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
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.