| pubmed-article:6974609 | pubmed:abstractText | The state of the literature led to a re-investigation of the alkylation products caused by vinyl chloride metabolites in DNA. When rat liver microsomes, an NADPH-regenerating system, DNA and [14C]vinyl chloride were incubated and, when the DNA was subsequently re-isolated and (enzymatically) hydrolyzed, chromatograms (on Aminex A-6) showed the presence of 1,N6-ethenodeoxyadenosine, 3,N4-ethenodeoxycytidine and 7-N-(2-oxoethyl)guanine (the product of hydrolysis of 7-N-(2-oxoethyl)-deoxyguanosine). By contrast, when rats were exposed to [1,2-14C]vinyl chloride and when the liver DNA of these rats was subjected to similar procedures, no radioactive 'etheno' derivatives could be detected, but a radioactive peak was eluted with 7-N-(2-oxoethyl)guanine. This peak could be transformed into 7-N-(2-hydroxyethyl)guanine; the chromatographic behaviour of which was identical to the reference compound used by Ostermann-Golkar et al. (Biochem. biophys. Res. Commun., 76 (1977) 259). Thus, it is concluded that the compound described by these authors, 7-N-(2-oxoethyl)guanine is in fact the major product of base alkylation in DNA after exposure to vinyl chloride. | lld:pubmed |
