SINCE the suggestion was made that replicating liver cells may be especially sensitive to chemical carcinogens (Pound, 1968), much evidence has accumulated which supports this idea. As an instance of this, certain carcinogenic alkylating agents, dimethylnitrosamine (DMN) and nitrosomethylurea (NMU), which do not usually induce liver cancer by a single treatment, are hepatocarcinogens if given during the period of restorative hyper-plasia following partial hepatectomy (Craddock, 1971; Craddock and Frei, 1974). These results suggest that repli-cation of alkylated DNA is an initial event in carcinogenesis. Another methy-lating agent, methyl methanesulphonate (MMS), on the other hand, was not found to be a hepatocarcinogen, even when given after partial hepatectomy (Craddock, 1973a). Evidence suggests that this difference may be due to a difference in the nature of the reaction products formed in DNA. It appears likely that 06-alkylguanine rather than 7-alkylgua-nine is relevant in carcinogenesis (Love-less, 1969). DMN and NMU give rise to both these methylated bases, whereas no 06-methylguanine was detectable in rat liver after treatment with MMS (Craddock, 1973b). A small amount was measured after treatment of DNA with MMS in vitro (Lawley and Shah, 1972), and in mice treated with MMS in vivo (Frei and Lawley, 1976). In the case of ethy
