| pubmed-article:6433187 | pubmed:abstractText | L-Ethionine is an ethyl analogue of the amino acid, methionine, well known as a carcinogen but not as a mutagen. Its activity is clearly related to its capacity to hypomethylate DNA and RNA. At a final concentration of 5 mM, L-ethionine completely inhibits DNA synthesis in PHA-stimulated human lymphocytes, probably acting on a methylation reaction critical for the initiation of the S phase. This block can be reversed. Utilizing this capacity of L-ethionine to block cell proliferation, we have studied the influence of G0 and G1 repair of premutational damage (PMD) (equivalent to liquid-holding recovery in bacteria) on spontaneous and MMC-induced SCEs in human lymphocytes. Our results clearly show that L-ethionine in our experimental conditions significantly increases the frequencies of spontaneous and MMC-induced SCEs. In view of the hypomethylating activity of the analogue, we hypothesize that this action at the replication fork level may increase the error-prone ligation of unrepaired lesions, thus influencing the frequency of occurrence of SCEs. | lld:pubmed |
