Category: 55662-66-3

On August 31, 2012, Olipitz, Werner; Wiktor-Brown, Dominika; Shuga, Joe; Pang, Bo; McFaline, Jose; Lonkar, Pallavi; Thomas, Aline; Mutamba, James T.; Greenberger, Joel S.; Samson, Leona D.; Dedon, Peter C.; Yanch, Jacquelyn C.; Engelward, Bevin P. published an article.Formula: C6H5N3O The title of the article was Integrated molecular analysis indicates undetectable change in DNA damage in mice after continuous irradiation at ∼ 400-fold natural background radiation. And the article contained the following:

Background: In the event of a nuclear accident, people are exposed to elevated levels of continuous low dose-rate radiation. Nevertheless, most of the literature describes the biol. effects of acute radiation. Objectives: DNA damage and mutations are well established for their carcinogenic effects. We assessed several key markers of DNA damage and DNA damage responses in mice exposed to low dose-rate radiation to reveal potential genotoxic effects associated with low dose-rate radiation. Methods: We studied low dose-rate radiation using a variable low dose-rate irradiator consisting of flood phantoms filled with 125Iodine-containing buffer. Mice were exposed to 0.0002 cGy/min (∼400-fold background radiation) continuously over 5 wk. We assessed base lesions, micronuclei, homologous recombination (HR; using fluorescent yellow direct repeat mice), and transcript levels for several radiation-sensitive genes. Results: We did not observe any changes in the levels of the DNA nucleobase damage products hypoxanthine, 8-oxo-7,8-dihydroguanine, 1,N6-ethenoadenine, or 3,N4-ethenocytosine above background levels under low dose-rate conditions. The micronucleus assay revealed no evidence that low dose-rate radiation induced DNA fragmentation, and there was no evidence of double strand break-induced HR. Furthermore, low dose-rate radiation did not induce Cdkn1a, Gadd45a, Mdm2, Atm, or Dbd2. Importantly, the same total dose, when delivered acutely, induced micronuclei and transcriptional responses. Conclusions: These results demonstrate in an in vivo animal model that lowering the dose-rate suppresses the potentially deleterious impact of radiation and calls attention to the need for a deeper understanding of the biol. impact of low dose-rate radiation. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Formula: C6H5N3O

The Article related to ionizing radiation background radioactivity dna damage, Radiation Biochemistry: Effects In Mammals and other aspects.Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 30, 1993, Helmenstine, A.; Uziel, M.; Vo-Dinh, T. published an article.Application of 55662-66-3 The title of the article was Measurement of DNA adducts using surface-enhanced Raman spectroscopy. And the article contained the following:

Many hazardous pollutants have chem. groups of toxicol. importance that can be characterized and detected by Raman spectroscopy. Raman spectroscopists have recently been able to analyze dilute biol. samples as a result of enhancements in the Raman scattering cross section by factors up to 1010 when a compound is adsorbed on or near a special electron-conducting surface. These spectacular enhancement factors of the normally weak Raman scattering process help overcome the low sensitivity of Raman spectroscopy through a combination of electromagnetic and chem. interactions between the analyte mol. and the surface. The technique associated with this phenomenon is known as surface-enhanced Raman scattering spectroscopy (SERS). The special conductive surface responsible for the scattering enhancement is referred to as a SERS substrate. For the past few years the authors have developed the SERS technique, using practical SERS-active substrate materials based on silver-coated microspheres deposited on glass. A wide variety of biomarkers have been investigated, including benzo[a]pyrene, dibenz[a,h]anthracene epoxides, 1,N6-ethenoadenine, 3,N4-ethenocytosine, and other substances. These biomarkers were measured at a nanogram and subnanogram levels. The exptl. results are of great anal. interest, since these chems. are difficult to detect by other techniques, such as luminescence spectroscopy, because of the weak luminescence quantum yields of these DNA adducts. In this paper the potential usefulness of the SERS technique for assessing environmental and health effects from human exposure to toxic pollutants is demonstrated. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Application of 55662-66-3

The Article related to dna adduct carcinogen determination raman spectroscopy, surface enhanced raman spectroscopy dna adduct, Toxicology: Methods (Including Analysis) and other aspects.Application of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On July 31, 2004, Chen, Hauh-Jyun Candy; Wu, Chan-Fu; Hong, Chia-Liang; Chang, Chia-Ming published an article.Product Details of 55662-66-3 The title of the article was Urinary Excretion of 3,N4-Etheno-2′-deoxycytidine in Humans as a Biomarker of Oxidative Stress: Association with Cigarette Smoking. And the article contained the following:

Smokers are known to have elevated levels of lipid peroxidation, a form of oxidative stress. Etheno DNA adduct formation can originate from endogenous lipid peroxidation or from exogenous exposure of carcinogens. Using a modified stable isotope dilution GC/neg. ion chem. ionization/MS assay originally developed for urinary 3,N4-ethenocytosine (εCyt), the nucleoside 3,N4-etheno-2′-deoxycytidine (εdCyd) was detected for the first time in human urine. The presence of εdCyd in human urine was confirmed by LC/electrospray ionization/tandem MS. Concentrations of εdCyd in the 24 h urine samples from healthy individuals not occupationally exposed to industrial chems. were in the range between 0 and 0.80 nM. A statistically significant correlation was established between cigarette smoking and urinary excretion of εdCyd after being adjusted for creatinine (p = 0.004). Furthermore, the urinary total antioxidant capacity was found to correlate inversely with the εdCyd levels (r = -0.50, p = 0.02). The results indicate that urinary εdCyd may provide a valuable noninvasive biomarker for oxidative DNA damage. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Product Details of 55662-66-3

The Article related to urine etheno deoxycytidine biomarker oxidative stress cigarette smoking, Toxicology: Methods (Including Analysis) and other aspects.Product Details of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On December 31, 2001, Chen, Hauh-Jyun Candy; Lin, Tai-Chun; Hong, Chia-Liang; Chiang, Li-Chang published an article.Formula: C6H5N3O The title of the article was Analysis of 3,N4-Ethenocytosine in DNA and in Human Urine by Isotope Dilution Gas Chromatography/Negative Ion Chemical Ionization/Mass Spectrometry. And the article contained the following:

The promutagenic etheno DNA adducts have been detected in tissue DNA of rodents and humans from various exogenous and endogenous sources. While other etheno DNA adducts have been detected and quantified by isotope dilution gas chromatog./neg. ion chem. ionization/mass spectrometry (GC/NICI/MS), similar anal. for 3,N4-ethenocytosine (εCyt) has not been available. In this report, a GC/NICI/MS assay was developed for detection and quantification of εCyt in DNA and in human urine samples. The stable isotope of εCyt with 7 mass units higher than the normal εCyt was synthesized and used as internal standard of the assay. The adduct-enriched fraction of DNA hydrolyzate was derivatized with pentafluorobenzyl bromide before GC/NICI/MS anal. with selective ion monitoring at [M – 181]- fragments of pentafluorobenzylated εCyt and its isotope analog. One femtogram (S/N > 40) of pentafluorobenzylated εCyt was detected when injected on column with selective ion monitoring mode. The limit of quantification for the entire assay was 7.4 fmol of εCyt, which was approx. one thousand times lower than that of the HPLC/fluorescence assay for the nucleoside 3,N4-etheno-2′-deoxycytidine in DNA. Anal. of chloroacetaldehyde-treated calf thymus DNA by both GC/NICI/MS and HPLC/fluorescence methods provided similar adduct levels and thus verified the assay. This GC/NICI/MS method was used for anal. of εCyt in two smokers’ urine samples and the average level of εCyt was 101±17 pg/mL/g of creatinine. Thus, quantification of Cyt in DNA and in urine by this highly specific and ultrasensitive isotope dilution GC/NICI/MS assay may facilitate research on the role of εCyt in carcinogenesis and in cancer development. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Formula: C6H5N3O

The Article related to ethenocytosine dna adduct human urine isotope dilution gc ms, Toxicology: Methods (Including Analysis) and other aspects.Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On February 28, 2007, Chen, Hauh-Jyun Candy; Kao, Chi-Fu published an article.Product Details of 55662-66-3 The title of the article was Effect of gender and cigarette smoking on urinary excretion of etheno DNA adducts in humans measured by isotope dilution gas chromatography/mass spectrometry. And the article contained the following:

Endogenous formation of the promutagenic DNA adducts 1,N6-ethenoadenine (εAde) and 3,N4-ethenocytosine (εCyt) has been considered as biomarkers originated from lipid peroxidation Elevated levels of εAde and εCyt were observed in cancer-prone tissues, suggesting the validity of these adducts in cancer risk assessment. The presence of DNA base adducts in biol. fluids is considered to derive primarily from base excision repair (BER) systems. In this study, a modified gas chromatog./mass spectrometry (GC/MS) method is developed for simultaneous anal. of εAde and εCyt in human urine. After adjusting for creatinine concentration, urinary excretion of εAde, as well as εCyt, is much higher in 18 male smokers than in 10 male nonsmokers (p = 0.003 for εAde and p = 0.04 for εCyt). Furthermore, excretion of εAde and εCyt in 14 female nonsmokers is much higher than in 10 male nonsmokers (p = 0.002 for εAde and p = 0.005 for εCyt). These results suggest a statistically significant association between gender, as well as smoking, and excretion of εAde and εCyt. Moreover, urinary excretion of εAde in these 42 subjects correlates with that of εCyt (R2 = 0.6846, p < 0.0001). Measurement of urinary εAde and εCyt excretion should provide valid noninvasive biomarkers for carcinogenesis and chemoprevention studies. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Product Details of 55662-66-3

The Article related to gender cigarette smoking urine etheno dna adduct, Toxicology: Methods (Including Analysis) and other aspects.Product Details of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On September 30, 2001, Mokkapati, Sanath K.; Fernandez de Henestrosa, A. R.; Bhagwat, Ashok S. published an article.Category: imidazoles-derivatives The title of the article was Escherichia coli DNA glycosylase Mug: a growth-regulated enzyme required for mutation avoidance in stationary-phase cells. And the article contained the following:

The Escherichia coli DNA glycosylase Mug (mismatched uracil glycosylase) excises 3,N4-ethenocytosines (εC) and uracils from DNA, but its biol. function is obscure. This is because εC is not found in E. coli DNA, and uracil-DNA glycosylase (Ung), a distinct enzyme, is much more efficient at removing uracils from DNA than Mug. We find that Mug is overexpressed as cells enter stationary phase, and it is maintained at a fairly high level in resting cells. This is true of cells grown in rich or minimal media, and the principal regulation of mug is at the level of mRNA. Although the expression of mug is strongly dependent on the stationary-phase sigma factor, σS, when cells are grown in minimal media, it shows only a modest dependence on σS when cells are grown in rich media. When mug cells are maintained in stationary phase for several days, they acquire many more mutations than their mug+ counterparts. This is true in ung as well as ung+ cells, and a majority of new mutations may not be C to T. Our results show that the biol. role of Mug parallels its expression in cells. It is expressed poorly in exponentially growing cells and has no apparent role in mutation avoidance in these cells. In contrast, Mug is fairly abundant in stationary-phase cells and has an important anti-mutator role at this stage of cell growth. Thus, Mug joins a very small coterie of DNA repair enzymes whose principal function is to avoid mutations in stationary-phase cells. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Category: imidazoles-derivatives

The Article related to dna glycosylase mug stationary phase mutation avoidance, escherichia dna glycosylase mug stationary phase mutation avoidance, gene mug escherichia stationary phase, Biochemical Genetics: Genomic Processes and other aspects.Category: imidazoles-derivatives

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 25, 1997, Hang, B.; Singer, B.; Margison, G. P.; Elder, R. H. published an article.Synthetic Route of 55662-66-3 The title of the article was Targeted deletion of alkylpurine-DNA-N-glycosylase in mice eliminates repair of 1,N6-ethenoadenine and hypoxanthine but not of 3,N4-ethenocytosine or 8-oxoguanine. And the article contained the following:

It has previously been reported that 1,N6-ethenoadenine (εA), deaminated adenine (hypoxanthine, Hx), and 7,8-dihydro-8-oxoguanine (8-oxoG), but not 3,N4-ethenocytosine (εC), are released from DNA in vitro by the DNA repair enzyme alkylpurine-DNA-N-glycosylase (APNG). To assess the potential contribution of APNG to the repair of each of these mutagenic lesions in vivo, we have used cell-free extracts of tissues from APNG-null mutant mice and wild-type controls. The ability of these extracts to cleave defined oligomers containing a single modified base was determined The results showed that both testes and liver cells of these knockout mice completely lacked activity toward oligonucleotides containing εA and Hx, but retained wild-type levels of activity for εC and 8-oxoG. These findings indicate that (i) the previously identified εA-DNA glycosylase and Hx-DNA glycosylase activities are functions of APNG; (ii) the two structurally closely related mutagenic adducts εA and εC are repaired by sep. gene products; and (iii) APNG does not contribute detectably to the repair of 8-oxoG. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Synthetic Route of 55662-66-3

The Article related to apng glycosylase dna excision repair, ethenoadenine hypoxanthine ethenocysteine apng glycosylase repair, mouse apng glycosylase dna excision repair, Biochemical Genetics: Genomic Processes and other aspects.Synthetic Route of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On April 29, 2003, Sung, Jung-Suk; Mosbaugh, Dale W. published an article.Category: imidazoles-derivatives The title of the article was Escherichia coli Uracil- and Ethenocytosine-Initiated Base Excision DNA Repair: Rate-Limiting Step and Patch Size Distribution. And the article contained the following:

The rate, extent, and DNA synthesis patch size of base excision repair (BER) were measured using Escherichia coli GM31 cell-free extracts and a pGEM (form I) DNA substrate containing a site-specific uracil or ethenocytosine target. The rate of complete BER was stimulated (∼3-fold) by adding exogenous E. coli DNA ligase to the cell-free extract, whereas addition of E. coli Ung, Nfo, Fpg, or Pol I did not stimulate BER. Hence, DNA ligation was identified as the rate-limiting step in the E. coli BER pathway. The addition of exogenous DNA polymerase I caused modest inhibition of BER, which was overcome by concomitant addition of DNA ligase. Repair patch size determinations were performed to assess the distribution of DNA synthesis associated with both uracil- and ethenocytosine-initiated BER. During the early phase (0-5 min) of the BER reaction, the large majority of repair events resulted from short patch (1-nucleotide) DNA synthesis. However, during the late phase (>10 min) both short and long (2-20 nucleotide) patches were observed, with long patch BER progressively dominating the repair process. In addition, the patch size distribution was influenced by the ratio of DNA polymerase I to DNA ligase activity in the reaction. A novel mode of BER was identified that involved DNA synthesis tracts of >205 nucleotides in length and termed very-long patch BER. This BER process was dependent upon DNA polymerase I since very-long patch BER was inhibited by DNA polymerase I antibody and addition of excess DNA polymerase I reversed this inhibition. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Category: imidazoles-derivatives

The Article related to escherichia uracil ethenocytosine excision repair dna ligase polymerase, dna base excision repair mechanism rate patch size escherichia, Biochemical Genetics: Genomic Processes and other aspects.Category: imidazoles-derivatives

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On December 1, 2007, Al Mamun, Abu Amar M. published an article.COA of Formula: C6H5N3O The title of the article was Elevated expression of DNA polymerase II increases spontaneous mutagenesis in Escherichia coli. And the article contained the following:

Escherichia coli DNA polymerase II (Pol-II), encoded by the SOS-regulated polB gene, belongs to the highly conserved group B (α-like) family of “high-fidelity” DNA polymerases. Elevated expression of polB gene was recently shown to result in a significant elevation of translesion DNA synthesis at 3, N4-ethenocytosine lesion with concomitant increase in mutagenesis. Here, I show that elevated expression of Pol-II leads to an approx. 100-fold increase in spontaneous mutagenesis in a manner that is independent of SOS, umuDC, dinB, recA, uvrA and mutS functions. Cells grow slowly and filament with elevated expression of Pol-II. Introduction of carboxy terminus (“β interaction domain”) mutations in polB eliminates elevated spontaneous mutagenesis, as well as defects in cell growth and morphol., suggesting that these abilities require the interaction of Pol-II with the β processivity subunit of DNA polymerase III. Introduction of a mutation in the proofreading exo motif of polB elevates mutagenesis by a further 180-fold, suggesting that Pol-II can effectively compete with DNA polymerase III for DNA synthesis. Thus, Pol-II can contribute to spontaneous mutagenesis when its expression is elevated. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).COA of Formula: C6H5N3O

The Article related to escherichia dna polymerase ii expression motif spontaneous mutagenesis, Biochemical Genetics: Genomic Processes and other aspects.COA of Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 29, 2006, Al Mamun, Abu Amar M.; Humayun, M. Zafri published an article.Related Products of 55662-66-3 The title of the article was Escherichia coli DNA polymerase II can efficiently bypass 3,N4-ethenocytosine lesions in vitro and in vivo. And the article contained the following:

Escherichia coli DNA polymerase II (pol-II) is a highly conserved protein that appears to have a role in replication restart, as well as in translesion synthesis across specific DNA adducts under some conditions. Here, we have investigated the effects of elevated expression of pol-II (without concomitant SOS induction) on translesion DNA synthesis and mutagenesis at 3,N 4-ethenocytosine (εC), a highly mutagenic DNA lesion induced by oxidative stress as well as by exposure to industrial chems. such as vinyl chloride. In normal cells, survival of transfected M13 single-stranded DNA bearing a single εC residue (εC-ssDNA) is about 20% of that of control DNA, with about 5% of the progeny phage bearing a mutation at the lesion site. Most mutations are C → A and C → T, with a slight predominance of transversions over transitions. In contrast, in cells expressing elevated levels of pol-II, survival of εC-ssDNA is close to 100%, with a concomitant mutation frequency of almost 99% suggesting highly efficient translesion DNA synthesis. Furthermore, an overwhelming majority of mutations at εC are C → T transitions. Purified pol-II efficiently catalyzes translesion synthesis at εC in vitro, accompanied by high levels of mutagenesis with the same specificity. These results suggest that the observed in vivo effects in pol-II over-expressing cells are due to pol-II-mediated DNA synthesis. Introduction of mutations in the carboxy terminus region (β interaction domain) of polB eliminates in vivo translesion synthesis at εC, suggesting that the ability of pol-II to compete with pol-III requires interaction with the β processivity subunit of pol-III. Thus, pol-II can compete with pol-III for translesion synthesis. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Related Products of 55662-66-3

The Article related to escherichia dna polymerase ii ethenocytosine lesion bypass mutagenesis, Biochemical Genetics: Genomic Processes and other aspects.Related Products of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem