The alterations in the immune system caused by ethanol appear to be a compl
ex combination of direct and indirect effects. The role of ethanol as an os
molyte has previously been studied in this laboratory with rat splenocytes.
In the present study the osmotic effects of ethanol were investigated in l
ymphocytes from human normal subjects and alcohol abusers. Mitogen-stimulat
ed lymphocytes were cultured in vitro with ethanol in hyperosmotic isotonic
or iso-osmotic hypotonic conditions. The former conditions mimic the physi
ological situation where ethanol increases osmolality in an electrolyte-bal
anced environment. Under these conditions, lymphocyte proliferation was una
ffected Ethanol addition in iso-osmotic hypotonic conditions, where there i
s electrolyte imbalance, was associated with inhibition of T-lymphocyte pro
liferation. Hyperosmotic hypertonic solutions in the absence of ethanol als
o resulted in inhibition of T-lymphocyte proliferation. Electron microscopy
and measurement of cell viability and metabolic activity (lactate and ATP
levels) indicated that the decreased proliferation associated with NaCl-ind
uced hyperosmotic hypertonic conditions was at least partially attributable
to cell death together with, and possibly caused by, detrimental effects o
n mitochondria. Conversely, decreased T-lymphocyte proliferation in iso-osm
otic hypotonic high ethanol solutions, appeared nor to be due to changes in
cell viability, nor alterations to energy metabolism. It is proposed that
ion fluxes involved in the maintenance of cell volume, in particular K+ mov
ement, may be important in facilitating normal lymphocyte proliferation in
the presence of ethanol in pathological conditions associated with electrol
yte imbalance.