10R-epoxide. The UGT1A1*28 allelic variant contains an additional (TA) dinucleotide repeat in the "TATAA" box [(TA)(6)>(TA)(7)] of the UGT1A1 promoter that has been linked to decreased expression of the UGT1A1 gene and decreased bilirubin conjugation, leading to the relatively nondebilitating condition known as Gilbert's syndrome. To determine whether the UGT1A1 TATAA box polymorphism may play a role in the overall glucuronidation of BPD(-) in humans, we compared UGT1A1 TATAA box genotype with BPD(-) glucuronidating activity in normal liver microsomes. Significant decreases in UGT1A1 protein (P < 0.005) and bilirubin conjugation activity (P < 0.001) were observed in liver microsomes from subjects homozygous for the UGT1A1*28 allelic variant compared with subjects homozygous for the wild-type UGT1A1*1 allele. Significant decreases in BPD(-) glucuronidation activity (P < 0.02) were observed in subjects with the UGT1A1(*28/*28) genotype compared with subjects having the wild-type UGT1A1(*1/*1) genotype in assays of liver microsomes that included 0.1 mM alpha-naphthylamine, a competitive inhibitor of UGT1A9 and not UGT1A1. Similar phenotype:genotype correlations were observed when we compared subjects with the UGT1A1(*28/*28) genotype with subjects having the UGT1A1(*1/*28) genotype. In assays with alpha-naphthylamine, the K(m) of liver microsomes against BPD(-) was similar to that reported for UGT1A1-overexpressing baculosomes (319 micro M versus 290 micro M; Fang et al., Cancer Res., 62: 1978-1986, 2002). These data suggest that the UGT1A1 TATAA box polymorphism plays a role in an individual's overall ability to detoxify benzo(a)pyrene and in cancer risk.

Dihydroxydihydrobenzopyrenes↗

PubMed1978

Carcinogenic benzo(a)pyrene metabolites bound to DNA: metabolic formation by human cultured lymphocytes and by human liver microsomes.

Sonicates of human cultured lymphocytes metabolize (benzo(a)pyrene to at least two intermediates that bind covalently to deproteinized DNA in vitro. The major peak represents the 4,5-oxide bound to nucleoside(s). No correlation is found between 'aryl hydrocarbon hydroxylase activity' (or its inducibility) and benzo(a)pyrene metabolites generated by human lymphocytes and bound to DNA in vitro. Human liver microsomes produce in vitro at least six such reactive intermediates which, bound to deproteinized DNA nucleosides, are separable by chromatography. The major peak represents the 7,8-diol-9,10-epoxides bound to nucleoside(s): this highly reactive intermediate is believed to be one of the ultimate carcinogenic forms of benzo(a)pyrene.

Aryl Hydrocarbon Hydroxylases↗

PubMed1986

Photosensitization to ultraviolet irradiation and selective killing of cells following uptake of pyrene-containing fatty acid.

Cells were incubated with 12-(1-pyrene)-dodecanoic acid (P12), a long-chain fatty acid to which a pyrene ring has been attached covalently. This acid was transported across the plasma membranes of cells and subsequently incorporated into their neutral lipids and phospholipids. Irradiation of these pyrene-containing cells for short periods (0.5-4 min) with ultraviolet light at 366 nm resulted in eventual cell death. Similar irradiation had no effect on cells that had not been exposed to P12. The time of the period of irradiation necessary for inducing the toxic process was related to the quantity of P12 incorporated, the latter being a function of the respective metabolic activity of the individual cell type. The degree of incorporation of P12 into a cell, and consequently its acquired sensitivity to killing by ultraviolet irradiation at 366 nm, was affected by the incubation temperature and addition of non-fluorescent fatty acid, albumin or other serum proteins. Different degrees of incorporation of P12 into various cell types were used for selective killing and elimination of cell populations by irradiation at 366 nm. The combined procedure of preincubation with P12 followed by ultraviolet irradiation thus permitted selection of cell types with a greater resistance to this procedure.

Cell Line↗

PubMed2003

Inhibition of benzo(a)pyrene-induced carcinogenesis by vitamin C alone and by vitamin C/vitamin E and selenium/glutathione.

The reduction on peroxidation caused by benzopyrenes by some naturally occurring antineoplastic agents was studied in this experimental work. Inhibition/reduction of experimental carcinogenesis induced by benzo(a)pyrene by vitamin C alone and by vitamin C/vitamin E and selenium/ glutathione was attempted in 224 female Wistar rats divided in four groups. Injected with 10.08 mL benzo(a)pyrene, the animals were treated with some naturally occurring substances like vitamin C alone and a combination of anticarcinogens. By calculating the carcinogenic potency of benzo(a)pyrene and the anticarcinogenic potency of substances used as well as histological examination of developed tumors and survival time of treated animals, it was found that vitamin C exerts a significant anticarcinogenic effect of 8.3 units and that the combination of the two anticarcinogens used produced a significant prolongation of the animals survival time with anticarcinogenic potency of 22.1 and 22.2 units, respectively. This is considered a potent anticarcinogenic effect. The question of an additional supportive administration of such agents complementary to the conventional cancer chemotherapy in humans is raised. Of course, further studies are needed.

Animals↗

PubMedDate not supplied

Fluorescence studies on N-(3-pyrene)maleinimide-labeled sarcoplasmic reticulum ATPase in native and solubilized membranes.

Fluorescence polarization and formation of excimers were studied in N-(3-pyrene)maleinimide-labeled sarcoplasmic reticulum vesicles. 1. The polarization of pyrenemaleinimide labeled vesicles does not change with temperature and shows a pronounced decrease at labeling concentrations larger than 1 mol pyrenemaleinimide per 10 mol ATPase. 2. Solubilization of the membrane with myristoylglycerophosphocholine renders the polarization temperature dependent, but does not affect the concentration dependent depolarization observed in native vesicles. 3. The polarization of labeled vesicles is much smaller than to be expected from the temperature independent polarization indicating that the pyrenemaleinimide polarization did not monitor the rotation of the entire ATPase. Thus segmental motion occurs. 4. Pyrene excimers are observed at label concentrations larger than 1 mol label per 2.5 mol ATPase. 5. The amount of excimers was critically dependent on added detergents. From the fact that non-solubilizing amounts of myristoylglycerophosphocholine strongly reduced the amount of pyrene excimers it is concluded that in the native sarcoplasmic reticulum vesicles at least two ATPase molecules must be in close contact.

Animals↗

PubMed1978

The effect of some cigarette smoke constituents and other compounds on the metabolism of benzo(a)pyrene in rabbit lung 9000 g supernatant.

1. The inhibitory effects, of a number of compounds, on the formation of two groups of benzo(a)pyrene metabolites in rabbit lung homogenates (9000 g supernatant) have been investigated. 2. The inhibitors comprised two groups: those inhibiting primarily benzo(a)pyrene hydroxylase activity, and those inhibiting the activity of the epoxide-metabolizing enzymes as well as hydroxylase activity. Phenol, 1-naphthol, nicotine and acetone belong to the former group; naphthalene, anthracene and chlorpromazine to the latter group. 3. The most active inhibitors also caused a significant decrease in the amount of benzo(a)pyrene bound covalently to tissue macromolecules.

Acetone↗

PubMed1982

Inhibition of tissue aryl hydrocarbon (benzo[a]pyrene) hydroxylase by 7,8-benzoflavone in birds.

1. Addition of 7,8-benzoflavone (7,8-BF) inhibited both hepatic and renal constitutive activity of aryl hydrocarbon (benzo[a]pyrene) hydroxylase in vitro for a number of avian species. Inhibition of hepatic benzo[a]pyrene hydroxylase was 70-94% in wild pigeon; 46-88% in homing pigeon; 85-93% in house crow; 18-53% in common kite; 56-86% in cattle egret; and for the renal enzyme was 43-84, 52-88, 18-73 and 13-48% respectively. 2. 3-Methylcholanthrene treatment of homing pigeons resulted in the induction of liver and kidney benzo[a]pyrene hydroxylase activity. Induced enzyme activity was also significantly inhibited by 7,8-BF.

Animals↗

PubMed1986

Activities in chick embryos of 7-ethoxycoumarin O-deethylase and aryl hydrocarbon (benzo[a]pyrene) hydroxylase and their induction by 3,3',4,4'-tetrachlorobiphenyl in early embryos.

Basal activities of 7-ethoxycoumarin O-deethylase and aryl hydrocarbon (benzo[a]pyrene) hydroxylase were determined in whole-liver homogenates from chick embryos of different ages, from newly hatched chicks and from chicks a few days old. The enzyme activities increased substantially in chick embryo livers between days five and 10, remained at a fairly constant level until day 19, and reached a peak in activity one day after hatching. The optimal pH value was lower than 7.0 for both enzyme activities. The total increase in activity from day five to one day after hatching was about 300-fold for 7-ethoxycoumarin O-deethylase and about 75-fold for aryl hydrocarbon (benzo[a]pyrene) hydroxylase. Treatment of eggs with 3,3',4,4'-tetrachlorobiphenyl resulted in increased metabolism of both substrates by five-day-old chick embryo livers. The increase in aryl hydrocarbon (benzo[a]pyrene) hydroxylase activity was 14-fold while that of 7-ethoxycoumarin O-deethylase was approximately double.

7-Alkoxycoumarin O-Dealkylase↗

PubMedDate not supplied

Comparative response of normal and of human papillomavirus-16 immortalized human epithelial cervical cells to benzo[a]pyrene.

Laboratory evidence suggests synergism of human papillomavirus (HPV) infection with cigarette smoking behaviors in enhancing the risk of cervical cancer. In this preliminary investigation, we tested the hypothesis that HPV infection may alter the metabolic activation of tobacco smoke carcinogens, such as benzo[a]pyrene (B[a]P), thereby playing a role in the etiology of cervical cancer. We examined in vitro the metabolism and DNA adduct formation of [3H]B[a]P in normal and HPV-16 immortalized human epithelial cervical cells in culture, and investigated the effect of [3H]B[a]P on growth of these cells. Cultures of normal human cervical cells and of HPV-16 immortalized cervical epithelial cells were exposed to 0.2 microM [3H]B[a]P for 24 and 48 h. [3H]B[a]P inhibited growth of both normal and HPV-16 immortalized cervical cells. However, the growth inhibition of normal cells was more profound than that of HPV-16 immortalized cells. Comparison of the metabolism of [3H]B[a]P in these cells indicated that they both metabolize [3H]B[a]P predominantly to [3H]trans-9,10-dihydroxy-9,10-dihydrobenzo[a]pyrene ([3H]B[a]P-9, 10-diol), [3H]r-7,t-8, 9,c-10-tetrahydroxy-7,8,9, 10-tetrahydrobenzo[a]pyrene ([3H]trans-anti-B[a]P-tetraol), and unknown polar products. Enzymatic hydrolysis of water-soluble metabolites indicated that the levels of glucuronide and sulfate conjugates in these cells are negligible. Similarly, both cell lines form similar [3H]B[a]P-DNA adducts. However, the level of the (+)[3H] anti-B[a]P diol epoxide (BPDE)-deoxyguanosine adduct in HPV-16 immortalized cells after 24 and 48 h exposures was 3.8 and 3. 1 pmol/mg DNA, respectively, which is 2.2-fold and 2.6-fold greater than the level of this adduct in normal cells. Under the conditions and within the time frame employed in these assays, both the cell growth and DNA damage induced by [3H]B[a]P appear to be higher in HPV-16 immortalized cells than those detected in normal cells. The results, although preliminary, suggest that HPV-16 immortalized cervical cells are more susceptible to DNA damage by BaP which, in part, may enhance their transformation to malignant cells.

Benzopyrenes↗

PubMed1975

Factors influencing augmentation and/or acceleration of lymphoreticular tumors in mice by benzo(a)pyrene treatment.

The response of lymphoreticular tissues to a single i.p. injection of benzo(a)pyrene was studied in the first generation of C57BL/6J X C3HeB/FeJ F1 and C3HeB/FeJ X A/J F1 mice. Groups of 1-, 15-, and 42-day-old animals of both sexes received 75 or 150 mug of the carcinogen per g body weight. After a period of approximately 90 weeks, a high incidence (up to 43%) of reticulum cell sarcomas was observed in C57BL/6J X C3HeB/FeJ F1 mice treated with benzo(a)pyrene at 40 days of age. Animals treated with carcinogen at younger ages had a lower incidence of reticulum cell sarcomas. These sarcomas showed marked cellular pleomorphism and were classified into histiocytic, epitheloid-nodular, reticulocytic, and fibrocytic forms according to the predominant cell type. Lymphomas of thymic and extrathymic lymphoid origin and leukemia of granulocytic type were seen in a descending order of frequency. Control animals of either strain that were killed at 90 weeks of age were basically free of lymphoreticular tumors, while those kept under observation up to 170 weeks developed these tumors in 24% (C57BL X C3H F1) and 10% (C3H X A/J F1), respectively. Studies revealed that the augmentation and/or acceleration of development of the lymphoreticular neoplasms and specifically reticulum cell sarcomas by benzo(a)pyrene was dependent upon the strain and sex of mice used and the age at which the animals were exposed to carcinogen.

Age Factors↗

PubMed1975

Species differences in the effect of benzo(alpha)pyrene-ferric oxide on the respiratory tract of rats and hamsters.

When given intratracheal injections of a suspension of benzo(alpha)pyrene-ferric oxide, rats and hamsters showed striking species differences in the response of their respiratory tracts to the carcinogen. Hamsters produced squamous metaplasia of the trachea and large bronchi; in contrast, squamous cell nodules of bronchioloalveolar origin developed in rats within a few weeks after carcinogen application. The different sites of the early proliferative and metaplastic responses correlated in their location with the sites of later tumor development. There were no obvious differences between the two species in retention of benzo(alpha)pyrene in the lungs or tracheas. A species difference was observed, however, in the localization of the benzo(alpha)pyrene in the tracheal tissues using ultraviolet fluorescence microscopy. Carcinogen was found to be present in the epithelium of hamsters but not in the epithelium of rats, suggesting a species difference in penetration of carcinogen from the lumen into the tracheal tissues.

Animals↗

PubMed1975

Inhibition of benzo(alpha)pyrene metabolism catalyzed by mouse and hamster lung microsomes.

Induced and constitutive microsomal enzymes of mouse and hamster lungs catalyze both the hydroxylation of benzo(alpha)pyrene and reactions that lead to its irreversible binding to macromolecules. For mouse and hamster, the induced lung hydroxylases have Km values of 1.10 and 0.52 muM, respectively. The induced hydroxylases are strongly inhibited by 7,8-benzoflavone and are stimulated by cyclohexene oxide, an inhibitor of epoxide hydrase. Formation of the macromolecular product by the induced "binding" enzyme follows. Michaelis-Menten kinetics, except for substrate inhibition, and has Km values of 0.52 and 0.25 muM for lung microsomes from mouse and hamster, respectively. These reactions are also inhibited by 7,8-benzoflavone. The reaction catalyzed by the constitutive hydroxylase of mouse lungs is characterized by a brief lag period but proceeds in a linear fashion after the lag. The enzyme requires 60 muM benzo(alpha)pyrene to achieve maximum reaction velocity. Above this concentration, strong substrate inhibition is observed; accurate values for Vmax and Km cannot be derived. The constitutive hydroxylases are moderately inhibited by butylated hydroxytoluene, retinol, cyclohexene oxide, and 7,8-benzoflavone. The product of the constitutive "binding" enzyme is formed in a reaction that follows Michaelis-Menten kinetics. The Km value for enzymes from mouse and hamster lungs are 11.8 and 4.9 muM, respectively. Formation of this product is strongly inhibited by butylated hydroxytoluene and by retinol but not strongly by 7,8-benzoflavone or cyclohexene oxide. Since other evidence indicates that a constitutive enzyme may be involved in carcinogenesis by benzo(alpha)pyrene and since this reaction is inhibited by two known anticarcinogens, we suggest that it may be involved in this process.

Animals↗

PubMed1975

In vitro metabolism of benzo(a)pyrene by human liver microsomes and lymphocytes.

The metabolism of benzo(a)pyrene by human liver microsomes and human lymphocytes has been analyzed by high-pressure liquid chromatography. Human liver forms seven known metabolites and at least five additional unidentified metabolites that migrate as distinct peaks. Lymphocytes incubated with benzo(a)pyrene for 30 min do not form dihydrodiols. Lymphocytes incubated for 24 hr with benzo(a)pyrene form all of the metabolites produced by liver including dihydrodiols as well as additional metabolites. The ratios of phenols formed by liver and lymphocytes are different, and preparations from humans form a different profile of metabolites than that formed by rat liver.

Animals↗

PubMed2002

Curcumin activates the aryl hydrocarbon receptor yet significantly inhibits (-)-benzo(a)pyrene-7R-trans-7,8-dihydrodiol bioactivation in oral squamous cell carcinoma cells and oral mucosa.

The development of oral squamous cell carcinoma (SCC) shows a positive correlation with the carcinogen exposure that occurs during tobacco and alcohol use. The purpose of this study was to investigate whether the naturally occurring chemopreventive agent, curcumin, modulates expression and function of carcinogen- metabolizing enzymes in human keratinocytes isolated from oral SCC tumors. Dose-response studies demonstrated that curcumin concentrations of >or=25 micro M were cytotoxic for oral SCC cells. Curcumin increased both expression (reverse transcription-PCR analyses) and function (high-performance liquid chromatography determination of ethoxyresorufin metabolism) of cytochrome P-450 (CYP) 1A1 and/or CYP1B1. The aryl hydrocarbon receptor (AhR), which up-regulates a battery of genes associated with carcinogen metabolism, is activated by polycyclic aromatic hydrocarbons such as the tobacco-associated carcinogen benzo(a)pyrene. Electromobility shift assays demonstrated that similar to the established AhR ligand 2,3,7,8,-tetrachlorodibenzo-p-dioxin, curcumin inclusion resulted in AhR nuclear translocation and formation of the transcriptionally active AhR-aryl hydrocarbon receptor nuclear translocator complex. Cellular capacity to bioactivate the tobacco-associated carcinogen (-)-benzo(a)pyrene-7R-trans-7,8-dihydrodiodiol was determined by evaluating conversion of the carcinogenic metabolite diol epoxide to stable tetrols via high-performance liquid chromatography. Results of our metabolism studies showed that curcumin significantly inhibited CYP1A1-mediated benzo(a)pyrene diol bioactivation in both oral SCC cells and intact oral mucosa. Because CYP1A1 is one of the primary carcinogen-activating enzymes in oral mucosa, the use of curcumin as an oral cavity chemopreventive agent could have significant clinical impact via its ability to inhibit carcinogen bioactivation.

Adult↗

PubMed1977

Inhibition of Herpesvirus saimiri replication by phosphonoacetic acid, benzo(a)pyrene, and methylcholanthrene.

The present investigations were undertaken to determine the possible effects of two carcinogenic polycyclic aromatic hydrocarbons, benzo(a)pyrene and 3-methylcholanthrene on Herpesvirus saimiri replication. The results from these experiments were compared with the effects of phosphonoacetic acid on the virus replication cycle. Phosphonoacetic acid inhibited the synthesis of virus-induced intracellular late antigens, membrane antigens and infectious virus but not the synthesis of the early antigens induced by H. saimiri. In contrast, benzo(a)pyrene and 3-methylcholanthrene inhibited primarily membrane antigen expression and infectious virus production. Benzo(a)pyrene was the most effective of the two compounds, with significant inhibition occurring with 2 mug/ml, whereas a minimum concentration of 10 mug/ml was required with 3-methylcholanthrene. Both compounds were most effective when present continuously during the 4-day infection process. However, exposure of infected cultures to a 3-hr pulse with each chemical also inhibited membrane antigen expression. Furthermore, pretreatment of cells for 48 hr before virus infection resulted in the inhibition of membrane antigen expression but not that of early or late antigens. These result demonstrate that some carcinogenic chemicals are capable of altering the H. saimiri replication cycle, primarily by inhibiting some but not all late events.

Acetates↗

PubMed1990

Monoclonal antibody characterization of NADH- and NADPH-dependent hydroxylation of benzo(a)pyrene in liver microsomes from 5,6-benzoflavone-induced C57Bl/6 mice.

Monoclonal antibodies (MAb 1-7-1) directed against the isoenzymes of rat liver cytochrome P-450 induced by methylcholanthrene, inhibited benzo(a)pyrene hydroxylase less strongly at low (0.04 mM) than at high (2 mM) NADH concentration. Inhibition of NADPH dependent hydroxylation was the same irrespective of NADPH concentrations and corresponded to that observed at high NADH concentration. The same was also the h.p.l.c. pattern of the reaction products of benzo(a)pyrene hydroxylation supported by high concentration of both coenzymes. It is postulated that different cytochrome P-450 isoenzymes participate in benzo(a)pyrene hydroxylation, whereas the second one acts at high concentration of both NADH and NADPH.

Animals↗

PubMed1990

Oxidation and DNA binding of (+)-7,8-dihydroxy-7,8-dihydrobenzo(a)pyrene in mouse epidermis in vivo and effects of coadministration of catechol.

Using a stereochemical probe as described by Marnett (Carcinogenesis (Lond.), 8: 1365-1373, 1987), we have investigated the mechanism of oxidation of (+)-[3H]BaP-7,8-dihydroxy-7,8-dihydrobenzo(a)pyrene [(+)-[3H]BaP-7,8-diol] in mouse epidermis in vivo. Groups of mice were topically treated with (+)-[3H]BaP-7,8-diol (60 nmol/mouse) and sacrificed at intervals from 1/2 to 8 h post treatment. (-)-Anti- and (+)-syn-7,8-[3H]dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDE) were formed as metabolites in a ratio of about 4 to 1, respectively, as determined by HPLC analysis of the hydrolysis products. Pretreatment of mice with indomethacin, an inhibitor of prostaglandin H synthase, did not alter the ratio of anti- to syn-BPDE-derived hydrolysis products. Pretreatment of mice with the cytochrome P-450 inducer, beta-naphthoflavone, yielded twice the level of syn-[3H]BPDE in mouse skin at the 1/2-h survival point. However, this enhancing effect diminished over time. Coadministration of 1,2-dihydroxybenzene (catechol) with (+)-[3H]BaP-7,8-diol decreased the formation of (-)-anti-[3H]BPDE and also decreased lipid peroxidation, as measured by the extent of formation of thiobarbituric acid-reactive material in mouse epidermis. Analysis of mouse epidermal DNA adducts 24 h after topical application (+)-[3H]BaP-7,8-diol indicated that the major adduct is not formed from the major metabolite (-)-anti-BPDE. Acid hydrolysis of the major adduct resulted in the formation of a small amount of r-7,c-9,c-10,t-8-tetrahydroxy-7,8,9,10-tetrahydrobenzo(a)pyrene and two unidentified products different from 7,8,9,10-tetrahydroxy-7,8,9,10-tetrahydro-BaP. Coadministered catechol suppressed the formation of this adduct by 30%. The present observation suggests that a peroxyl radical-mediated epoxidation pathway is involved in the oxidation of (+)-[3H]BaP-7,8-diol in mouse skin in vivo.

Animals↗