Tag: 100-200

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 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 October 31, 1998, Fan, M.; Byrd, C.; Compadre, C. M.; Compadre, R. L. published an article.Related Products of 5709-67-1 The title of the article was Comparison of CoMFA models for Salmonella typhimurium TA98, TA100, TA98 + S9 and TA100 + S9 mutagenicity of nitroaromatics. And the article contained the following:

Comparative Mol. Field Anal. (CoMFA) was applied to a comprehensive data set of heterogeneous nitroaroms. tested in Salmonella typhimurium TA98 and TA100 with and without S9 microsomal activation. The four CoMFA models developed agree with postulated mechanisms of mutagenicity, and explain over 70% of the corresponding mutagenic variance. The standard deviation coefficient contours common in the four models included high electronic d. regions equivalent to C4-C5 in the pyrene ring, and an electron deficient site equivalent to C6. These areas are associated with high mutagenicity. Electron deficient areas may be related with the nitroreductive bioactivation of nitroaroms. Electron rich sites may be involved with oxidative mechanisms analogous to the bioactivation pathway of polycyclic aromatic hydrocarbons. The contribution of steric factors to mutagenicity follows the order TA98 + S9 > TA98 > TA100 + S9 > TA100. The models indicated that increasing bulk perpendicular to the aromatic plane would decrease mutagenicity, but increasing the aromatic ring system along a region corresponding to C6-C7 in 1-nitropyrene would increase mutagenicity. The experimental process involved the reaction of 2-Nitro-1H-benzo[d]imidazole(cas: 5709-67-1).Related Products of 5709-67-1

The Article related to salmonella mutagenicity nitroarom compound, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Related Products of 5709-67-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On March 19, 2020, Pirez, Cyril; Nagashima, Hiroki; Dumeignil, Franck; Lafon, Olivier published an article.Product Details of 5036-48-6 The title of the article was Probing Functionalities and Acidity of Calcined Phenylene-Bridged Periodic Mesoporous Organosilicates Using Dynamic Nuclear Polarization NMR, Diffuse Reflectance Infrared Fourier Transform Spectroscopy, and X-ray Photoelectron Spectroscopy. And the article contained the following:

Owing to their high surface area, their high stability, and their hydrophobicity, periodic mesoporous organosilica (PMO) materials represent promising catalytic support for environmentally friendly chem. processes in water. We investigate here how the calcination of PMO material with benzene linkers (PMOB) allows its functionalization. Conventional and dynamic nuclear polarization (DNP)-enhanced NMR spectroscopy, diffuse reflectance IR Fourier transform spectroscopy, and XPS prove that calcination at 450°C results in the oxidation of phenylene bridges into (poly)phenols but also into carboxylic acids. Ketone, aldehyde, as well as allyl and aliphatic alc. functionalities are also observed, but their amount is much lower than that of carboxylic acids. The calcination also cleaves the Si-C bonds. Nevertheless, N2 adsorption-desorption measurements, powder X-ray diffraction, and transmission electron microscopy indicate that the PMOB materials calcined up to 600°C still exhibit ordered mesopores. We show that the phenol and carboxylic acid functionalities of PMOB calcined at 450°C protonate the NH2 group of 1-(3-aminopropyl)imidazole (API) in water at room temperature, but no formation of a covalent bond between API and the calcined PMOB functionalities has been detected. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).Product Details of 5036-48-6

The Article related to organosilica surface acidity calcination, Surface Chemistry and Colloids: Solid-Gas Systems and other aspects.Product Details of 5036-48-6

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On March 31, 1986, Vance, William A.; Okamoto, Howard S.; Wang, Yi Y. published an article.Recommanded Product: 5709-67-1 The title of the article was Structure-activity relationships of nitro and methyl-nitro derivatives of indoline, indole, indazole and benzimidazole in Salmonella typhimurium. And the article contained the following:

The mutagenic activities of I (R = H or Me) and II (R = H or Me; X = Y = CH or N) were investigated in Salmonella TA 98 and 100. The presence of a NO2 group at C4 or C7 resulted in only weakly or nonmutagenic compounds, while a NO2 group at C2, C5 or C6 usually resulted in measurable mutagenic activity in the non-N-methylated compounds Methylation of a ring N usually reduced the mutagenic activity of these nitroheterocyclics except 2-nitrobenzimidazole  [5709-67-1], which resulted in a better than 300-fold increase in mutagenic activity. A proposed mechanism for the increased mutagenic activity obtained by methylation of imidazole N may provide insights into the reasons for the potent mutagenicities observed for several similarly methylated cooked-food mutagens. 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 nitro nitrogen heterocycle, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Recommanded Product: 5709-67-1

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