Month: November 2022

Oesch, Franz; Doerjer, Gerhard published an article in 1982, the title of the article was Detection of N2,3-ethenoguanine in DNA after treatment with chloroacetaldehyde in vitro.Electric Literature of 55662-66-3 And the article contains the following content:

The reaction of chloroacetaldehyde  [107-20-0], a reactive metabolite of the carcinogen vinyl chloride, with DNA produces in addition to the hitherto known adducts, 1,N6-ethenoadenine  [13875-63-3] and 3,N4-ethenocytosine  [55662-66-3], an ethenoguanine adduct, namely N2,3-ethenoguanine (I) [62962-42-9]. This adduct is formed in the reaction of chloroacetaldehyde with the free base as well. After DNA hydrolysis followed by isolation of this new adduct by high-performance liquid chromatog., its mass spectrum and fluorescence spectrum are identical with those reported in the literature. The formation of only I out of several theor. possible reaction products allows the formulation of a reaction scheme. The absence of 7-(2-oxoethyl)guanine, another recently detected DNA adduct of vinyl chloride, in chloroacetaldehyde-treated DNA suggests its origin from the other reactive metabolite of vinyl chloride, chloroethylene oxide. The potential of I to lead to misincorporation of deoxythymidine monophosphate opposite to guanine and the high fluorescence of this adduct provide it with potentially high biol. significance and ease of anal. monitoring. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Electric Literature of 55662-66-3

The Article related to ethenoguanine formation dna chloroacetaldehyde, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Electric Literature of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On July 21, 1998, Saparbaev, Murat; Laval, Jacques published an article.Electric Literature of 55662-66-3 The title of the article was 3,N4-ethenocytosine, a highly mutagenic adduct, is a primary substrate for Escherichia coli double-stranded uracil-DNA glycosylase and human mismatch-specific thymine-DNA glycosylase. And the article contained the following:

Exocyclic DNA adducts are generated in cellular DNA by various industrial pollutants such as the carcinogen vinyl chloride and by endogenous products of lipid peroxidation The etheno derivatives of purine and pyrimidine bases 3,N4-ethenocytosine (εC), 1,N6-ethenoadenine (εA), N2,3-ethenoguanine, and 1,N2-ethenoguanine cause mutations. The εA residues are excised by the human and the Escherichia coli 3-methyladenine-DNA glycosylases (ANPG and AlkA proteins, resp.), but the enzymes repairing εC residues have not yet been described. We have identified two homologous proteins present in human cells and E. coli that remove εC residues by a DNA glycosylase activity. The human enzyme is an activity of the mismatch-specific thymine-DNA glycosylase (hTDG). The bacterial enzyme is the double-stranded uracil-DNA glycosylase (dsUDG) that is the homolog of the hTDG. In addition to uracil and εC-DNA glycosylase activity, the dsUDG protein repairs thymine in a G/T mismatch. The fact that εC is recognized and efficiently excised by the E. coli dsUDG and hTDG proteins in vitro suggests that these enzymes may be responsible for the repair of this mutagenic lesion in vivo and be important contributors to genetic stability. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Electric Literature of 55662-66-3

The Article related to ethenocytosine mutagenic adduct dna glycosylase, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Electric Literature of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On August 31, 1993, Villemin, D.; Cherqaoui, D.; Cense, J. M. published an article.HPLC of Formula: 5709-67-1 The title of the article was Neural networks studies: quantitative structure-activity relationship of mutagenic aromatic nitro compounds. And the article contained the following:

The application of neural networks to the study of quant. structure-activity relationship (QSAR) of mutagenic aromatic and heteroaromatic nitro compounds is reported. The results obtained are compared with the results given by a multiple linear regression. It is shown that neural networks prediction is more accurate than regression anal. prediction. The experimental process involved the reaction of 2-Nitro-1H-benzo[d]imidazole(cas: 5709-67-1).HPLC of Formula: 5709-67-1

The Article related to aromatic nitro compound mutagenicity qsar model, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.HPLC of Formula: 5709-67-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On April 20, 1993, Palejwala, Vaseem A.; Rzepka, Robert W.; Humayun, M. Zafri published an article.Reference of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was UV irradiation of Escherichia coli modulates mutagenesis at a site-specific ethenocytosine residue on M13 DNA. Evidence for an inducible recA-independent effect. And the article contained the following:

Mutagenic action of chem. and phys. mutagens is mediated through DNA damage and subsequent misreplication at sites of unrepaired damage. Most DNA damage is noninstructive in the sense that the causative chem. modification either destroys the template information or renders it inaccessible to the DNA polymerase. Noninstructive adducts possess high genotoxicity because they stop DNA replication. Replication past noninstructive adducts is thought to depend on induced functions in addition to the regular replication machinery. In E. coli, noninstructive DNA damage leads to induction of the SOS regulon, which in turn is thought to provide the inducible functions required for replicative bypass of the lesion. Because of the absence of accessible template instruction, base incorporation opposite noninstructive lesions is inherently error-prone and results in mutagenesis. Ethenocytosine (εC), an exocyclic DNA lesion induced by carcinogens such as vinyl chloride and urethane, is a highly mutagenic, noninstructive lesion on the basis of its template characteristics in vivo and vitro. However, mutagenesis at εC does not require SOS functions, as evidenced by efficient mutagenesis in recA-deleted E. coli. Even though efficient mutagenesis in recA-deleted cells shows a lack of SOS dependence, the question remains whether SOS induction can modulate mutagenesis opposite εC. To exam. the possible contribution of SOS functions to mutagenesis at εC, an M13 duplex circular DNA mol. containing an εC residue was constructed at a unique site. The construct was transfected into nonirradiated or UV-irradiated E. coli. The frequency as well as specificity of the mutations induced under a number of conditions was determined by using a multiplex DNA sequencing technol. Without prior UV irradiation, ∼33% of the host cells show a significant increase in mutagenesis, with most of the increase accounted for by an increase in C→A transversions. Surprisingly, essentially identical effects were observed in irradiated recA-deleted cells as well as in umuC-deficient cells, suggesting that the observed UV modulation of mutagenesis is independent of the SOS pathway. These observations suggest the existence of a recA-independent UV-inducible mutagenic mechanism in E. coli. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Reference of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to uv mutagenesis dna ethenocytosine site escherichia, Radiation Biochemistry: Effects In Microorganisms and other aspects.Reference of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On October 31, 1992, Kusmierek, J. T.; Singer, B. published an article.Quality Control of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was 1,N2-Ethenodeoxyguanosine: properties and formation in chloroacetaldehyde-treated polynucleotides and DNA. And the article contained the following:

1,N2-Etheno-2′-deoxyguanosine (1,N2-εdGuo) (I), not previously reported as a product of chloroacetaldehyde (CAA) reaction, was synthesized and characterized. Reaction of deoxyguanosine with CAA in DMF in the presence of K2CO3 led to the preparation of pure 1,N2-εdGuo with a 55% yield. PKa values are 2.2 and 9.2. The anionic form of the compound exhibits weak but defined fluorescence; the intensity is similar to that of N2,3-etheno-2′-deoxyguanosine (N2,3-εdGuo) at neutrality. The stability of the glycosyl bond of 1,N2-εdGuo (t1/2 = 2.3 h at 37°, pH 1) is 10-fold greater than of unmodified deoxyguanosine and at least 1000-fold greater than that of isomeric N2,3-εdGuo. Reaction of CAA with model polynucleotides indicates that hydrogen bonding of guanine residues in the double-stranded structures is, as expected, an important factor in the formation of 1,N2-ethenoguanine. In contrast, the formation of isomeric N2,3-ethenoguanine is relatively independent of whether the DNA is single- or double-stranded. In salmon sperm DNA, reacted with CAA at neutrality, the formation of 1,N2-ethenoguanine could be demonstrated. However, the authors find the efficiency of formation of this adduct in double-stranded DNA is lower than that of all other etheno derivatives The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Quality Control of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to chloroacetaldehyde ethenodeoxyguanosine polynucleotide dna, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Quality Control of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On February 3, 2009, Knutson, Charles G.; Rubinson, Emily H.; Akingbade, Dapo; Anderson, Carolyn S.; Stec, Donald F.; Petrova, Katya V.; Kozekov, Ivan D.; Guengerich, F. Peter; Rizzo, Carmelo J.; Marnett, Lawrence J. published an article.COA of Formula: C6H5N3O The title of the article was Oxidation and Glycolytic Cleavage of Etheno and Propano DNA Base Adducts. And the article contained the following:

Non-invasive strategies for the anal. of endogenous DNA damage are of interest for the purpose of monitoring genomic exposure to biol. produced chems. The authors have focused the authors’ research on the biol. processing of DNA adducts and how this may impact the observed products in biol. matrixes. Preliminary research has revealed that pyrimidopurinone DNA adducts are subject to enzymic oxidation in vitro and in vivo and that base adducts are better substrates for oxidation than the corresponding 2′-deoxynucleosides. The authors tested the possibility that structurally similar exocyclic base adducts may be good candidates for enzymic oxidation in vitro. The authors investigated the in vitro oxidation of several endogenously occurring etheno adducts [1,N2-ε-guanine (1,N2-ε-Gua), N2,3-ε-Gua, heptanone-1,N2-ε-Gua, 1,N6-ε-adenine (1,N6-ε-Ade), and 3,N4-ε-cytosine (3,N4-ε-Cyt)] and their corresponding 2′-deoxynucleosides. Both 1,N2-ε-Gua and heptanone-1,N2-ε-Gua were substrates for enzymic oxidation in rat liver cytosol; heteronuclear NMR experiments revealed that oxidation occurred on the imidazole ring of each substrate. In contrast, the partially or fully saturated pyrimidopurinone analogs [i.e., 5,6-dihydro-M1G and 1,N2-propanoguanine (PGua)] and their 2′-deoxynucleoside derivatives were not oxidized. The 2′-deoxynucleoside adducts, 1,N2-ε-dG and 1,N6-ε-dA, underwent glycolytic cleavage in rat liver cytosol. Together, these data suggest that multiple exocyclic adducts undergo oxidation and glycolytic cleavage in vitro in rat liver cytosol, in some instances in succession. These multiple pathways of biotransformation produce an array of products. Thus, the biotransformation of exocyclic adducts may lead to an addnl. class of biomarkers suitable for use in animal and human studies. 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 etheno propano dna base adduct oxidation glycolytic cleavage, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.COA of Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On December 21, 2004, Choi, Jun-Hyuk; Pfeifer, Gerd P. published an article.COA of Formula: C6H5N3O The title of the article was DNA damage and mutations produced by chloroacetaldehyde in a CpG-methylated target gene. And the article contained the following:

Chloroacetaldehyde (CAA) is a metabolite of the human carcinogen vinyl chloride. CAA produces several types of DNA adducts including the exocyclic base adducts 3,N4-ethenocytosine, 1,N6-ethenoadenine, N2,3-ethenoguanine, and 1,N2-ethenoguanine. Adducts of CAA with 5-methylcytosine have not yet been characterized. Here the authors have analyzed the mutational spectra produced by CAA in the supF gene of the pSP189 shuttle vector when present in either an unmethylated or CpG-methylated state. The vectors were replicated in human nucleotide excision repair-deficient XP-A fibroblasts. The mutational spectra obtained with the unmethylated and methylated supF target genes were generally similar with a preponderance of C/G to T/A transitions and C/G to A/T transversions. CAA-induced DNA adducts were mapped along the supF gene by using thermostable thymine DNA glycosylase (TDG) in conjunction with ligation-mediated PCR or by a Taq polymerase stop assay. Prominent CAA-induced TDG-sensitive sites were seen at several CpG positions but were independent of methylation. Methylated CpG sites were sites of CAA-induced mutations but were not the major mutational hotspots. Taq polymerase arrest sites were observed at numerous sequence positions in the supF gene and reflected the rather broad distributions of mutations along the sequence. We conclude that methylated CpG sites are not preferential targets for chloroacetaldehyde-induced mutagenesis. 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 dna damage mutation chloroacetaldehyde cpg methylation supf gene, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.COA of Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On March 7, 2003, Abu, Mika; Waters, Timothy R. published an article.COA of Formula: C6H5N3O The title of the article was The Main Role of Human Thymine-DNA Glycosylase Is Removal of Thymine Produced by Deamination of 5-Methylcytosine and Not Removal of Ethenocytosine. And the article contained the following:

Metabolites of vinyl chloride react with cytosine in DNA to form 3,N4-ethenocytosine. Recent studies suggest that ethenocytosine is repaired by the base excision repair pathway with the ethenobase being removed by thymine-DNA glycosylase. Here single turnover kinetics have been used to compare the excision of ethenocytosine by thymine-DNA glycosylase with the excision of thymine. The effect of flanking DNA sequence on the excision of ethenocytosine was also investigated. The 34-bp duplexes studied here fall into three categories. Ethenocytosine base-paired with guanine within a CpG site (i.e. CpG·εC-DNA) was by far the best substrate having a specificity constant (k2/Kd) of 25.1×106 M-1 s-1. The next best substrates were DNA duplexes containing TpG·εC, GpG·εC, and CpG·T. These had specificity constants 45-130 times smaller than CpG·εC-DNA. The worst substrates were DNA duplexes containing ApG·εC and TpG·T, which had specificity constants, resp., 1,600 and 7,400 times lower than CpG·εC-DNA. DNA containing ethenocytosine was bound much more tightly than DNA containing a G·T mismatch. This is probably because thymine-DNA glycosylase can flip out ethenocytosine from a G·εC base pair more easily than it can flip out thymine from a G·T mismatch. Because thymine-DNA glycosylase has a larger specificity constant for the removal of ethenocytosine, it has been suggested its primary purpose is to deal with ethenocytosine. However, these results showing that thymine-DNA glycosylase has a strong sequence preference for CpG sites in the excision of both thymine and ethenocytosine suggest that the main role of thymine-DNA glycosylase in vivo is the removal of thymine produced by deamination of 5-methylcytosine at CpG sites. 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 thymine dna glycosylase deamination methylcytosine ethenocytosine, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.COA of Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 16, 1994, Simha, Devendranath; Yadav, Deepmala; Rzepka, Robert W.; Palejwala, Vaseem A.; Humayun, M. Zafri published an article.Computed Properties of 55662-66-3 The title of the article was Base incorporation and extension at a site-specific ethenocytosine by Escherichia coli DNA polymerase I Klenow fragment. And the article contained the following:

Ethenocytosine (εC) is a highly mutagenic exocyclic DNA lesion induced by carcinogens vinyl chloride and urethane. The authors have examined base incorporation and extension at a site-specific εC residue by a quant. gel electrophoretic assay using an exonuclease-deficient version of Escherichia coli DNA polymerase I (Klenow fragment) as the model enzyme. The data show that the KM for incorporation of adenine or thymine opposite εC by is about 5 orders of magnitude higher than that for the incorporation of guanine opposite normal cytosine. The KM for base extension past εC:A and εC:T pairs is 1-2 orders of magnitude higher than that observed for a C:G pair. Although adenine misinsertion is favored over that of thymine, base extension occurs more readily when the base incorporated opposite εC is thymine. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Computed Properties of 55662-66-3

The Article related to ethenocytosine base incorporation extension escherichia polymerase, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Computed Properties of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Kowalczyk, Pawel; Ciesla, Jaroslaw M.; Saparbaev, Murat; Laval, Jacques; Tudek, Barbara published an article in 2006, the title of the article was Sequence-specific p53 gene damage by chloroacetaldehyde and its repair kinetics in Escherichia coli.Related Products of 55662-66-3 And the article contains the following content:

Oxidative stress and certain environmental carcinogens, e.g. vinyl chloride and its metabolite chloroacetaldehyde (CAA), introduce promutagenic exocyclic adducts into DNA, among them 1,N6-ethenoadenine (εA), 3,N4-ethenocytosine (εC) and N2,3-ethenoguanine (εG). We studied sequence-specific interaction of the vinyl-chloride metabolite CAA with human p53 gene exons 5-8, using DNA Polymerase Fingerprint Anal. (DPFA), and identified sites of the highest sensitivity. CAA-induced DNA damage was more extensive in p53 regions which revealed secondary structure perturbations, and were localized in regions of mutation hot-spots. These perturbations inhibited DNA synthesis on undamaged template. We also studied the repair kinetics of CAA-induced DNA lesions in E. coli at nucleotide resolution level. A plasmid bearing full length cDNA of human p53 gene was modified in vitro with 360 mM CAA and transformed into E. coli DH5α strain, in which the adaptive response system had been induced by MMS treatment before the cells were made competent. Following transformation, plasmids were re-isolated from transformed cultures 35, 40, 50 min and 1-24 h after transformation, and further subjected to LM-PCR, using ANPG, MUG and Fpg glycosylases to identify the sites of DNA damage. In adaptive response-induced E. coli cells the majority of DNA lesions recognized by ANPG glycosylase were removed from plasmid DNA within 35 min, while MUG glycosylase excised base modifications only within 50 min, both in a sequence-dependent manner. In non-adapted cells resolution of plasmid topol. forms was perturbed, suggesting inhibition of one or more bacterial topoisomerases by unrepaired ε-adducts. We also observed delayed consequences of DNA modification with CAA, manifesting as secondary DNA breaks, which appeared 3 h after transformation of damaged DNA into E. coli, and were repaired after 24 h. 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 p53 gene dna damage repair kinetics chloroacetaldehyde escherichia, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Related Products of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem