Disease relevance of CCRIS 1208

• Mucin histochemistry by paradoxical concanavalin A staining in experimental gastric cancers induced in Wistar rats by N-methyl-N-nitro-N-nitrosoguanidine or 4-nitroquinoline 1-oxide [1].
• Fibroblasts from patients with hereditary cutaneous malignant melanoma are abnormally sensitive to the mutagenic effect of simulated sunlight and 4-nitroquinoline 1-oxide [2].
• The T4 enzyme was effective in xeroderma pigmentosum cells on DNA damaged by UV light but not in cells damaged by 4-nitroquinoline 1-oxide [3].
• Fischer rat embryo cells infected with xenotropic mouse type-C RNA viruses isolated from either NIH Swiss mice or C57L inbred mice were transformed by 4-nitroquinoline oxide or 3-methylcholanthrene under conditions in which neither treatment alone sufficed to induce transformation [4].
• The incidence of tongue carcinomas (TCs) induced by oral administration of 4-nitroquinoline 1-oxide in rats is strain dependent [5].

High impact information on CCRIS 1208

• The glandular stomach carcinogens N-methyl-N'-nitro-N-nitrosoguanidine (CAS: 70-25-7), N-ethyl-N'-nitro-N-nitrosoguanidine (CAS: 63885-23-4), N-propyl-N'-nitro-N-nitrosoguanidine, 4-nitroquinoline 1-oxide (CAS: 56-57-5), and N-nitroso-N-methylurethane (CAS: 615-53-2) induced UDS in the pyloric mucosa of the stomach [6].
• Skin fibroblasts from patients with familial adenomatosis coli (AC) and normal individuals were treated once with the carcinogen 4-nitroquinoline 1-oxide or N-methyl-N'-nitro-N-nitrosoguanidine and then passaged sequentially [7].
• Molecular biology of the carcinogen, 4-nitroquinoline 1-oxide [8].
• Nonterminal differentiation induces spontaneously transformed 3T3 T cells to revert to a nontransformed state and induces the revertant cell clones to become resistant to retransformation by UV irradiation or 4-nitroquinoline oxide treatment [9].
• Induction of the RAD2 gene after treatment of untransformed cells with 4-nitroquinoline 1-oxide was confirmed by direct examination of RAD2 mRNA [10].

Chemical compound and disease context of CCRIS 1208

• Sensitivity of subpopulations of mouse skin papillomas to malignant conversion by urethane or 4-nitroquinoline N-oxide [11].
• Hypersensitivity to cell killing and faulty repair of 1-beta-D-arabinofuranosylcytosine-detectable sites in human (ataxia-telangiectasia) fibroblasts treated with 4-nitroquinoline 1-oxide [12].
• Spleen cells from control and wasted (wst) mice, a putative animal model for the human genetic disease ataxia-telangiectasia, were tested for inhibition of replicative (semiconservative) DNA synthesis after treatments with bleomycin, gamma-irradiation, 4-nitroquinoline 1-oxide, and ultraviolet irradiation [13].
• Multidrug resistance protein and glutathione S-transferase P1-1 act in synergy to confer protection from 4-nitroquinoline 1-oxide toxicity [14].
• Mutation spectra of the two guanine adducts of the carcinogen 4-nitroquinoline 1-oxide in Escherichia coli. Influence of neighbouring base sequence on mutagenesis [15].

Biological context of CCRIS 1208

• CDC8 was also found to be inducible by DNA damage, but POL1 and URA3 were not inducible by 4-nitroquinoline 1-oxide [16].
• Detection of in vivo DNA repair synthesis in mouse liver and lung induced by treatment with benzo(a)pyrene or 4-nitroquinoline 1-oxide [17].
• Some characteristics of these cell lines, such as growth rates, chromosome numbers, UV sensitivities, and activities of unscheduled DNA syntheses induced by UV, 4-nitroquinoline 1-oxide, and N-methyl-N'-nitro-N-nitrosoguanidine, were determined [18].
• The spontaneous sister chromatid exchanges (SCEs) and SCEs induced by 50 microM methyl methanesulfonate, 1 microM 4-nitroquinoline 1-oxide, and 5 microM 3-amino-1-methyl-5H-pyrido[4,3-b]indole were examined in phytohemagglutinin-activated peripheral lymphocytes from 53 healthy adult donors [19].
• Quantitative trait loci affecting 4-nitroquinoline 1-oxide-induced tongue carcinogenesis in the rat [5].

Anatomical context of CCRIS 1208

• The level of mRNAs corresponding to the two groups of cDNAs is increased in the cytoplasm of human epidermal keratinocytes after both UV irradiation and treatment with 4-nitroquinoline 1-oxide or 12-O-tetradecanoylphorbol 13-acetate [20].
• Here we report the development of an effective colony-forming assay in which a SV40-transformed Werner fibroblast cell line is 6-18-fold more sensitive to 4-nitroquinoline 1-oxide than SV40-transformed normal cell lines [21].
• Induction of covalent DNA modifications and micronucleated erythrocytes by 4-nitroquinoline 1-oxide in adult and fetal mice [22].
• The DNA-damaging agent 4-nitroquinoline 1-oxide was applied to NIH-3T3 cells overexpressing normal IGF-IRs (NWTb3 cells) [23].
• A rat model was used for this purpose, in which dysplasia in the epithelium of the palate was induced by topical application of the carcinogen 4-nitroquinoline 1-oxide [24].

Associations of CCRIS 1208 with other chemical compounds

• The means of the mean spontaneous SCEs and SCEs induced by methyl methanesulfonate, 4-nitroquinoline 1-oxide, and 3-amino-1-methyl-5H-pyrido[4,3-b]indole in cells of these donors had coefficients of variability of 12, 14, 24, and 28%, respectively [19].
• Breakage of a DNA-protein complex induced by 4-nitroquinoline 1-oxide, 4-nitropyridine 1-oxide, and their derivatives in cultured mouse fibroblasts [25].
• Genetic characterization of adenine-3 mutants induced by 4-nitroquinoline 1-oxide and 4-hydroxyaminoquinoline 1-oxide in Neurospora crassa [26].
• The effects of three widely differing chemical carcinogens, 4-nitroquinoline 1-oxide, Adriamycin, and ethyleneimine, on DNA replication were studied by pulse labeling of DNA with [3H]thymidine and sedimentation analysis with alkaline sucrose gradients [27].
• Chemoprevention of 4-nitroquinoline 1-oxide-induced rat oral carcinogenesis by the dietary flavonoids chalcone, 2-hydroxychalcone, and quercetin [28].

Gene context of CCRIS 1208

• The SNQ2 gene of Saccharomyces cerevisiae, which encodes an ATP binding cassette protein responsible for resistance to the mutagen 4-nitroquinoline oxide, is regulated by the DNA-binding proteins PDR1 and PDR3 [29].
• Yeast gene YRR1, which is required for resistance to 4-nitroquinoline N-oxide, mediates transcriptional activation of the multidrug resistance transporter gene SNQ2 [30].
• However, exposure of cells to UV radiation, 4-nitroquinoline 1-oxide, or gamma radiation results in 4- to 6-fold enhanced expression of the RAD2 gene [31].
• RNR2 encodes a 1.5-kilobase mRNA whose levels increase 18-fold after treatment with the DNA-damaging agent 4-nitroquinoline 1-oxide [16].
• We showed that after 4-nitroquinoline 1-oxide-induced DNA damage, IGF-I induced exclusion of the p53 protein from the nucleus and led to its degradation in the cytoplasm, whereas p53 mRNA was unaffected [23].

Analytical, diagnostic and therapeutic context of CCRIS 1208

• Microscopic autoradiography of the complex spread on a Millipore filter, demonstrated that treatment of the cells with 4-nitroquinoline 1-oxide, or of the complex with Pronase E, gave rise to a relaxed mass of DNA fibers, in contrast to a compact mass of DNA from control cells [32].
• The formation of superoxide anion radical catalyzed by flavin-containing enzymes such as cytochrome P450 reductase or xanthine oxidase in the presence of 4-NQO or 4-nitroquinoline N-oxide was studied by spin-trapping experiments [33].
• Chemopreventive efficacy of all-trans-retinoic acid in biodegradable microspheres against epithelial cancers: results in a 4-nitroquinoline 1-oxide-induced oral carcinogenesis model [34].
• Effects of partial hepatectomy on initiation of liver cell foci by 4-nitroquinoline 1-oxide, a non-hepatocarcinogen, and generation of DNA adducts in rats [35].
• It involves the in vitro treatment of tooth germs with 4-nitroquinoline 1-oxide (4NQO) at the early bell stage and their subsequent transplantation into the kidney subcapsular space [36].

References