Antioxidant enzymes are present in nerves supplying the sphincter of O
ddi and regulate its motor function. Oxygen free radicals (O-2(.-)) pr
oduce hydrogen peroxide (H2O2) by the action of superoxide dismutase (
SOD). Hydroxyl radical (OH.), an important mediator of H2O2 toxicity,
oxidizes ETOH. Thus, the aim of our study was determine the effects of
ETOH on sphincter of Oddi motility. The sphincter of Oddi was removed
from opossums and force transducers recorded tension in its transvers
e axis. Alcohol (ETOH) was added to the tissue bath in concentrations
from 0.1 to 0.4%. OH. was generated by the addition of 0.01% H2O2. Nit
ric oxide production was inhibited by the addition of 0.3 mM N-omega-n
itro-L-arginine (L-NNA). H2O2 increased the frequency of sphincter of
Oddi contractions. Concentrations of ETOH >0.3% decreased contractile
frequency; however, 0.2% ETOH alone had no affect on the basal frequen
cy of contraction but inhibited the increase in contractile frequency
caused by H2O2. L-NNA also increased the contractile frequency; howeve
r, this effect was not inhibited by ETOH. We conclude that ETOH attenu
ates the effect of H2O2 on sphincter of Oddi motility. (C) 1997 Academ
ic Press.