The effects of a single ethanol administration on ornithine decarboxylase induction, polyamine metabolism and DNA synthesis in rat liver after partial hepatectomy were studied. Ethanol given 1 hr before partial hepatectomy at the dose of 2 , 3 or 5 gm/kg body wt inhibited the increase in ornithine decarboxylase activity and that in the putrescine level in the liver 4 hr after partial hepatectomy. The hepatectomy increased the amount of ornithine decarboxylase messenger RNA expressed, and this amount was unaffected by ethanol administration. Further, ethanol did not accelerate the degradation of ornithine decarboxylase 4 hr after partial hepatectomy, indicating that the inhibition of ornithine decarboxylase activity caused by ethanol was not caused by a decrease in the ornithine decarboxylase messenger RNA level or by the acceleration of ODC degradation. The single dose of ethanol inhibited [sH]thymidine incorporation into the hepatic DNA 24 hr after partial hepatectomy. The suppression of [SH]thymidine incorporation was partially reversed by the administration of putrescine. These results suggested that ethanol inhibits the increase in ornithine decarboxylase activity after transcription, suppressing the accumulation of putrescine, which prevents DNA synthesis in response to hepatectomy. (HEPATOLOGY 1991; 14696.700.) When ornithine decarboxylase (ODC; EC 4.1.1.17), a rate-limiting enzyme of polyamine biosynthesis, is induced, polyamines accumulate in growing cells and tissues as a response to growth stimuli (1). The suppression of the accumulation of polyamines inhibits cell growth. These findings suggest that polyamines are indispensable for cell growth (2).
The effect of ethanol consumption on liver regeneration is poorly understood. Several studies (3-5) suggest that ethanol inhibits DNA synthesis and liver regeneration. However, other studies (6, 7) suggest that it does not. Poso and Poso (8,9) report that short-term ethanol