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-Endorphin1
*
Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901; and
Department of Pharmaceutical Sciences, Cancer Prevention and Research Center, Washington State University, Pullman, WA 99164
The role of 
-endorphin (-EP) in ethanol-altered NK cell
cytolytic activity is studied using male Fischer-344 rats as an animal
model. Ethanol was administered for 1, 2, 3, or 4 wk in a liquid diet
containing 8.7% ethanol (v/v), which means that 37% of the total
calories were derived from ethanol. Rats treated with ethanol for 1 wk
showed an increase in hypothalamic and plasma levels of immunoreactive
(IR)--EP, but displayed no significant effect on NK cell activity
determined by 51Cr release assay, as compared with those in
pair-fed and ad libitum-fed animals. However, animals treated with
ethanol for 2, 3, or 4 wk showed decreased hypothalamic and plasma
levels of IR--EP and decreased splenic NK cell activity. No
significant decrease in the number of splenocytes and NK cells or in
the percentage of NK cells was seen until after 3 and 4 wk of ethanol
treatment. Exposure in vitro of splenic lymphocytes obtained from
control animals to various concentrations of -EP increased NK cell
activity. The opiate antagonist naltrexone blocked the
-EP-stimulated effect. The in vitro NK cell response to -EP was
reduced in the splenocytes obtained from animals treated with ethanol
for 2 wk, but not in those obtained from animals treated with ethanol
for 1 wk as compared with those in control animals. Additionally,
-EP administration into the paraventricular nucleus of the
hypothalamus stimulated NK cell cytolytic activity, whereas the opiate
blocker administration reduced NK cell activity. The NK cell responses
to paraventricular nucleus -EP were reduced in the animals treated
with ethanol for 2 wk. These data provide evidence for the first time
that ethanol inhibits NK cell cytolytic activity, possibly by reducing
-EP-regulated splenic NK cell function.
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