ETHANOLS EFFECT ON TISSUE POLYAMINES AND ORNITHINE DECARBOXYLASE ACTIVITY - A CONCISE REVIEW

Citation
Ia. Shibley et al., ETHANOLS EFFECT ON TISSUE POLYAMINES AND ORNITHINE DECARBOXYLASE ACTIVITY - A CONCISE REVIEW, Alcoholism, clinical and experimental research, 19(1), 1995, pp. 209-215
Citations number
81
Categorie Soggetti
Substance Abuse
ISSN journal
01456008
Volume
19
Issue
1
Year of publication
1995
Pages
209 - 215
Database
ISI
SICI code
0145-6008(1995)19:1<209:EEOTPA>2.0.ZU;2-F
Abstract
An extraordinarily diverse literature describes the cellular/tissue sy stems in which the molecular effects of both acute and chronic alcohol exposure seem to be mediated by changes in polyamine levels and/or or nithine decarboxylase (ODC) activity. The single unifying factor that links most of these studies is that they all, in some way, involve tis sues that are undergoing relatively rapid cell division. Nondividing c ells expressing the NMDA receptor are a notable exception in that etha nol and the polyamines seem to act via discrete regions of that recept or. Under most cellular conditions, ODC activity is a reflection of th e relative tissue polyamine content, and an increase in ODC activity a nd polyamine content seems to be one of the early events in the progre ssion of quiescent cells toward cell division. Thus, it is not surpris ing that ethanol, which has been widely reported to delay cell divisio n, should be found to interact with the ODC/polyamine pathway. Perhaps the most unique aspect of these studies is the fact that, with rare e xception, both acute and chronic ethanol exposure have been found to s low growth and to lower tissue polyamine (putrescine) content. Further more, in most studies, the ethanol-induced suppression of cell divisio n could be overcome by the administration of exogenous putrescine. The se data suggest that the ethanol-induced suppression of cell division resulted from the loss of putrescine. In addition, because the cells w ere able to respond to the exogenous putrescine, the studies suggest t hat the signaling pathway remained intact beyond the polyamine synthes is step. Increased ODC activity (and polyamines?) has been reported du ring the perinatal and postnatal periods in fetal animals exposed to e thanol during early development. Although not examined in all models, the perinatal/postnatal increase in fetal ODC activity may be a compen satory response to an initial loss of ODC activity, as the organism at tempted to overcome the alcohol-induced growth suppression.