Changes in polyamine acetylation in human cancer cells.

In the pancreatic-biliary diversion model, D F M O significantly reduced intestinal spermidine and spermine levcls and the spermidinc/spermine ratio. This was associated with a marked reduction or complete prevention of the adaptive mucosal hyperplasia in both the jejunum and the ileum 1201. D F M O has also been used t o inhibit intestinal growth in other experimental models. D F M O produced intestinal villous atrophy in the dog and monkey [22], inhibited the adaptive growth associated with post-starvation refeeding 11-1. 231 and at least partially reversed the intestinal growth induced by plant lectins [ 171. However. it is important to note that not all increases in intestinal mucosal polyamines during intestinal growth may be due to increased polyamine biosynthesis. In the plant lcctin intestinal hyperplasia model, mucosal polyamines are markedly increased, but O D C activity is only minimally increased. and D F M O exhibited only a minimal antiproliferative effect [ 171. I t was subsequently shown that the uptake of polyamines in the enterocytes was increased and there was a preferential uptake of spermine over putrcscine in the crypt I 1x1. These results support a ro le for the polyamines themselves in inducing intestinal growth. In addition. the administration of exogenous polyamincs by themselvcs can also induce intestinal growth. T h e luminal infusion o f putrescine stimulated rat intestinal mucosal growth 1231. T h e oral feeding o f spermidine and spermine induces the precocious maturation o f the newborn rat intestine. both enzymatically and morphologically [ 25. 261. T h e ahovc results would appear t o support a primary role for the polyrimines in at least some models of intestinal growth.