It seems therefore that the induction of N1-SAT has a number of facets: some stabilization of the enzyme protein; stabilization of mRNA; requirement for new protein and RNA synthesis; and a Ca(2+)-sensitive induction site. It may be there is a polyamine-analogue-binding/induction site as well as an induction site which binds agents such as doxorubicin and butyrate (Figure 3). At present it is not clear whether the polyamine analogues interact directly with the active site of N1-SAT and it will be interesting to determine the effect of site-specific mutagenesis on the inducibility of N1-SAT by both polyamine analogues and antitumour agents like doxorubicin. Alternatively, it may be that agents such as doxorubicin and butyrate alter the conformation of DNA and thus release polyamines from intracellular binding sites. This increase in intracellular polyamine content may then induce N1-SAT activity which in turn will activate polyamine efflux with the net result being a decrease in intracellular polyamine content and the rate of cell growth.