Month: November 2022

On April 23, 2004, Gros, Laurent; Maksimenko, Andrei V.; Privezentzev, Cyril V.; Laval, Jacques; Saparbaev, Murat K. published an article.Name: Imidazo[1,2-c]pyrimidin-5(6H)-one The title of the article was Hijacking of the Human Alkyl-N-purine-DNA Glycosylase by 3,N4-Ethenocytosine, a Lipid Peroxidation-induced DNA Adduct. And the article contained the following:

Lipid peroxidation generates aldehydes, which react with DNA bases, forming genotoxic exocyclic etheno(ε)-adducts. E-bases have been implicated in vinyl chloride-induced carcinogenesis, and increased levels of these DNA lesions formed by endogenous processes are found in human degenerative disorders. E-adducts are repaired by the base excision repair pathway. Here, the authors report the efficient biol. hijacking of the human alkyl-N-purine-DNA glycosylase (ANPG) by 3,N4-ethenocytosine (εC) when present in DNA. Unlike the ethenopurines, ANPG does not excise, but binds to εC when present in either double-stranded or single-stranded DNA. The authors developed a direct assay, based on the fluorescence quenching mechanism of mol. beacons, to measure a DNA glycosylase activity. Mol. beacons containing modified residues have been used to demonstrate that the εC·ANPG interaction inhibits excision repair both in reconstituted systems and in cultured human cells. Furthermore, the authors show that the εC·ANPG complex blocks primer extension by the Klenow fragment of DNA polymerase I. These results suggest that εC could be more genotoxic than 1,N6-ethenoadenine (εA) residues in vivo. The proposed model of ANPG-mediated genotoxicity of εC provides a new insight in the mol. basis of lipid peroxidation-induced cell death and genome instability in cancer. 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 genotoxicity ethenocytosine lipid peroxidation dna adduct human anpg, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Name: Imidazo[1,2-c]pyrimidin-5(6H)-one

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On December 31, 2020, Jiang, Long; Lei, Xiang; Wang, Kaijie; Zhang, Zhijie; Wang, Fang; Lu, Sheng; Chen, Xiaoqiang published an article.Safety of N-(3-Aminopropyl)-imidazole The title of the article was Colorimetric and fluorometric detection of NADPH using imidazolium functionalized polydiacetylenes with high sensitivity and selectivity. And the article contained the following:

The NAD derivatives (NADPH, NADP+, NADH, and NAD+) are important redox cofactors that involve in many biol. activities, and their concentration levels are associated with a variety of diseases. In this work, an imidazolium functionalized polydiacetylenes sensing system (IM-PDAs) is reported to selectively detect the reduced form of NADP (NADPH). Depending on the electrostatic attraction between the pos. charged imidazolium heads and the neg. charged phosphate groups, the sensing system exhibits colorimetric and fluorescent responses when exposed to NADPH and its oxidized form (NADP+); while the system does not respond to the less neg. charged NADH and NAD+ at the concentration range tested in this study. Owing to the pos. charged nicotinamide of NADP+, the detection sensitivity of IM-PDAs towards NADP+ is much lower than that towards NADPH, successfully differentiating NADPH from the rest three cofactors. Furthermore, IM-PDAs loaded paper-based sensor is constructed and demonstrates the potentials of IM-PDAs based sensing device for practical applications in NADPH detection. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).Safety of N-(3-Aminopropyl)-imidazole

The Article related to colorimetry fluorometry nadph imidazolium functionalized polydiacetylene, Biochemical Methods: Spectral and Related Methods and other aspects.Safety of N-(3-Aminopropyl)-imidazole

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On January 1, 2021, Nayim, Sk; Jana, Gopal Chandra; Aktara, Mt Nasima; Khatun, Munira; Dhal, Asima; Beg, Maidul; Sahoo, Nandan Kumar; Maji, Anukul; Hossain, Maidul published an article.Safety of N-(3-Aminopropyl)-imidazole The title of the article was 9-N-substituted novel berberine derivative for selective and sensitive nanomolar level fluorometric detection of human hemoglobin: A synthesis, sensing and interaction study. And the article contained the following:

Quant. determination of Hb (Hb) level is an obligatory part of diagnostic proceedings and an undisputed health index for a number of chronic diseases. In this study, we have tried to introduce a new 9-N-substituted berberine analog (BR-N) as a triumphant fluorescent sensor for aptly selective and extremely sensitive nanomolar detection of Hb. The probe was found to endure a rampant quenching in its highly intensified inherent fluorescence emission with successive addition of Hb. Though, the other available proteins and biomols. were proved to be failure in causing any significant change in fluorescence of BR-N under equivalent exptl. condition. Again, the sensitivity of the probe was such that it provided an astonishing detection limit of 0.41 nM having linearity range 1-70 nM. Noteworthy, the presence of Hb caused significant alternation in the nature of the intrinsic fluorescence curve of the probe which was also a differentiating aspect during Hb identification. Experiments revealed that ground state probe-protein complex formation was behind the reduction of fluorescence intensity through static quenching mechanism. The interaction study unearthed the binding constant value to be 2.8 × 105 M-1. Moreover, the probe was also successful when applied in real samples for quant. Hb determination which spoke for its reliable practical utility in the field of clin. diagnosis from today onwards. The experimental process involved the reaction of N-(3-Aminopropyl)-imidazole(cas: 5036-48-6).Safety of N-(3-Aminopropyl)-imidazole

The Article related to substituted berberine derivative sensitive nanomolar fluorometric sensor hb human, Biochemical Methods: Spectral and Related Methods and other aspects.Safety of N-(3-Aminopropyl)-imidazole

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On October 26, 1982, Kusmierek, J. T.; Singer, B. published an article.Recommanded Product: 55662-66-3 The title of the article was Chloroacetaldehyde-treated ribo- and deoxyribopolynucleotides. 1. Reaction products. And the article contained the following:

The in vitro reaction of the vinyl chloride metabolite chloracetaldehyde (CAA) [107-20-0] with cytosine and adenine residues in ribo- and deoxyribopolynucleotides leads to the formation of the relatively stable hydrated etheno derivatives 3,N4-(N4-α-hydroxyethano)cytosine (εC.H2O) [66547-58-8] and 1,N6-(N6-α-hydroxyethano)adenine (εA.H2O) [69260-72-6]. Under physiol. conditions, the hydrates are slowly converted to 3,N4-ethenocytosine (εC)(I) [55662-66-3] and 1,N6-ethenoadenine (εA) [13875-63-3]. The half-life at pH 7.25 of εC.H2O in poly(C) is 4.9 h at 50° and of εA.H2O in poly(A) is 1.4 h at 37°. These dehydration rates in polymers are similar to those for hydrates in monomers. The reactivity of adenine and cytosine residues is greatly suppressed in double-stranded polymers. Adenine residues are ∼10 times less reactive in poly(A).poly(U) than adenine in single-stranded polymers. Under similar reaction conditions no reaction of cytosine residues in poly(C).poly(G) was detected. In vinyl chloride exposed cells, where CAA is formed, the cyclic etheno derivatives of adenine and cytosine are likely to occur preferentially in single-stranded regions of nucleic acids, with the hydrate forming a major proportion of the modification. The experimental process involved the reaction of Imidazo[1,2-c]pyrimidin-5(6H)-one(cas: 55662-66-3).Recommanded Product: 55662-66-3

The Article related to chloracetaldehyde reaction nucleic acid, polynucleotide reaction chloracetaldehyde, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Recommanded Product: 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

On February 3, 2010, Maciejewska, Agnieszka M.; Ruszel, Karol P.; Nieminuszczy, Jadwiga; Lewicka, Joanna; Sokolowska, Beata; Grzesiuk, Elzbieta; Kusmierek, Jaroslaw T. published an article.Related Products of 55662-66-3 The title of the article was Chloroacetaldehyde-induced mutagenesis in Escherichia coli: The role of AlkB protein in repair of 3,N4-ethenocytosine and 3,N4-α-hydroxyethanocytosine. And the article contained the following:

Etheno (ε) adducts are formed in reaction of DNA bases with various environmental carcinogens and endogenously created products of lipid peroxidation Chloroacetaldehyde (CAA), a metabolite of carcinogen vinyl chloride, is routinely used to generate ε-adducts. The authors studied the role of AlkB, along with AlkA and Mug proteins, all engaged in repair of ε-adducts, in CAA-induced mutagenesis. The test system used involved pIF102 and pIF104 plasmids bearing the lactose operon of CC102 or CC104 origin which allowed to monitor Lac+ revertants, the latter arose by GC → AT or GC → TA substitutions, resp., as a result of modification of guanine and cytosine. The plasmids were CAA-damaged in vitro and replicated in Escherichia coli of various genetic backgrounds. To modify the levels of AlkA and AlkB proteins, mutagenesis was studied in E. coli cells induced or not in adaptive response. Formation of εC proceeds via a relatively stable intermediate, 3,N4-α-hydroxyethanocytosine (HEC), which allowed to compare repair of both adducts. The results indicate that all three genes, alkA, alkB and mug, are engaged in alleviation of CAA-induced mutagenesis. The frequency of mutation was higher in AlkA-, AlkB- and Mug-deficient strains in comparison to alkA +, alkB +, and mug + controls. Considering the levels of CAA-induced Lac+ revertants in strains harboring the pIF plasmids and induced or not in adaptive response, the authors conclude that AlkB protein is engaged in the repair of εC and HEC in vivo. Using the modified TTCTT 5-mers as substrates, the authors confirmed in vitro that AlkB protein repairs εC and HEC although far less efficiently than the reference adduct 3-methylcytosine. The pH optimum for repair of HEC and εC is significantly different from that for 3-methylcytosine. The authors propose that the protonated form of adduct interact in active site of AlkB protein. 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 chloroacetaldehyde mutagen escherichia alkb ethenocytosine hydroxyethanocytosine repair, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Related Products of 55662-66-3

Referemce:
Imidazole – Wikipedia,
Imidazole | C3H4N2 – PubChem

Barbin, Alain; Bartsch, Helmut; Lecomte, Philippe; Radman, Miroslav published an article in 1981, the title of the article was On the possible role of the miscoding DNA lesions, 1,N6-ethenoadenine and 3,N4-ethenocytosine, in vinyl chloride-induced mutagenesis and carcinogenesis.Related Products of 55662-66-3 And the article contains the following content:

chloroacetaldehyde  [107-20-0] And chloroethylene oxide (CEO) [7763-77-1], 2 reactive metabolites of vinyl chloride  [75-01-4], were used to introduce increasing amounts of 1,N6-ethenoadenine (εA)(I) [13875-63-3] and 3,N4-ethenocytosine (εC)(II) [55662-66-3] residues in poly(dA) [25191-20-2] and poly(dC) [25609-92-1], resp. The modified polynucleotides were assayed with Escherichia coli DNA polymerase I for their template activity and misincorporation. The miscoding properties observed of εA and εC may explain the mutagenic effects reported for vinyl chloride and its metabolites; these lesions may also represent one of the initial steps in vinyl chloride- or CEO-induced carcinogenesis. 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 vinyl chloride mutagenesis dna miscoding, carcinogenesis vinyl chloride ethenoadenine ethenocytosine, Toxicology: Carcinogens, Mutagens, and Teratogens and other aspects.Related Products of 55662-66-3

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

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

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 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