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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Compensatory route of spermidine acetylation and oxidation can supply sufficient putrescine for hepatic DNA synthesis at an early stage after partial hepatectomy in diaminopropane-treated rats.

Hepatic ornithine decarboxylase activity in rats increased 2 h after partial hepatectomy, showing two peaks at 4 and 10 h. When the rats received 1,3-diaminopropane (DAP) from 0 to 4 h or from 6 to 10 h, this increase was suppressed at 6 or 12 h, respectively, whereas hepatic spermidine N1-acetyltransferase activity was enhanced by DAP administration at 6 as well as 12 h, though the levels at 12 h were one-fifth of those at 6 h. An increase in hepatic DNA synthesis at 22 h did not occur in the rats given DAP from 6 to 10 h. It recovered after administration of putrescine, but not that of spermidine. In contrast, such an inhibition was not seen in the rats given DAP from 0 to 4 h; it occurred when quinacrine, a polyamine oxidase inhibitor, was concomitantly dosed, and disappeared with further addition of putrescine. Hepatic DNA synthesis changed in close association with hepatic putrescine content irrespective of spermidine and spermine contents in these rats. Putrescine may be essential for liver regeneration after partial hepatectomy, and can be produced in sufficient quantity to support hepatic DNA synthesis by the compensatory route of spermidine acetylation and oxidation when ornithine decarboxylase activity is suppressed at an early stage.[1]


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