Tag: 100-200

On September 10, 1991, Simha, Devendranath; Palejwala, Vaseem A.; Humayun, M. Zafri published an article.Related Products of 55662-66-3 The title of the article was Mechanisms of mutagenesis by exocyclic DNA adducts. Construction and in vitro template characteristics of an oligonucleotide bearing a single site-specific ethenocytosine. And the article contained the following:

It is widely accepted that mutagenic DNA lesions fall into two categories: mispairing lesions hydrogen bond with an incorrect incoming base, generally do not stop replication, and possess high mutagenic efficiency without any requirement for induced functions; noninstructional lesions lack accessible template information, act as strong blocks to DNA replication (and are therefore toxic), and their mutagenic effects are SOS-dependent. The recent results show that a noninstructional exocyclic DNA lesion induced by vinyl chloride, may have unusual mutagenic properties. To obtain more definitive exptl. evidence for the observed effects, a single ethenocytosine (εC) residue was introduced at a specific site of coliphage M13AB28 replicative form DNA by a single-stranded linker-ligation technique. The resulting DNA was purified and transfected into appropriate recA+ or recA- Escherichia coli host cells. The effect of εC on survival was determined from transfection efficiency. Both the frequency and specificity of mutations induced by εC were determined by direct sequence anal. of randomly picked progeny phage plaques. The results indicated that εC has little effect on the survival of M13 DNA. Approx. 30% of the progeny phage obtained by transfecting εC DNA had a base substitution mutation precisely at the lesion site. No such mutations were observed in progeny plaques obtained by transfecting the control DNA construct. All εC-induced mutations were either C-to-T transitions or C-to-A transversions. Neither survival nor mutagenic efficiency was significantly affected in recA- host cells. The findings reported here and in the preceding paper suggest that ethenocytosine may represent a novel type of RecA-independent, highly mutagenic noninstructional DNA lesion. These and other results argue that a requirement for SOS functions is neither a defining attribute nor an exclusive attribute of noninstructional lesions. These data also support the possibility that mutation recovery (i.e., lesion bypass) rather than misincorporation may be the major role of SOS functions in mutagenesis. Finally, the high mutagenic efficiency observed makes εC a reasonable candidate for mediating the genotoxic properties of vinyl chloride, a suspected human carcinogen, and a major industrial chem. that is produced in large quantities around the world. 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 ethenocytosine lesion dna mutagenicity, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Related Products of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On May 31, 2020, Nazir, Ahsan; Yu, Haojie; Wang, Li; Liu, Jinhua; Li, Songbiao; Ul Amin, Bilal; Naveed, Kaleem-ur-Rahman; Ullah Khan, Rizwan; Khan, Amin; Usman, Muhammad; Elshaarani, Tarig; Uddin, Alim Md. published an article.Name: N-(3-Aminopropyl)-imidazole The title of the article was Electromagnetic interference shielding effectiveness of ferrocene-based polyimidazole/carbon material composites. And the article contained the following:

Ferrocene-based polyimidazole (PPIFc) composites containing multiwalled carbon nanotube (MWCNT), reduced graphene oxide (RGO), and carbon black (CB) were prepared by chem. oxidative polymerization, resp. The prepared PPIFc/MWCNT, PPIFc/RGO, and PPIFc/CB composites were characterized by scanning electron microscope, transmission electron microscope, Fourier transform IR, X-ray diffraction, XPS, and thermogravimetric anal. The elec. conductive property of the PPIFc/MWCNT, PPIFc/RGO, and PPIFc/CB composites was tested by a four-probe method. The electromagnetic interference (EMI) shielding properties of the composites were measured by a coaxial method in the 1 to 4.5 GHz. These PPIFc/MWCNT, PPIFc/RGO, and PPIFc/CB composites showed good EMI shielding performance and total shielding effectiveness (SET) for PPIFc/CB was -11.2 dB, PPIFc/RGO was -13.1 dB, and PPIFc/MWCNT was -25.4 dB by using 50 wt% of the composite in the paraffin wax. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).Name: N-(3-Aminopropyl)-imidazole

The Article related to ferrocene based polyimidazole mwcnt graphene oxide carbon black composite, electromagnetic interference shielding oxidative polymerization, Plastics Fabrication and Uses: Plastic Product Uses and other aspects.Name: N-(3-Aminopropyl)-imidazole

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On September 1, 2020, Xu, Zhaozan; Tang, Hongying; Li, Nanwen published an article.Application In Synthesis of N-(3-Aminopropyl)-imidazole The title of the article was Enhanced proton/iron permselectivity of sulfonated poly(ether ether ketone) membrane functionalized with basic pendant groups during electrodialysis. And the article contained the following:

High permselectivity of cation exchange membrane for H+ and divalent metallic ions is essential for waste acid recovery by electrodialysis. Basic tertiary amine and imidazole groups were introduced into sulfonated poly(ether ether ketone) (SPEEK) membrane via a facile and controllable reaction, named as TA-x and IM-x (x was the basic group content), to construct acid-base pairs and reduce the swelling degree of membranes. 1H NMR confirmed the chem. structure of the as-obtained materials and protonation of tertiary amine and imidazole groups. As expected, all TA-x and IM-x membranes showed lower Fe2+ fluxes than pristine SPEEK membrane during electrodialysis because of their lower swelling degree and the electrostatic repulsion of protonated tertiary amine and imidazole groups. Remarkably, their H+ fluxes were kept similar to that of pristine SPEEK membrane. Therefore, the H+/Fe2+ permselectivity of membrane was improved considerably. Among them, IM-30 membrane showed the highest H+/Fe2+ permselectivity of 65.4, which was over three times that of pristine SPEEK membrane (19.1). Therefore, the introduction of basic groups into cation exchange membrane could reduce the swelling degree of membrane and improve the permselectivity between H+ and divalent metallic ions. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).Application In Synthesis of N-(3-Aminopropyl)-imidazole

The Article related to sulfonated peek electrodialysis proton permselective membrane waste acid reclamation, Plastics Fabrication and Uses: Plastic Product Uses and other aspects.Application In Synthesis of N-(3-Aminopropyl)-imidazole

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On February 15, 2021, Shahid, Salman; Baron, Gino V.; Denayer, Joeri F. M.; Martens, Johan A.; Wee, Lik H.; Vankelecom, Ivo F. J. published an article.COA of Formula: C6H11N3 The title of the article was Hierarchical ZIF-8 composite membranes: Enhancing gas separation performance by exploiting molecular dynamics in hierarchical hybrid materials. And the article contained the following:

Mixed matrix membranes (MMM) incorporating metal-organic framework (MOF) fillers have gained increasing attention in addressing environmental and sustainability challenges. Hierarchical materials combining pore sizes of different length scales are expected to facilitate mol. diffusion and mass transfer for the optimization of catalysis and separation processes. Herein, a novel preparation method for hierarchical ZIF-8 (H-ZIF-8) particles is presented for the synthesis of polyimide (PI)-based MMMs with good compatibility between filler and polymer. Gas permeability measurements of polyimide-Matrimid/H-ZIF-8 MMMs showed 4-fold improvements in permeability of both CO2 and CH4 coupled with a marked increase in selectivity and plasticization resistance for MMM with 30 wt% H-ZIF-8 loading. Gas transport anal. in these MMMs revealed that the enhanced gas separation performance of the MMMs can be related to the imidazolate modification of the PI structure and the hierarchical structure of H-ZIF-8, as confirmed by N2, Ar, mercury porosimetry, SEM, TEM anal. CO2 permeability for all MMMs increases with increasing CO2 concentration and by decreasing temperature The proof of concept, as demonstrated in this study, could be extended for the preparation of other hierarchical ZIFs and related MMMs. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).COA of Formula: C6H11N3

The Article related to hierarchical zif8 composite membrane gas separation mol dynamic, Plastics Fabrication and Uses: Plastic Product Uses and other aspects.COA of Formula: C6H11N3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 31, 1989, Eberle, Gertrud; Barbin, Alain; Laib, Reinhold J.; Ciroussel, Francoise; Thomale, Juergen; Bartsch, Helmut; Rajewsky, Manfred F. published an article.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was 1,N6-etheno-2′-deoxyadenosine and 3,N4-etheno-2′-deoxycytidine detected by monoclonal antibodies in lung and liver DNA of rats exposed to vinyl chloride. And the article contained the following:

1,N6-Etheno-2′-deoxyadenosine (εdAdo) and 3,N4-etheno-2′-deoxycytidine (εdCyd) are formed in vitro by reaction of DNA with the electrophilic metabolites of vinyl chloride (VC), chloroethylene oxide and chloroacetaldehyde. To detect and quantitate these DNA adducts in vivo, a series of specific monoclonal antibodies (Mab) were raised. Among those, Mab EM-A-1 and Mab EM-C-1, resp., were used for detection of εdAdo and εdCyd by competitive RIA, following preseparation of the etheno adducts from DNA hydrolyzates by HPLC. At 50% inhibition of tracer-antibody binding, both Mab had a detection limit of 187 fmol and antibody affinity constants (K) of 2 × 109 L/mol. The levels of εdAdo and εdCyd were quantitated in the DNA of lung and liver tissue of young rats exposed to 2000 ppm of VC for 10 days. The εdAdo/2′-deoxyadenosine and εdCyd/2′-deoxycytidine molar ratios were 1.3 × 10-7 and 3.3 × 10-7, resp., in lung DNA, and 5.0 × 10-8 and 1.6 × 10-7 in liver DNA. When hydrolyzates of 3 mg of DNA were analyzed by RIA at 25% inhibition of tracer-antibody binding, εdAdo and εdCyd were not detected in liver DNA from untreated rats above the limiting εdAdo/2′-deoxyadenosine and εdCyd/2′-deoxycytidine molar ratios of 2.2 × 10-8 and 3.1 × 10-8, resp. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to vinyl chloride ethenodeoxyadenosine ethenodeoxycytidine dna, lung dna adduct vinyl chloride, liver dna adduct vinyl chloride, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 30, 1993, Basu, Ashis K.; Wood, Michael L.; Niedernhofer, Laura J.; Ramos, Leilani A.; Essigmann, John M. published an article.Reference of Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Mutagenic and genotoxic effects of three vinyl chloride-induced DNA lesions: 1,N6-ethenoadenine, 3,N4-ethenocytosine, and 4-amino-5-(imidazol-2-yl)imidazole. And the article contained the following:

The mutagenic and genotoxic properties of 1,N6-ethenoadenine (εAde), 3,N4-ethenocytosine (εCyt), and 4-amino-5-(imidazol-2-yl)imidazole (β) were investigated in vivo. The former two modified bases are known DNA adducts formed by the human carcinogen vinyl chloride; β is formed by pyrimidine ring-opening of εAde. Chem. synthesized deoxyhexanucleotides containing εAde and β, d[GCT(εA)GC], and d[GCT(β)GC], resp., were described previously [(1987) Biochem. 26, 5626-5635]. εCyt was inserted into an oligonucleotide, d[GCTAG(εC)], by a mild enzymic synthetic procedure, which avoided exposure of the base to alk. conditions. 3,N4-etheno-2′-deoxycytidine 3′,5′-bisphosphate coupled with reasonable efficiency (30-40%) to the 3′-nucleoside of an acceptor pentamer, d(GCTAG), in a reaction catalyzed by T4 RNA ligase in the presence of ATP. Each of the three modified hexanucleotides and an unmodified control were inserted into a six-base gap positioned at a known site in the genome of bacteriophage M13-NheI. A nick was placed in the DNA strand opposite that containing the single DNA lesions, enabling the formation of singly adducted single-stranded genomes by denaturation. After transfection of the adducted phage DNAs into Escherichia coli, each of the adducts was found to be genotoxic. The most toxic lesion was β, which reduced survival of the genome by 97%. εCyt and εAde reduced survival by 90% and 65%, resp. An examination of the surviving phage populations revealed that each of the three adducts was mutagenic. The least mutagenic lesion was εAde (0.1% of the survivors were mutant), which showed primarily A → G transitions. The εAde rearrangement product, β, was also found to induce mutations but at a 20-fold higher frequency (∼2%). In this case, however, mutagenesis was random, possibly because the hydrogen-bonding face of this lesion has been obliterated. εCyt induced mutations at a frequency of 1.5-2%; its mutations were mainly C → T transitions, although targeted C → A and -1 deletions were also detected. The possible resp. roles of these three DNA lesions in the mutagenic and carcinogenic activities of vinyl chloride and related haloalkanes are discussed. 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 mutation genotoxicity vinyl chloride dna damage, ethenoadenine ethenocytosine aminoimidazolylimidazole dna genotoxicity, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Reference of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On November 15, 2003, Barbin, Alain; Wang, Rong; O’Connor, Peter J.; Elder, Rhoderick H. published an article.Related Products of 55662-66-3 The title of the article was Increased Formation and Persistence of 1,N6-Ethenoadenine in DNA Is Not Associated with Higher Susceptibility to Carcinogenesis in Alkylpurine- DNA-N-Glycosylase Knockout Mice Treated with Vinyl Carbamate. And the article contained the following:

Ethenobases are promutagenic DNA adducts formed by some environmental carcinogens and products of endogenous lipid peroxidation Mutation spectra in tumors induced in mice by urethane or its metabolite vinyl carbamate (Vcar) are compatible with 1,N6-ethenoadenine (εA) being an initiating lesion in the development of these tumors. As alkylpurine-DNA-N-glycosylase (APNG) releases εA from DNA in vitro, wild-type and APNG-/- C57Bl/6J mice were treated with Vcar and levels of εA and 3,N4-ethenocytosine (εC), which is not a substrate of APNG, were analyzed in liver and lung DNA. At 6 h after the last dose, levels of εA were 1.6-fold higher in DNA from APNG-/- mice and subsequently persisted at higher levels for longer than in DNA from wild-type animals, confirming that εA is released by APNG in vivo. In contrast, ∼14-fold lower levels of εC were induced by Vcar, and the kinetics of formation and persistence of εC was similar in the two mouse strains. The carcinogenicity of Vcar was compared in APNG-/- and wild-type suckling mice given a single dose of Vcar (30 or 150 nmol/g). After 1 yr, only mice in the high-dose group developed hepatocellular carcinoma; however, the incidence was not higher in APNG-/- mice. Although higher levels and increased persistence of εA was observed in hepatic DNA from APNG-/- mice at 150 nmol/g Vcar, apoptosis and cell proliferation levels were similar in both strains of mice. This may explain why differences in εA formation/persistence observed here did not result in higher susceptibility of APNG-/- mice to hepatocarcinogenesis. 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 ethenoadenine genetic susceptibility vinyl carbamate, alkylpurine n glycosylase gene vinyl carbamate carcinogenesis, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Related Products of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On March 31, 1988, Dirr, A.; Wild, D. published an article.Synthetic Route of 5709-67-1 The title of the article was Synthesis and mutagenic activity of nitroimidazoarenes. A study on the mechanism of the genotoxicity of heterocyclic arylamines and nitroarenes. And the article contained the following:

A series of nitroimidazoarenes (nitro-IAs) (I and II, X = CH or N, R = H or Me) were synthesized from the corresponding aminoimidazoarenes (amino-IAs). These 2 classes of compounds are structurally related to the potent food mutagen and carcinogen, 2-amino-3-methylimidazo[4,5-f]quinoline (IQ). The mutagenic activities of the I and II were assayed in the Salmonella typhimurium frameshift tester strains TA98, TA98/1,8-DNP6 and TA98NR without use of extracellular metabolization. I (X = N, R = Me) the nitro counterpart of IQ, was 2-fold more mutagenic than IQ. In general, the mutagenic activities of the I varied >50,000-fold. The relation between the chem. structures and mutagenic activities are identical with those previously reported for the corresponding amino-IAs: the Me group on the imidazole ring and the quinoline N were required for potent mutagenic activity. The reductive activation of the nitro-IAs is not carried out primarily by the classical nitroreductase of Salmonella which is defective in TA98NR. The O-acetyltransferase defective in TA98/1,8-DNP6 is required for the efficient production of the ultimate mutagens of the nitro-IAs. The interchangeability of the structure-activity relations of the nitro-IAs and amino-IAs reflects a basic similarity of the mechanisms of the mutagenicity of the 2 classes of compounds Probably, the N-hydroxy compounds are proximate metabolites common to the nitro-IAs and amino-IAs; they are further activated by an acetyl-CoA-dependent O-acetyltransferase of Salmonella. It is very likely a property of the ultimate mutagen, possibly a nitrenium ion, which governs the mutagenic potency of the different nitro- and amino-IAs and thus determines the structure-activity relations. The experimental process involved the reaction of 2-Nitro-1H-benzo[d]imidazole(cas: 5709-67-1).Synthetic Route of 5709-67-1

The Article related to nitroimidazoarene toxicity preparation, imidazoarene toxicity preparation, genotoxicity imidazoarene preparation, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Synthetic Route of 5709-67-1

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On June 30, 1985, Barbin, Alain; Laib, Reinhold J.; Bartsch, Helmut published an article.COA of Formula: C6H5N3O The title of the article was Lack of miscoding properties of 7-(2-oxoethyl)guanine, the major vinyl chloride-DNA adduct. And the article contained the following:

Chloroethylene oxide  [7763-77-1], an ultimate carcinogenic metabolite of vinyl chloride, was reacted with poly(deoxyguanylate-deoxycytidylate) [36786-90-0]; the nucleic acid base adducts, 7-(2-oxoethyl)guanine  [73100-87-5] and 3,N4-ethenocytosine  [55662-66-3], were analyzed by reversed-phase HPLC. Chloroethylene oxide-modified poly(deoxyguanylate-deoxycytidylate) was assayed as template in a replication fidelity assay with Escherichia coli DNA polymerase I  [9012-90-2], and the newly synthesized product was subjected to nearest-neighbor anal. Misincorporation rates of dAMP  [653-63-4] and TMP  [365-07-1] were increased with the level of template modification. About 80% of the mispairing events were located opposite minor cytosine lesions. 7-(2-Oxoethyl)guanine, the major adduct identified (>98% of the adducts), did not miscode for either thymine or adenine, failing to support an earlier hypothesis that the cyclic hemiacetal form, O6,7-(1′-hydroxyethano)guanine, could, by anal. with O6-methyl- and O6-ethylguanine, simulate adenine. Thus, direct miscoding of 7-(2-oxoethyl)guanine may contribute only slightly to the induction of mutations by chloroethylene oxide. 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 oxyethylguanine chloroethylene oxide dna coding, ethenocytosine nucleic acid coding chloroethylene oxide, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.COA of Formula: C6H5N3O

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Barbin, A. published an article in 1999, the title of the article was Role of etheno DNA adducts in carcinogenesis induced by vinyl chloride in rats.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one And the article contains the following content:

A review and discussion with many references Vinyl chloride, a hepatocarcinogen in humans and rodents, can form promutagenic ethano bases in DNA after metabolic activation. The formation of 1,N6-ethenoadenine (εA) and 3,N4-ethenocytosine (εC) was measured in adult Sprague-Dawley rats by immunoaffinity purification and 32P-post-labeling. A highly variable background was found in all tissues from untreated animals: the mean molar ratios of εA:A and εC:C in DNA ranged from 0.043 × 10-8 to 31.2 × 10-8 and from 0.062 × 10-8 to 20.4 × 10-8, resp. After exposure to 500 ppm vinyl chloride by inhalation (4 h/day, 5 days/wk for 8 wk), increased levels of εA were found in the liver, lung, circulating lymphocytes and testis, the mean (± SD) of induced levels (treated-control values) being (4.1±1.5) × 10-8 for these tissues. No increase in the εA:A ratio was observed in kidney, brain or spleen. The levels of εC increased in all the tissues examined except the brain. The mean value of the induced εC:C ratios was (7.8±1.2) × 10-8 for the liver, kidney, lymphocytes and spleen, and these ratios were higher in the lung (28×10-8) and testis (19×10-8). The results suggest a variable repair capacity for εA or εC in different tissues. The results are discussed in relation to published studies on the accumulation and persistence of etheno bases in the liver during and after exposure to vinyl chloride and on mutation spectra in the ras and p53 genes in liver tumors induced by vinyl chloride. In addition, we show that the linear relationship established for monofunctional alkylating agents between their carcinogenic potency in rodents and their covalent binding index for promutagenic bases in hepatic DNA holds for vinyl chloride. It is concluded that etheno bases are critical lesions in hepatocarcinogenesis induced by vinyl chloride. For a better understanding of the mechanism of action of this compound, further work is needed on the role of DNA repair pathways and of endogenous lipid peroxidation products in the formation and persistence of etheno bases in vivo. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

The Article related to etheno dna adduct carcinogenesis vinyl chloride, review etheno dna adduct carcinogenesis vinyl chloride, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Safety of Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem