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