Tag: 100-200

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 29, 2008, Nair, Pramod C.; Sobhia, M. Elizabeth published an article.Electric Literature of 5709-67-1 The title of the article was Comparative QSTR studies for predicting mutagenicity of nitro compounds. And the article contained the following:

Mutagenicity and carcinogenicity are toxicol. endpoints which pose a great concern being the major determinants of cancers and tumors. Nitroarenes possess genotoxic properties as they can form various electrophilic intermediates and adducts with biol. systems. Different QSTR techniques were employed to develop models for the prediction of mutagenicity of nitroarenes using a diverse set of 197 nitro aromatic and hetero aromatic mols. The 2D and 3D QSTR methods used for model development gave statistically significant results. The alignment for 3D methods was obtained by maximum common substructures (MCS) approach, by taking the most mutagenic mol. of the dataset as the template. All the QSTR models were developed with the same set of training and test set mols. The 3D contours and 2D contribution maps along with mol. fingerprints provide useful information about the mutagenic potentials of the mols. The GFA based model shows thermodn. and topol. descriptors play an important role in characterizing mutagenicity of nitroarenes. At.-level thermodn. descriptor namely AlogP throws light on hydrophobic features and helps to understand the bilinear model. Topol. aspects of these classes of compounds were depicted by the fragment fingerprints and Balaban indexes obtained from HQSAR and GFA models, resp. The predictive abilities of 2D and 3D QSTR models may be useful as a vibrant predictive tool to screen out mutagenic nitroarenes and design safer non-mutagenic nitro compounds The experimental process involved the reaction of 2-Nitro-1H-benzo[d]imidazole(cas: 5709-67-1).Electric Literature of 5709-67-1

The Article related to mutagenicity nitroarene structure activity relationship, Toxicology: Methods (Including Analysis) and other aspects.Electric Literature of 5709-67-1

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 March 31, 2015, Liu, Yang-hua; Zhou, Zhi-xiang; Zhang, Xiao-long; Li, Han-dong published an article.Recommanded Product: 5709-67-1 The title of the article was Development of QSAR model for predicting mutagenicity of aromatic compounds. And the article contained the following:

Quant. structure-activity relationship (QSAR) model was developed for predicting the mutagenicity of aromatic compounds The log revertants data of S. typhimurium TA98 strain from Ames test have been collected. 225 Aromatic compounds were randomly divided into the training set with 186 mols. and test set with 39 mols. Multiple linear regression (MLR) anal. was used to select six descriptors from thousands of descriptors calculated by semi-empirical AM1 and E-dragon methods. The final QSAR model with six descriptors was internal and external validated. In addition, to validate the utility of our QSAR model for the chem. evaluation, three aromatic compounds were taken to test the predictive ability and reliability of the model exptl. The compounds selected for testing were not based on the predictions, thus spanning the range of predicted probabilities. The subsequently generated results of the Ames test were in good correspondence with the predictions and confirmed this approach as a useful means of predicting likely mutagenic risk of aromatic compounds The experimental process involved the reaction of 2-Nitro-1H-benzo[d]imidazole(cas: 5709-67-1).Recommanded Product: 5709-67-1

The Article related to mutagenicity aromatic compound qsar model, Toxicology: Methods (Including Analysis) and other aspects.Recommanded Product: 5709-67-1

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 January 31, 2021, Khanal, Jhabindra; Lim, Dae Young; Tayara, Hilal; Chong, Kil To published an article.Related Products of 443-72-1 The title of the article was A stacking ensemble-based computational prediction of DNA N6-methyladenine (6mA) sites in the Rosaceae genome. And the article contained the following:

DNA N6-methyladenine (6 mA) is an epigenetic modification that plays a vital role in a variety of cellular processes in both eukaryotes and prokaryotes. Accurate information of 6 mA sites in the Rosaceae genome may assist in understanding genomic 6 mA distributions and various biol. functions such as epigenetic inheritance. Various studies have shown the possibility of identifying 6 mA sites through experiments, but the procedures are time-consuming and costly. To overcome the drawbacks of exptl. methods, we propose an accurate computational paradigm based on a machine learning (ML) technique to identify 6 mA sites in Rosa chinensis (R.chinensis) and Fragaria vesca (F.vesca). To improve the performance of the proposed model and to avoid overfitting, a recursive feature elimination with cross-validation (RFECV) strategy is used to extract the optimal number of features (ONF) subset from five different DNA sequence encoding schemes, i.e., Binary Encoding (BE), Ring-Function-Hydrogen-Chem. Properties (RFHC), Electron-Ion-Interaction Pseudo Potentials of Nucleotides (EIIP), Dinucleotide Physicochem. Properties (DPCP), and Trinucleotide Physicochem. Properties (TPCP). Subsequently, we use the ONF subset to train a double layers of ML-based stacking model to create a bioinformatics tool named ‘i6mA-stack’. The experimental process involved the reaction of N-Methyl-7H-purin-6-amine(cas: 443-72-1).Related Products of 443-72-1

The Article related to rosaceae genome dna n6 methyladenine computational prediction, dna n6-methyladenine, machine learning, rfecv, sequence analysis, stacking, Biochemical Genetics: Genomic Processes and other aspects.Related Products of 443-72-1

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