Category: 55662-66-3

On March 15, 2017, Chaim, Isaac A.; Gardner, Alycia; Wu, Jie; Iyama, Teruaki; Wilson, David M. III; Samson, Leona D. published an article.Computed Properties of 55662-66-3 The title of the article was A novel role for transcription-coupled nucleotide excision repair for the in vivo repair of 3,N4-ethenocytosine. And the article contained the following:

Etheno (ε) DNA base adducts are highly mutagenic lesions produced endogenously via reactions with lipid peroxidation (LPO) products. Cancer-promoting conditions, such as inflammation, can induce persistent oxidative stress and increased LPO, resulting in the accumulation of ε-adducts in different tissues. Using a recently described fluorescence multiplexed host cell reactivation assay, we show that a plasmid reporter bearing a site-specific 3,N4-ethenocytosine (εC) causes transcriptional blockage. Notably, this blockage is exacerbated in Cockayne Syndrome and xeroderma pigmentosum patient-derived lymphoblastoid and fibroblast cells. Parallel RNA-Seq expression anal. of the plasmid reporter identifies novel transcriptional mutagenesis properties of εC. Our studies reveal that beyond the known pathways, such as base excision repair, the process of transcription-coupled nucleotide excision repair plays a role in the removal of εC from the genome, and thus in the protection of cells and tissues from collateral damage induced by inflammatory responses. 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 transcription coupled nucleotide dna excision repair nethenocytosine, Biochemical Genetics: Genomic Processes and other aspects.Computed Properties of 55662-66-3

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 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 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 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 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

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 September 8, 1998, Gelfand, Craig A.; Plum, G. Eric; Grollman, Arthur P.; Johnson, Francis; Breslauer, Kenneth J. published an article.Name: Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was The Impact of an Exocyclic Cytosine Adduct on DNA Duplex Properties: Significant Thermodynamic Consequences Despite Modest Lesion-Induced Structural Alterations. And the article contained the following:

The exocyclic base adduct 3,N4-deoxyethenocytosine (εC) is a common DNA lesion that can arise from carcinogen exposure and/or as a byproduct of cellular processes. We have examined the thermal and thermodn. impact of this lesion on DNA duplex properties, as well as the structural alterations imparted by the lesion. For these studies, we used calorimetric and spectroscopic techniques to investigate a family of 13-mer DNA duplexes of the form (5’CGCATGNGTACGC3′)•(3’GCGTACNCATGCG5′), where the central N•N base pair represents the four standard Watson-Crick base pairs (corresponding to four control duplexes), and where either one of the N bases has been replaced by εC, yielding eight test duplexes. Studies on these 12 duplexes permit us to assess the impact of the εC lesion as a function of sequence context. Our spectroscopic and calorimetric data allow us to reach the following conclusions: (i) The εC lesion imparts a large penalty on duplex stability, with sequence context only modestly modulating the extent of this lesion-induced destabilization. This result contrasts with our recent studies of duplexes with abasic sites, where sequence context was found to be the predominant determinant of thermodn. damage. (ii) For the εC-containing duplexes, sequence context effects are most often observed in the enthalpic contribution to lesion-induced duplex destabilization. However, due to compensating entropies, the free energy changes associated with this lesion-induced duplex destabilization are nearly independent of sequence context. (iii) Despite significant lesion-induced changes in duplex energetics, our spectroscopic probes detect only modest lesion-induced changes in duplex structure. In fact, the overall duplex maintains a global B-form conformation, in agreement with NMR structural data. We discuss possible interpretations of the apparent disparity between the severe thermodn. and relatively mild structural impacts of the εC lesion on duplex properties. We also note and discuss the implications of empirical correlations between biophys. and biol. properties of lesion-containing duplexes. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Name: Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to exocyclic cytosine adduct dna duplex thermodn, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Name: Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 30, 1995, Wang, Ge; Palejwala, Vaseem A.; Dunman, Paul M.; Aviv, Daniel H.; Murphy, Holly S.; Rahman, M. Sayeedur; Humayun, M. Zafri published an article.Application of 55662-66-3 The title of the article was Alkylating agents induce UVM, a recA-independent inducible mutagenic phenomenon in Escherichia coli. And the article contained the following:

Noninstructive DNA damage in Escherichia coli induces SOS functions hypothesized to be required for mutagenesis and translesion DNA synthesis at noncoding DNA lesions. We have recently demonstrated that in E. coli cells incapable of SOS induction, prior UV-irradiation nevertheless strongly enhances mutagenesis at a noninstructive lesion borne on M13 DNA. Here, we address the question whether this effect, named UVM for UV modulation of mutagenesis, can be induced by other DNA damaging agents. Exponentially growing ΔrecA cells were pretreated with alkylating agents before transfection with M13 single-stranded DNA bearing a site-specific ethenocytosine residue. Effect of cell pretreatment on survival of the transfected DNA was determined as transfection efficiency. Mutagenesis at the ethenocytosine site in pretreated or untreated cells was analyzed by multiplex DNA sequencing, a phenotype-independent technol. Our data show that 1-methyl-3-nitro-1-nitrosoguanidine N-nitroso-N-methylurea and dimethylsulfate, but not Me iodide, are potent inducers of UVM. Because alkylating agents induce the adaptive response to defend against DNA alkylation, we asked if the genes constituting the adaptive response are required for UVM. Our data show that MNNG induction of UVM is independent of ada, alkA and alkB genes and define UVM as an inducible mutagenic phenomenon distinct from the E. coli adaptive and SOS responses. 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 uv modulation mutagenesis alkylating agent, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Application of 55662-66-3

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