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1.
Dibenzo[a,l]pyrene-induced DNA adduction, tumorigenicity, and Ki-ras oncogene mutations in strain A/J mouse lung 总被引:1,自引:0,他引:1
Prahalad AK; Ross JA; Nelson GB; Roop BC; King LC; Nesnow S; Mass MJ 《Carcinogenesis》1997,18(10):1955-1963
Dibenzo[a,l]pyrene (DB[a,l]P), an environmental polycyclic aromatic
hydrocarbon, is the most potent carcinogen ever tested in mouse skin and
rat mammary gland. In this study, DB[a,l]P was examined for DNA adduction,
tumorigenicity, and induction of Ki-ras oncogene mutations in tumor DNA in
strain A/J mouse lung. Groups of mice received a single i.p. injection of
0.3, 1.5, 3.0, or 6.0 mg/kg DB[a,l]P in tricaprylin. Following treatment,
DNA adducts were measured at times between 1 and 28 days, while tumors were
counted at 250 days and analyzed for the occurrence of point mutations in
codons 12 and 61 of the Ki-ras oncogene. DB[a,l]P in strain A/J mouse lung
induced six major and four minor DNA adducts. Maximal levels of adduction
occurred between 5 and 10 days after injection followed by a gradual
decrease. DB[a,l]P-DNA adducts in lung tissue were derived from both anti-
and syn-11,12- dihydroxy-13,14-epoxy-
11,12,13,14-tetrahydrodibenzo[a,l]pyrene (DB[a,l]PDE) and both
deoxyadenosine (dAdo) and deoxyguanosine (dGuo) residues in DNA as revealed
by cochromatography. The major adduct was identified as a product of the
reaction of an anti-DB[a,l]PDE with dAdo in DNA. DB[a,l]P induced
significant numbers of lung adenomas in a dose- dependent manner, with the
highest dose (6.0 mg/kg) yielding 16.1 adenomas/mouse. In
tricaprylin-treated control animals, there were 0.67 adenomas/mouse. Based
on the administered dose, DB[a,l]P was more active than other environmental
carcinogens including benzo[a]pyrene. As a function of time-integrated DNA
adduct levels, DB[a,l]P induced lung adenomas with about the same potency
as other PAHs, suggesting that the adducts formed by DB[a,l]P are similar
in carcinogenic potency to other PAHs in the strain A/J mouse lung model.
Analysis of the Ki- ras mutation spectrum in DB[a,l]P-induced lung tumors
revealed the predominant mutations to be G-->T transversions in the
first base of codon 12, A-->G transitions in the second base of codon
12, and A-->T transversions in the second or third base of codon 61,
concordant with the DNA adduct profile.
相似文献
2.
A D Kligerman M M Moore G L Erexson K H Brock C L Doerr J W Allen S Nesnow 《Cancer letters》1986,31(2):123-131
The genotoxicity of the cyclopenta-fused polycyclic aromatic hydrocarbon, benz[l]aceanthrylene (B[l]A), was evaluated in vitro using the L5178Y/TK+/- mouse lymphoma assay and in vivo using the mouse peripheral blood lymphocyte (PBL) culture system. The mutagenicity and sister chromatid exchange (SCE) inducing potential of B[l]A was then compared to that of benzo[a]pyrene (B[a]P). B[l]A appeared to be slightly less mutagenic than B[a]P at the TK locus, and each compound produced both small and large colony mutants indicating that they are clastogenic as well as mutagenic. Gross chromosome aberration analysis of treated L5178Y/TK+/- mouse lymphoma cells confirmed the clastogenicity of B[l]A in vitro. In the mouse PBL system, after administration by gavage, B[l]A was more cytotoxic and produced a sharper elevation in SCE frequency than B[a]P. 相似文献
3.
The field of mechanistic chemical carcinogenesis has evolved with the advent and advances in genomic, proteomic and metabolomic technologies. These advances allow mechanistic events along the process of exposure to frank tumors to be studied in great detail. Herein is reviewed an example of this approach using, propiconazole, a triazole-containing antifungal agent that is a mouse hepatocarcinogen. This review will highlight those toxicological, genomic, proteomic and metabolomic findings in mice that were used to describe a set of linked events that lead to propiconazole-induced hepatocarcinogenesis. Independent experimental proof of many of these events is presented that solidified this proposed mechanism of carcinogenic action for propiconazole. 相似文献
4.
Benzo[b]fluoranthene: tumorigenicity in strain A/J mouse lungs, DNA adducts and mutations in the Ki-ras oncogene 总被引:1,自引:0,他引:1
Mass Marc J.; Abu-Shakra Amal; Roop Barbara C.; Nelson Garret; Galati Anthony J.; Stoner Gary D.; Nesnow Stephen; Ross Jeffrey A. 《Carcinogenesis》1996,17(8):1701-1704
The polycyclic aromatic hydrocarbon benzo[b]fluoranthene (B[b]F)is a pervasive constituent of environmental combustion products.We sought to examine the lung tumorigenic activity of B[b]Fin strain A/J mice, to study the relationship between formationand decay of B[b]F-DNA adducts and to examine mutations in theKi-ras proto-oncogene in DNA from B[b]F-induced tumors. Micewere given i.p. injections of 0, 10, 50, 100 or 200 mg/kg bodywt and lung adenomas were scored after 8 months. B[b]F inducedsignificant numbers of mouse lung adenomas in a dose-relatedfashion, with the highest dose (200 mg/kg) yielding 6.95 adenomas/mouse, with 100% of the mice exhibiting an adenoma. In micegiven tricaprylin, the vehicle control, there were 0.60 adenomas/mouse,with 55% of the mice exhibiting an adenoma. Based on dose, B[b]Fwas less active than benzo[ 相似文献
5.
Linda A. Oglesby Claire Cudak Gaynelle Curtis Helen Garland Betty Hyatt Linda Montgomery Stephen Nesnow 《Cancer letters》1982,16(3):231-237
The C3H10T1/2CL8 mouse embryo oncogenic transformation bioassay system detects a wide variety of chemical carcinogens. However, one carcinogen that does not transform C3H10T1/2CL8 cells is the liver carcinogen N-2-fluorenylacetamide (FAA). Previous reports indicate that an activated form of FAA,N-acetoxy-FAA (N-OAc-FAA), transforms these fibroblasts. In an effort to understand these results, the metabolism and binding to cellular macromolecules of FAA and N-OAc-FAA using C3H10T1/2CL8 cells was investigated. C3H10T1/2CL8 cells metabolized FAA to 7-hydroxy-FAA, 2-fluorenylamine and N-hydroxy-FAA (N-OH-FAA) at rates of 5.03, 2.22 and 3.33 pmol/h/106 cells, respectively. N-OAc-FAA was bound to the DNA and RNA in C3H10T1/2CL8 cells to the extent of 10.6 and 3.6 FAA residues/106 nucleotides, respectively, and to protein at 21.9 pmol FAA residues/mg protein. However, binding of FAA to DNA and RNA at similar concentrations to N-OAc-FAA was less than 0.3 and 0.6 residues/106 nucleotides, respectively. These results strongly indicate that the inability of FAA to transform C3H10T1/2CL8 cells resides in the cells' inability to metabolize it sufficiently to the proximate carcinogen N-OH-FAA and not an inherent insensitivity to its activated forms. 相似文献
6.
A murine keratinocyte cell-mediated mutagenesis assay was characterizedand examined as an in vitro model system for studying the biotransformationof promutagens/procarcinogens by mouse skin. The assay usedliving cultured newborn SENCAR keratinocytes for the metabolicactivation of promutagens and Chinese hamster lung V-79 fibroblastsfor detection of resulting mutagens. Mutations at, or affecting,the hypoxanthine-guanine phosphoribosyltransferase locus werescored by resisistance to 6-thioguanine. The relative mutagenicitiesof several polycyclic aromatic hydrocarbons (PAHs) in the cell-mediatedassay correlated with the in vivo skin tumongenicity of thePAHs determined in a two-stage carcinogenesis protocol. Metabolicactivation of the promutagenic PAHs to ultimate mutagens wasdependent upon the presence of the cultured keratinocyte feederlayer. 7,8-Benzoflavone, a potent inhibitor of 7, 12-dimethylbenz-[a]anthracene (DMBA)-dependent initiation in mouse skin, inhibitedDMBA-dependent mutagenesis in the cell-mediated assay in a concentrationresponsive manner. The non-PAH promutagens, dimethylnitrosamine(DMN) and sterigmatocystin (STC) were both activated by culturedkeratinocytes to cytotoxic derivatives. DMN was neither mutagenicin the cell-mediated assay nor tumorigenic in mouse skin whentested in a two-stage carcinogenesis protocol. STC was weaklymutagenic and tumorigenic in mouse skin. 相似文献
7.
El-Bayoumy K Sharma AK Lin JM Krzeminski J Boyiri T King LC Lambert G Padgett W Nesnow S Amin S 《Chemical research in toxicology》2004,17(12):1591-1599
The environmental pollutant 6-nitrochrysene (6-NC) is a potent carcinogen in several animal models including the rat mammary gland. 6-NC can be activated to intermediates that can damage DNA by simple nitroreduction, ring oxidation, or a combination of ring oxidation and nitroreduction. Only the first pathway (nitroreduction) has been clearly established, and DNA adducts derived from this pathway have been fully characterized in in vitro systems. We also showed previously that the second pathway, ring oxidation leading to the formation of the bay region diol epoxide of 6-NC, is not responsible for the formation of the major DNA adduct in the mammary gland of rats treated with 6-NC. Therefore, in the present study, we explored the validity of the third pathway that involves the combination of both ring oxidation and nitroreduction of 6-NC to form trans-1,2-dihydroxy-1,2-dihydro-6-hydroxylaminochrysene (1,2-DHD-6-NHOH-C). During the course of this study, we synthesized for the first time 1,2-DHD-6-NHOH-C, N-(deoxyguanosin-8-yl)-6-aminochrysene, and N-(deoxyguanosin-8-yl)-1,2-dihydroxy-1,2-dihydro-6-aminochrysene. Incubation of 1,2-DHD-6-NHOH-C with calf thymus DNA resulted in the formation of three adducts. Upon LC/MS combined with 1H NMR analyses, the first eluting adduct was identified as 5-(deoxyguanosin-N2-yl)-1,2-dihydroxy-1,2-dihydro-6-aminochrysene [5-(dG-N2-yl)-1,2-DHD-6-AC], the second eluting adduct was identified as N-(deoxyguanosin-8-yl)-1,2-dihydroxy-1,2-dihydro-6-aminochrysene, and the last was identified as N-(deoxyinosin-8-yl)-1,2-dihydroxy-1,2-dihydro-6-aminochrysene. We also report here for the first time that among those adducts identified in vitro, only 5-(dG-N2-yl)-1,2-DHD-6-AC is the major DNA lesion detected in the mammary glands of rats treated with 6-NC. 相似文献
8.
Five doses of either N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or ethylnitrosourea (ENU) were tested as complete carcinogens, tumor initiators and tumor promoters in the SENCAR skin tumorigenesis model. As tumor initiators, MNNG-induced papillomas at all doses tested, while ENU was active from 10-40 mumol. As complete carcinogens, MNNG from doses of 0.5-5.0 mumol and ENU from doses of 10 mumol-40 mumol were potent inducers of both papillomas and carcinomas indicating that these agents are active as both tumor initiators and tumor promoters. 相似文献
9.
Previous work with low passage synchronized human foreskin fibroblast cell populations has indicated that benzo[a]pyrene (BP) can induce a carcinogenic event [3]. BP additionally has shown to damage DNA in logarithmically growing low passage cultures [9]. High passage cells, on the other hand, seem to be refractory to transformation by BP, even though this agent can induce DNA damage, similar to that seen in low passage cells. When low passage cells were treated with BP, the initial binding of the hydrocarbon was primarily to a cytoplasmic protein complex of molecular weight 12,500, while in high passage cells, a major portion of BP was bound to a protein complex of molecular weight 200,000. High-pressure liquid chromatography (HPLC) profiles of ethyl acetate extractable fractions from the BP-cytoplasmic protein complexes of low and high passage cells demonstrated that the majority of the BP remained unmetabolized. When nuclei were isolated from low and high passage cells prior to the HPLC analysis, the major component (90%) was again unmetabolized BP. The results suggest selective attachment of BP to different cytoplasmic protein complexes of logarithmically growing human diploid fibroblast cells dependent on the passage level of the cells. 相似文献
10.
The metabolism of alpha-naphthoflavone (ANF) was studied in hepatic microsomes from rats, mice, rabbits, and hamsters, species in which ANF exerts its biological activities. The major metabolites produced by all species were ANF-5,6-oxide, ANF-6-phenol, and ANF-7,8-dihydrodiol. Minor metabolites produced by all species were ANF-5,6-dihydrodiol, ANF-7-phenol, and ANF-9-phenol. In general, the total rates of metabolism were similar within all species: 22-32 nmol ANF metabolized/15 min/mg protein. Mouse liver microsomes were approximately 1.7 to 2.9 times as active as the other species on a nanomole of cytochrome P-450 basis. The major sites of enzymatic oxidation were the 5,6 and 7,8 bonds of ANF where for all species, 49-71% and 15-46% of the total metabolism occurred, respectively. 相似文献