piperidines and methional

piperidines has been researched along with methional* in 1 studies

Other Studies

1 other study(ies) available for piperidines and methional

Article	Year
Double base lesions of DNA by a metabolite of carcinogenic benzo[a]pyrene. Biochemical and biophysical research communications, 2002, Jan-18, Volume: 290, Issue:2 Carcinogenic benzo[a]pyrene (BP) is generally considered to show genotoxicity by forming DNA adducts of its metabolite, BP-7,8-diol-9,10-epoxide. We investigated oxidative DNA damage and its sequence specificity induced by BP-7,8-dione, another metabolite of BP, using (32)P-5'-end-labeled DNA. Formamidopyrimidine-DNA glycosylase treatment induced cleavage sites mainly at G residues of 5'-TG-3' sequence and at poly(C) sequences, in DNA incubated with BP-7,8-dione in the presence of NADH and Cu(II), whereas piperidine treatment induced cleavage sites at T mainly of 5'-TG-3'. BP-7,8-dione strongly damaged the G and C of the ACG sequence complementary to codon 273 of the p53 gene. Catalase and a Cu(I)-specific chelator attenuated the DNA damage, indicating the involvement of H(2)O(2) and Cu(I). BP-7,8-dione with NADH and Cu(II) also increased 8-oxo-7,8-dihydro-2'-deoxyguanosine formation. We conclude that oxidative DNA damage, especially double base lesions, may participate in the expression of carcinogenicity of BP in addition to DNA adduct formation. Topics: 8-Hydroxy-2'-Deoxyguanosine; Aldehydes; Animals; Benzopyrenes; Binding Sites; Carcinogens; Cattle; Copper; Cyclin-Dependent Kinase Inhibitor p16; Deoxyguanosine; DNA; DNA Damage; DNA-Formamidopyrimidine Glycosylase; Free Radical Scavengers; Genes, p53; Genes, ras; Humans; N-Glycosyl Hydrolases; NAD; Oxidation-Reduction; Piperidines	2002

Article

Year

Double base lesions of DNA by a metabolite of carcinogenic benzo[a]pyrene.

Biochemical and biophysical research communications, 2002, Jan-18, Volume: 290, Issue:2

Carcinogenic benzo[a]pyrene (BP) is generally considered to show genotoxicity by forming DNA adducts of its metabolite, BP-7,8-diol-9,10-epoxide. We investigated oxidative DNA damage and its sequence specificity induced by BP-7,8-dione, another metabolite of BP, using (32)P-5'-end-labeled DNA. Formamidopyrimidine-DNA glycosylase treatment induced cleavage sites mainly at G residues of 5'-TG-3' sequence and at poly(C) sequences, in DNA incubated with BP-7,8-dione in the presence of NADH and Cu(II), whereas piperidine treatment induced cleavage sites at T mainly of 5'-TG-3'. BP-7,8-dione strongly damaged the G and C of the ACG sequence complementary to codon 273 of the p53 gene. Catalase and a Cu(I)-specific chelator attenuated the DNA damage, indicating the involvement of H(2)O(2) and Cu(I). BP-7,8-dione with NADH and Cu(II) also increased 8-oxo-7,8-dihydro-2'-deoxyguanosine formation. We conclude that oxidative DNA damage, especially double base lesions, may participate in the expression of carcinogenicity of BP in addition to DNA adduct formation.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Aldehydes; Animals; Benzopyrenes; Binding Sites; Carcinogens; Cattle; Copper; Cyclin-Dependent Kinase Inhibitor p16; Deoxyguanosine; DNA; DNA Damage; DNA-Formamidopyrimidine Glycosylase; Free Radical Scavengers; Genes, p53; Genes, ras; Humans; N-Glycosyl Hydrolases; NAD; Oxidation-Reduction; Piperidines

2002