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J. Biol. Chem., Vol. 265, Issue 4, 1946-1951, Feb, 1990
LE Nagy, I Diamond, DJ Casso, C Franklin and AS Gordon
Chronic exposure to ethanol results in heterologous desensitization of
receptors coupled to adenylyl cyclase via Gs, the stimulatory guanine
nucleotide regulatory protein. Ethanol-induced accumulation of
extracellular adenosine is required for the development of heterologous
desensitization (Nagy, L. E., Diamond, I., Collier, K., Lopez, L., Ullman,
B., and Gordon, A. S., Mol. Pharmacol., in press). To understand the
mechanism underlying ethanol-induced increases in extracellular adenosine,
we examined the interaction of ethanol with the adenosine transport system
in S49 lymphoma cells. We found that ethanol inhibited nucleoside uptake
without affecting deoxyglucose or isoleucine transport. Inhibition of
adenosine uptake was due to decreased influx via the nucleoside
transporter. Thus, ethanol-induced increases in extracellular adenosine
appear to be due to inhibition of adenosine influx. After chronic exposure
to ethanol, cells became tolerant to the acute effects of ethanol, i.e.
ethanol no longer inhibited uptake. Consequently, ethanol no longer
increased extracellular adenosine concentrations. Taken together with our
previous studies, these results suggest that ethanol inhibition of
adenosine influx leads to an increase in extracellular adenosine which
causes an initial increase in intracellular cAMP levels and subsequent
development of heterologous desensitization of cAMP signal transduction.
Ethanol increases extracellular adenosine by inhibiting adenosine uptake via the nucleoside transporter
Ernest Gallo Clinic and Research Center, University of California, San Francisco 94143.
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