Disease relevance of 4-NITROQUINOLINE-N-OXIDE

• Effluent extracts coinjected with a direct-acting carcinogen [N-methyl-N'-nitro-N-nitrosoguanidine (CAS: 56-57-5)] did not increase the incidence of hepatic neoplasms (with and without exogenous S-9 activation) [1].
• In this study, we assessed the protective effect of topical application of a polyphenolic fraction isolated from green tea (GTP) against spontaneous as well as benzoyl peroxide (BPO)- and 4-nitroquinoline-N-oxide (4-NQO)-enhanced malignant conversion of chemically induced skin papillomas in SENCAR mice [2].
• Oral carcinomas of the tongue and palate were induced in Sprague-Dawley male rats by painting their palates three times weekly for 7-8 months with 0.5% (w/v) 4-nitroquinoline-N-oxide [3].
• Epithelial dendritic cells (EDC) and connective tissue macrophages were examined during the induction and growth of oral squamous cell carcinomas in Sprague-Dawley rats treated with the carcinogen 4-nitroquinoline N-oxide (4NQO) and the immune potentiator Corynebacterium parvum [4].
• After labelling with GS-I-B4, the fluorescent intensity of the basal and parabasal epithelial cells was significantly less after 9 months of 4NQO treatment and in overt squamous cell carcinomas compared to controls [5].

High impact information on 4-NITROQUINOLINE-N-OXIDE

• The incidences of neoplasms and preneoplastic lesions of the tongue in animals given 5 ppm 4-nitroquinoline-1-oxide (4-NQO; CAS: 56-57-5) in the drinking water for 16 weeks and followed by 20% betel nut in the diet for 40 weeks were significantly higher than those in animals given 4-NQO alone [6].
• Using a PHR1-lacZ fusion gene in which expression of beta-galactosidase is regulated by PHR1 5' regulatory elements, we found that exposure of cells to 254-nm light, 4-nitroquinoline-N-oxide, methyl methanesulfonate, and N-methyl-N'-nitro-N-nitrosoguanidine induced synthesis of increased amounts of fusion protein [7].
• We found that 4-nitroquinoline-N-oxide (4NQO) is a powerful inducer of soxS, > 10-fold more potent than paraquat [8].
• Potent intracellular oxidative stress exerted by the carcinogen 4-nitroquinoline-N-oxide [8].
• Human mononuclear leukocytes were exposed to prooxidants such as H2O2, phorbol-12-myristate-13-acetate, and 4-nitroquinoline-N-oxide, and the effects on induction of DNA damage and repair were evaluated [9].

Chemical compound and disease context of 4-NITROQUINOLINE-N-OXIDE

• The plasmid pSK1002 (umuC'-'lacZ) could increase the number of revertants induced by methyl methanesulfonate (MMS) and 4-nitroquinoline-N-oxide (4NQO) in Salmonella typhimurium TA 1535 (his-) [10].
• Pulsed field gel electrophoresis (PFGE) has been used to detect aberrations of the chromosomal banding pattern referred to as chromosomal aberrations arising after treatment of yeast strain S. cerevisiae MP1 with the three different genotoxic substances 4-nitroquinoline-N-oxide (4-NQO), methotrexate (MTX) and 2-amino-6-mercaptopurine (AMP) [11].
• Salmonella typhimurium strains TA98 and TA100 were exposed in an appropriate liquid medium to the direct mutagens 4-nitroquinoline-N-oxide and methyl methanesulphonate, respectively, and to the indirect mutagen 2-aminoanthracene [12].
• Toxicity, mutagenicity and suppression on the mutagenesis induced by a direct mutagen, 4-nitroquinoline-N-oxide (4-NQO) on Salmonella typhimurium TA 100, by the various methanol extracts of the prepared soybean koji and unfermented soybean were determined and compared [13].

Biological context of 4-NITROQUINOLINE-N-OXIDE

• Previous work has identified a novel Cys(6)-Zn(II)(2) transcription factor designated Yrr1p as mutant forms of this protein confer high level resistance to the cell cycle inhibitor reveromycin A and DNA damaging agent 4-nitroquinoline-N-oxide [14].
• We show here that a pdr1-3 mutant exhibits a PDR phenotype, including elevated resistance to the mutagen 4-nitroquinoline-N-oxide, a known substrate for Snq2 but not for Pdr5 [15].
• Loss of expression of basement membrane proteins reflects anomalies of chromosomes 3 and 12 in the rat 4-nitroquinoline-N-oxide model of oral carcinogenesis [16].
• This study examined the cytogenetic characteristics of keratinocyte cell lines derived from rat oral tissues treated in vivo with the carcinogen 4-nitroquinoline-N-oxide [16].
• In one cell line derived from 4NQO treatment in vitro, there was evidence that aneuploidy was an early marker, preceding anchorage independence and tumorigenicity in athymic mice [17].

Anatomical context of 4-NITROQUINOLINE-N-OXIDE

• There were no significant differences in the number of Ia+ EDC between the infiltrating and the non-invasive overlying epithelium of the lingual carcinomas and the non-invasive lingual epithelium treated with either 4NQO or 4NQO + C.parvum.(ABSTRACT TRUNCATED AT 400 WORDS)[4]
• This study examined the characteristics of premalignant oral epithelial cell lines derived from non-invasive palatal and lingual mucosa of rats painted with the carcinogen 4-nitroquinoline N-oxide (4NQO) in vivo [18].
• Stationary cultures of human fibroblasts were exposed to various doses of carcinogens (UV-light at 254 nm, N-acetoxy-acetyl-aminofluorene, ethyl-methane sulfonate, N-methylnitro-nitrosoguanidine, mitomycin C and 4-nitroquinoline-N-oxide) at different time-intervals before preparing crude cellular extracts and assaying for ligase activity [19].
• BALB/c-3T3 cells displayed a dose-dependent transformation response to a variety of carcinogens (polycyclic hydrocarbons, methylating agents, ethylating agents, aflatoxin B1 [AFB1], and 4-nitroquinoline-N-oxide [4-NQO]) [20].
• It is suggested that de novo formation of free oral sebaceous glands is caused by a metaplastic process due to local irritants among which the carcinogen 4NQO seems particularly powerful [21].

Associations of 4-NITROQUINOLINE-N-OXIDE with other chemical compounds

• The addition of 6.8 microM 1-methyl-3-nitro-1-nitrosoguanidine, 5.3 microM 4-nitroquinoline-N-oxide, and 4-20.3 microM 1-nitropyrene resulted in the induction of mutations at the HGPRT locus as determined by 6-thioguanine resistance [22].
• Using different plasmid-chromosome and direct-repeat recombination constructs in which transcription is driven from either the P(GAL1)- or the P(tet)-regulated promoters, we have shown that either 4-nitroquinoline-N-oxide (4-NQO) or methyl methanesulfonate (MMS) produces a synergistic increase of recombination when combined with transcription [23].
• Demethylation inhibitor (DMI)-resistant strains of the plant pathogenic fungus Penicillium digitatum were shown to be simultaneously resistant to cycloheximide, 4-nitroquinoline-N-oxide (4NQO), and acriflavine [24].
• MNNG does not belong to that class of compounds typified by ultraviolet light or 4-nitroquinoline-N-oxide which exhibit both random and non-random components of mutagenesis [25].
• Isopalmitic acid also inhibited mutagenesis induced 4-nitroquinoline-N-oxide (4NQO), and 7, 12-dimethyl benz[a]anthracene (DMBA), and was found to inhibit the metabolic activation of DMBA [26].

Gene context of 4-NITROQUINOLINE-N-OXIDE

• The isolated gene exhibited 48.9% identity with the S. cerevisiae ATR1 gene conferring resistance to aminotriazole and 4-nitroquinoline- N-oxide and encoded a protein of 553 amino acids [27].
• The results indicate that the autocrine production of TGF-alpha and TGF-beta are not accurate markers of tumour progression in the rat 4NQO model of oral carcinogenesis [28].
• Gene SNQ2 of Saccharomyces cerevisiae, which confers resistance to 4-nitroquinoline-N-oxide and other chemicals, encodes a 169 kDa protein homologous to ATP-dependent permeases [29].
• Keratinocytes from 4NQO-treated tissues predominantly had fewer epidermal growth factor (EGF) receptors than normal controls [18].
• Molecular characterization of the two genes SNQ and SFA that confer hyperresistance to 4-nitroquinoline-N-oxide and formaldehyde in Saccharomyces cerevisiae [30].

Analytical, diagnostic and therapeutic context of 4-NITROQUINOLINE-N-OXIDE

• The inflammatory infiltrate induced in palatal and lingual mucosae of Sprague-Dawley rats after treatment with the water-soluble carcinogen 4-nitroquinoline-N-oxide (4NQO) was investigated using immunohistochemical methods on acetone-fixed frozen sections [31].
• The comet assay was conducted after treatment of Episkin with UV, Lomefloxacin and UV or 4-nitroquinoline-N-oxide (4NQO) [32].
• Furthermore, ARC-G exhibited potent anti-tumor-promoting activity on two-stage carcinogenesis test of mouse pulmonary tumors induced by 4-nitroquinoline-N-oxide as an initiator and glycerol as a promoter [33].

References