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R C Garner

Publications and source records attributed to R C Garner.

At least 73 records · Page 4Linked to original sources

Rat liver immuno-ultrastructural localization of the specific (4-5S) 3-methylcholanthrene-binding protein; evidence for its involvement as a receptor protein in cytochrome P-4501A1 induction.

Two major specific carcinogen-binding proteins are thought to be involved in the regulation of hepatic cytochrome P-4501A1 induction in response to polycyclic aromatic hydrocarbons. We have raised both mono- and polyclonal antibodies which specifically interact with one of these proteins, the 4-5S-specific binding protein. Antibody binding was found to both the specific (4-5S) 3-methylcholanthrene (3MC) binding activity present in rat hepatic cytosol (as quantified on sucrose gradients or by Sephacryl S-300 gel filtration chromatography) and to the purified 39,000-dalton protein previously reported as the specific 3MC-binding protein (determined by Western blot analyses). No immunoreactivity was observed to cytosolic proteins in the region of 70,000 or 95,000 daltons (i.e. corresponding to the Ah receptor). We have used Western blot analyses and immunostaining of cryostat sections to demonstrate that the 4-5S-specific binding protein is present predominantly in the cytoplasm but also (at lower concentration) in the nuclei of untreated Wistar rat hepatocytes. Electron micrographs of immunostained sections indicate that, following exposure to 3MC, the concentration of specific binding proteins in the nucleus increases and this is assumed to be due to translocation of specific binding protein-3MC complexes from the cytoplasm.

Animals↗

The mutagenicity and DNA base sequence changes induced by 1-nitroso- and 1-nitropyrene in the cI gene of lambda prophage.

The mutagenicity of 1-nitropyrene and its reduced metabolite 1-nitrosopyrene was determined in the lambda cI gene of an Escherichia coli uvr- lysogen. 1-Nitropyrene induced a mutation frequency of 3.8 x 10(-6), which was approximately 2-fold higher than the background mutation frequency, whereas an equimolar dose of 1-nitrosopyrene induced a much higher mutation frequency of 1.4 x 10(-4). Previous studies have established that both compounds form the same premutagenic lesion, viz. N-(deoxyguanosin-8-yl)-1-aminopyrene in bacterial DNA. In order to determine how this initial premutational lesion is converted to a stable heritable mutation, DNA sequences were determined for 30 mutations induced by 1-nitrosopyrene that mapped between bp 1 and 352 in the lambda cI gene of E.coli lysogens. We show here that these mutations are mainly frameshifts involving the addition or deletion of a single GC or CG base pair. A small proportion of mutations were base substitutions which were equally divided between transitions and transversions. These also occurred primarily at GC or CG sites.

Bacteriophage lambda↗

A comparison of 32P-postlabelling and immunological methods to examine human lung DNA for benzo[a]pyrene adducts.

Human lung DNA isolated from surgical specimens has been examined for the presence of polycyclic aromatic hydrocarbon-DNA adducts using both 32P-postlabelling and immunological methods. Of 12 samples examined to date, five had detectable amounts of benzo[a]pyrene diol epoxide-DNA adducts (BPDE-DNA) as determined by the enzyme-linked immunosorbent assay (ELISA), after immunoaffinity concentration. Values ranged from 3.5 to 11.5 fmol/mg DNA. When the same group of samples was analysed using the 32P-postlabelling technique, adducts could be detected in all the samples examined. There was generally not a good correspondence between the two methods. The number of adducts measured by 32P-postlabelling ranged from 1-100 per 10(8) nucleotides, which is some two orders of magnitude higher than with the immunological method, indicating that the BPDE-DNA adduct is probably not the major adduct present in these samples.

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

Purification and photoaffinity labelling of a rat cytosolic binding protein specific for 3-methylcholanthrene.

Rat hepatic cytosolic proteins which sediment at 4-5 S on sucrose gradients exhibit high-affinity saturable binding for the carcinogen 3-methylcholanthrene. A rat liver protein of Stokes' radius 3 nm, Mr by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis of 39,000 and with specific 3-methylcholanthrene-binding activity sedimenting at 4.5 S, has been purified 315-fold to apparent homogeneity by using affinity chromatography on a column of 1-hydroxy-3-methylcholanthrene coupled to epoxy-activated Sepharose 6B, in conjunction with two gel-filtration steps. The protein purified by this technique was shown to be associated with the observed specific 3-methylcholanthrene-binding activity by photoaffinity labelling with 1-oxo-3-methylcholanthrene.

Affinity Labels↗

Aflatoxin B1 activation to a plasmid mutagen by a chemical model of cytochrome P-450.

Aflatoxin B1 (AFB1) was oxidised by a chemical model of cytochrome P-450 and the products obtained analysed by reversed-phase hplc. The oxidation system employs a water-insoluble iron(III)porphyrin catalyst (tetraphenylporphinatoiron(III) chloride; FeTPPCl) and an oxygen donor, iodosylbenzene (PhIO). The two AFB1 products obtained from this reaction were derived by initial oxidation across the 8-9 double bond of AFB1 and subsequent breakdown of AFB1-8,9-epoxide, the compound postulated to be the ultimate carcinogenic and mutagenic derivative of AFB1. Oxidation of AFB1 by the porphyrin-catalysed system in the presence of calf-thymus DNA, resulted in the formation of AFB1-DNA adducts identical to those formed in vivo and in vitro after liver mono-oxygenase activation. The chemical model system was therefore used on a microscale to react AFB1 with plasmid pHR1800, a plasmid containing the genes for beta-lactamase (amp-r) and galactokinase (galK). AFB1-modified plasmid DNA was then transformed into E. coli AB1886 (uvrA-) and the effects of the AFB1-DNA adducts on plasmid survival and the ability of pHR1800-transformed bacteria to metabolise galactose, were then studied. The results showed an AFB1 dose-dependent decrease in plasmid survival and increase in the mutation frequency of the galK gene only when the complete oxidation system was used to generate the reactive AFB1 metabolite.

Aflatoxin B1↗

Effect of histamine H2-receptor antagonist therapy on the mutagenic activity of gastric juice.

There is concern at present that treatment with histamine H2-receptor antagonists might promote the development of gastric cancer by producing conditions which favour intragastric formation of N-nitroso compounds. If H2-receptor antagonist therapy causes increased intragastric levels of N-nitroso compounds, an issue not yet resolved by analytical studies, corresponding changes in the mutagenic activity of gastric juice might be anticipated. In this study mutagenic activity and pH were measured in fasting gastric aspirate from 18 peptic ulcer patients before and during the final week of therapy with ranitidine (n = 10) or cimetidine (n = 8). Mutagenic activity was assessed using Salmonella typhimurium TA98 and TA100 in a modified pre-incubation "fluctuation" test. No significant change in mutagenic activity was detected after therapy. Of 15 patients found to have significant mutagenic activity in their fasting gastric juice before treatment, 14 remained mutagenic following treatment. Mutation frequencies (sum of positive wells in duplicate 96-well microtitre plates, mean +/- SD) for TA98 and TA100 were respectively, 20 +/- 34 and 100 +/- 64 before compared with 10 +/- 6 and 102 +/- 65 after therapy (p greater than 0.05). Changes in mutagenic activity were similar in both treatment groups and unrelated to duration of therapy, changes in gastric pH or ulcer healing. In vitro, neither cimetidine in aqueous solution, nor gastric juice preincubated with cimetidine showed significant mutagenic activity. These results provide no evidence that increased intragastric levels of genotoxic chemicals, such as N-nitroso compounds, occur during H2-receptor antagonist therapy.

Adult↗

Topical treatment of mice with benzo[a]pyrene or parenteral administration of benzo[a]pyrene diol epoxide-DNA to rats results in faecal excretion of a putative benzo[a]pyrene diol epoxide-deoxyguanosine adduct.

The administration of [3H]BPDE-DNA, whether by i.p. or i.v. injection, to male Wistar rats resulted in the majority of the radioactivity being recovered in the faeces. Excretion was rapid: within 24 h post-injection, 45% of the applied dose was recovered in the faeces. H.p.l.c. analysis of radioactive material extracted from the faeces by methanol showed that it contained a single component which co-chromatographed with [3H]BPDE-dGuo and which was not affected by treatment with alkaline phosphatase, aryl sulphatase or beta-glucuronidase. To determine if this phenomenon occurs after topical application of BP to a target tissue, such as mouse skin, animals were treated with [3H]BP and their faeces collected. After an extensive extraction procedure involving differential solubility in organic solvents, Sephadex LH-20 chromatography and h.p.l.c., a product was isolated from mice faeces which had characteristics consistent with a [3H]BPDE-dGuo adduct. These findings are discussed in relation to detection of BPDE adducts in human populations.

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

Bacterial mutagenicity and chemical analysis of polycyclic aromatic hydrocarbons and some nitro derivatives in environmental samples collected in West Germany.

Snow and air particulate samples collected in Upper Frankonia, Federal Republic of Germany, have been analyzed for nitro-polycyclic aromatic hydrocarbons (PAH) and PAH content. A novel clean-up technique has been developed enabling interfering organochlorine environmental contaminants to be removed prior to analysis of the hydrocarbons by GC-MS. Mass fragmentation patterns are presented for 1-nitropyrene, 6-nitrobenzo(a)pyrene, 6-nitrochrysene, and 3-nitrofluoranthene. The level of these compounds found in air samples was in the range of 0.2-2.0 ng.m-3 with the exception of 6-nitrobenzo(a)pyrene, which was not detected. This compares with PAH values of between 1 and 6 ng.m-3. The freshly fallen snow sample collected at the side of a motorway had no detectable PAHs or nitro-PAHs. Parallel studies on the bacterial mutagenicity of the collected air samples using Salmonella typhimurium TA98 and TA100 in the presence and absence of aroclor-induced rat liver "S9" revealed both "direct" and "indirect" activity. Larger numbers of mutants were induced in the presence of S9 than in its absence. The snow sample was devoid of mutagenic activity. These studies show the utility of the biological approach to screen environmental samples prior to expensive and time-consuming chemical analysis.

Air Pollutants↗

Aflatoxin B1 binding to plasma albumin and liver DNA upon chronic administration to rats.

The hepatocarcinogen aflatoxin B1 (AFB1) was administered to male Wistar rats by oral intubation in either single or repeated doses and the binding to plasma protein and liver DNA determined. Twenty-four hours after a single dose (3.5-200 micrograms/kg AFB1) a constant ratio was found between levels of aflatoxin bound to plasma protein and that bound to liver DNA. In total 0.98-2.15% of the administered dose was bound to the plasma protein at this time point. In the chronic study rats received two doses of 0.5 microgram AFB1/day and groups of animals were killed on days 2, 3, 7, 14, 21 and 24. Binding of aflatoxin to plasma protein accumulated to a level 3-fold higher than that seen after a single dose. Levels of binding reached a plateau between days 7 and 14 of treatment and then remained stable until the end of the experiment. Binding to DNA also accumulated, 2.5-fold and in parallel to plasma protein, binding reached a plateau between days 7 and 14 of treatment. In both the chronic and acute studies fractionation of the plasma proteins by Sephadex G-200 chromatography showed that all detectable bound aflatoxin was associated with a single peak corresponding to albumin. Thus, a constant ratio was observed, after chronic or single exposure, between the concentration of plasma albumin-bound aflatoxin and that bound to DNA of the liver, the target organ for carcinogenesis by AFB1. In order to investigate the proposed role of AFB1 in the aetiology of primary hepatocellular carcinoma in man it would be of great value to have a method for assessing long-term human exposure at an individual level. The relevance of the observations presented in this paper are discussed in the light of such a requirement.

Aflatoxin B1↗

Immunoaffinity chromatography of carcinogen DNA adducts with polyclonal antibodies directed against benzo[a]pyrene diol-epoxide-DNA.

Polyclonal antibodies specific for (+/-)-trans-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene [(BPDE) CAS: 58917-67-2]-DNA adducts were obtained from the sera of New Zealand White rabbits immunized with BPDE-DNA. These antibodies did not recognize benzo[a]pyrene [(BP) CAS: 50-32-8] or DNA alone or other carcinogen adducts, such as aflatoxin (CAS: 1402-68-2)-DNA or aminopyrene (CAS: 58-15-1)-DNA, up to the concentrations used. In a competitive enzyme-linked immunosorbent assay, 0.18 microgram BPDE-DNA/ml (single stranded), equivalent to 7 pmol BPDE adduct, caused 50% inhibition with this antibody. (When referring to the DNA content of BPDE-DNA, the authors gave the concentration in microgram/ml; when referring to the BPDE content of BPDE-DNA, the authors gave the concentration as pmol/ml.) Chemical and enzymic modifications of the BPDE-DNA substrate suggested that the epitope for the antibody is greater than that represented by a BPDE-nucleoside adduct. The specific BPDE-DNA antibodies were covalently bound to cyanogen bromide-activated Sepharose 4B, and the extent of ligand binding to the immunoaffinity column was measured with the use of [3H]BPDE-DNA as substrate. Maximum binding to the immunoaffinity column was obtained after DNase 1 digestion of [3H]BPDE-DNA: The bound adducts could be readily eluted from the column with 50 mM NaOH. The binding of DNase 1-digested [3H]BPDE-DNA to the immunoaffinity column was dose related and not affected by the addition of unmodified DNA. The columns have proven to be reusable. Samples of [3H]BP-DNA isolated from the skin of mice treated topically with either 0.75 mumol [3H]BP/mouse or 1.5 mumol [3H]BP/mouse were examined by immunoaffinity chromatography. Binding values of 6.0 and 12.2 pmol BP/mg DNA were obtained; these values from immunoaffinity chromatography were slightly lower than those determined by high-pressure liquid chromatography analysis (9 and 17 pmol BP/mg DNA). With chemically reacted BPDE-DNA, around 70% of that applied was retained by immunoaffinity chromatography, whereas with [3H]BP-DNA isolated from the in vivo treatment of mouse skin, only 40% was retained--a possible reflection of the greater heterogeneity of the in vivo BP-DNA adducts. This immunoaffinity chromatography technique should prove useful in the selective examination of levels of BPDE-DNA adducts present in biological samples.

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

Effect of increased intake of vitamin C on the mutagenic activity of gastric juice and intragastric concentrations of ascorbic acid.

Mutagenic activity, ascorbic acid levels and pH were measured in fasting gastric juice from eight patients given oral supplements of vitamin C (1 g qid X 7 days). Supplementation significantly reduced mutagenic activity and increased intragastric ascorbate levels without altering gastric pH. These results demonstrate for the first time the relation between intragastric ascorbate levels, mutagenic activity and oral supplements of vitamin C. The findings are discussed in relation to the possible chemoprevention of gastric cancer.

Adult↗

Evidence for N-(deoxyguanosin-8-yl)-1-aminopyrene as a major DNA adduct in female rats treated with 1-nitropyrene.

[3H]1-Nitropyrene was administered at a dose of 25 mg/kg by i.p. injection to female Wistar rats. Animals were killed 24 h later and DNA was isolated from kidney, liver and mammary gland, enzymically hydrolysed and analysed by reverse-phase h.p.l.c. A major adduct peak was detected in DNA from each of the three organs. Enzymic hydrolysates of DNA, which had been reacted in vitro with 1-nitropyrene in the presence of xanthine oxidase, were similarly analysed by h.p.l.c. One major adduct peak was obtained which had the same retention time as the in vivo product. Confirmatory evidence that the in vivo adduct and the in vitro adduct were structurally similar was obtained from the determination of the pH-dependent solvent partitioning profiles. Further, treatment of the in vivo adduct from liver, kidney or mammary gland DNA hydrolysates and the in vitro adduct with sodium hydroxide resulted in the formation of a more polar product which eluted earlier on h.p.l.c. This behaviour is consistent with scission of the imidazole ring of a deoxyguanosine adduct. The major DNA adduct formed in vitro following xanthine oxidase reduction of 1-nitropyrene has previously been identified by others as N-(deoxyguanosin-8-yl)-1-aminopyrene. The present data suggest that the in vivo 1-nitropyrene-DNA adduct has the same structure.

Animals↗

Studies on the detoxication of microsomally-activated aflatoxin B1 by glutathione and glutathione transferases in vitro.

Aflatoxin B1 (AFB1)-8,9-oxide, the proposed ultimate carcinogen is conjugated enzymically with glutathione (GSH) to give 8-(S-glutathionyl)-9-hydroxy-8,9-dihydro AFB1 (AFB1-SG). The GSH conjugate isolated from rat bile was shown, on the basis of 1H n.m.r. to be identical to AFB1-SG. Of the seven soluble rat liver GSH transferases tested, namely GSH transferases 1-1, 1-2, 2-2, 3-3, 3-4, 4-4 and 5-5 (see reference 1 for the new system of nomenclature), only the first three were active with microsomally generated AFB1-8,9-oxide, their rates of conjugation being 1.1, 0.61 and 0.64 nmol/min/mg enzyme, respectively. AFB1-SG is a thioacetal, but it was not formed from the incubation of the hemiacetal, AFB1-8,9-dihydrodiol, with GSH or GSH plus GSH transferase 1-1 plus 1-2. The covalent binding of in vitro microsomally activated AFB1 to DNA and the formation of AFB1-SG were linearly related to AFB1 concentration in the range of 0.2-2 micrograms/ml. DNA binding was decreased by 38% by the competing formation of AFB1-SG throughout this range of concentrations. These results are in accord with the observation of Scott Appleton et al. (Cancer Res., 42, 3659-3662) that, in the rat in vivo, there is no evident threshold for the binding of AFB1 to DNA. These findings are also consistent with the further observation, reported in this paper that GSH and GSH transferases have no effect on the mutagenicity of microsomally activated AFB1 to Salmonella typhimurium TA 100.

Aflatoxin B1↗

6-Nitrochrysene is a potent tumorigen in newborn mice.

A newborn mouse (BLU:Ha) lung adenoma bioassay demonstrated that 6-nitrochrysene was a highly potent tumorigen. It induced 100% incidence of lung tumors and a 150-fold increase in their number (20.84 tumors/mouse) at the lowest dose level tested (total dose: 38.5 micrograms/mouse). 70% of the 6-nitrochrysene treated mice had malignant lung tumors (adenocarcinomas). Lymphomas and nodular hyperplasia of the liver were also observed in treated, but not control, animals. The tumorigenicity of 6-nitrochrysene relative to other polynuclear aromatic hydrocarbons and their mononitro-derivatives has been discussed.

Adenoma↗

Rat and human explant metabolism, binding studies, and DNA adduct analysis of benzo(a)pyrene and its 6-nitro derivative.

Human colon and bronchus tissue explants were incubated with either [3H]benzo(a)pyrene ([3H]BP) or [3H]-6-nitrobenzo(a)pyrene ([3H]-6-NBP). The total percentage of metabolism of BP and 6-NBP was, respectively, 8-59% and 18-41% in bronchus and 11-23% and 36-50% in colon. A product tentatively identified as 3-hydroxy-6-NBP was isolated from the 6-NBP incubation medium. BP and 6-NBP when incubated at equivalent concentrations were found to bind covalently to the DNA of human bronchi from 15 cases at means of 42 and 50.9 pmol/10 mg DNA, respectively, and to the DNA of human colon from 6 cases at means of 66.5 and 35 pmol/10 mg DNA, respectively. The range among individuals was within one order of magnitude. High pressure liquid chromatography (HPLC) of enzymic hydrolysates of human bronchus explant DNA revealed one adduct from the BP-incubated bronchus which cochromatographed with (+/-)-7,8-dihydroxy-9,10-epoxy-7,8,9, 10-tetrahydrobenzo(a)pyrene-deoxyguanosine and a possible two adducts from the 6-NBP-incubated bronchus which eluted earlier than did the BP adduct. DNA obtained from the lung or liver of rats given 2.0-mg/kg doses of either [3H]BP or [3H]-6-NBP by i.p. injection was also enzymically hydrolyzed and analyzed on HPLC. Three DNA adducts were observed in liver and two were observed in lung DNA hydrolysates from rats given injections of [3H]BP. One adduct from each organ cochromatographed with (+/-)-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene- deoxyguanosine; however, the major adduct in each case eluted earlier. Only one adduct was detected in liver and lung DNA hydrolysates from rats given [3H]-6-NBP, and this had the same retention time as did the major adduct isolated from human bronchus that had been incubated previously with [3H]-6-NBP. Salmonella typhimurium TA98 was incubated with [3H]-6-NBP and Aroclor-induced rat liver S9. Enzymically hydrolyzed DNA analyzed by HPLC revealed three adducts, two of which cochromatographed with the two DNA adducts isolated from human bronchus DNA adduct which had the same retention time as did the major liver and lung DNA adduct from rats given i.p. injections of [3H]-6-NBP. In each case the major adduct from DNA hydrolysates of rat liver and lung, human bronchus, and S. typhimurium, all treated with [3H]-6-NBP, cochromatographed with the major DNA adduct isolated from liver and lung DNA of rats given [3H]BP.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Effect of storage at 4 degrees on prepared Salmonella/microsome test plates.

Salmonella/microsome soft-agar overlay ('Ames' test) plates were prepared using the previously published 'York' method. Plates treated with either added 3-methylcholanthrene (3MC) or 3,3'-dichlorobenzidine (DCB) and Aroclor-induced rat-liver S9 were stored at 4 degrees after preparation and removed at time intervals thereafter for incubation at 37 degrees. The number of 3MC-induced mutants in TA100 fell within 24 h of storage by 50% but then remained at this level until 96 h. Storage for a total of 336 h still showed some residual mono-oxygenase activity. On the other hand the ability to convert DCB to a mutagen for TA98 appeared to increase with storage, reaching a peak by 96 h. After this time the number of induced mutants fell until by 336 h the numbers were approximately equal to those plates which had not been stored in the cold.

3,3'-Dichlorobenzidine↗