Ethanol's Effect on Tissue Polyamines and Ornithine Decarboxylase Activity: A Concise Review

Ivan A. Shibley, Michael D. Gavigan, Sam N. Pennington

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

An extraordinarily diverse literature describes the cellular/tissue systems in which the molecular effects of both acute and chronic alcohol exposure seem to be mediated by changes in polyamine levels and/or ornithine decarboxylase (ODC) activity. The single unifying factor that links most of these studies is that they all, in some way, involve tissues that are undergoing relatively rapid cell division. Non‐dividing cells expressing the NMDA receptor are a notable exception in that ethanol and the polyamines seem to act via discrete regions of that receptor. Under most cellular conditions, ODC activity is a reflection of the relative tissue polyamine content, and an increase in ODC activity and polyamine content seems to be one of the early events in the progression of quiescent cells toward cell division. Thus, it is not surprising that ethanol, which has been widely reported to delay cell division, should be found to interact with the ODC/ polyamine pathway. Perhaps the most unique aspect of these studies is the fact that, with rare exception, both acute and chronic ethanol exposure have been found to slow growth and to lower tissue polyamine (putrescine) content. Furthermore, in most studies, the ethanol‐induced suppression of cell division could be overcome by the administration of exogenous putrescine. These data suggest that the ethanol‐induced suppression of cell division resulted from the loss of putrescine. In addition, because the cells were able to respond to the exogenous putrescine, the studies suggest that the signaling pathway remained intact beyond the polyamine synthesis step. Increased ODC activity (and polyamines?) has been reported during the perinatal and postnatal periods in fetal animals exposed to ethanol during early development. Although not examined in all models, the perinatal/postnatal increase in fetal ODC activity may be a compensatory response to an initial loss of ODC activity, as the organism attempted to overcome the alcohol‐induced growth suppression.

Original languageEnglish (US)
Pages (from-to)209-215
Number of pages7
JournalAlcoholism: Clinical and Experimental Research
Volume19
Issue number1
DOIs
StatePublished - Feb 1995

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Toxicology
  • Psychiatry and Mental health

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