Effect of hydroxyl radical (OH) on sphincter of oddi motility

Antioxidant enzymes are present in sphincter of Oddi nerves and regulate sphincter of Oddi motor function mediated by NO-releasing nerves. Oxygen free radicals (O./2) produce hydrogen peroxide (H₂O₂) by the action of superox-ide dismutase (SOD). Hydroxyl radical (OH) has been shown to play an important role as a mediator of H₂O₂ toxicity. The aims of our study were to determine the effects of H₂O₂ on sphincter of Oddi motility and if these effects are mediated by OH. Adult opossums were sacrificed and the sphincter of Oddi removed and placed in a tissue bath containing oxygenated Krebs solution. Force transducers recorded tension in a transverse orientation at two sites along the sphincter of Oddi specimen. H₂O₂ was added into the tissue bath at concentrations from 0.01 to 0.5%. O⁻₂ radicals were inhibited by the addition of SOD, while OH was scavenged by the addition of alcohol (ETOH) or dimethyl sulfoxide (DMSO). H₂O₂ produced a dose-dependent increase in baseline amplitude, frequency, and peak amplitude of contractions. The effect of 0.01% H₂O₂ on sphincter of Oddi contractile frequency was inhibited by 0.2% ETOH and DMSO, but not by SOD. We conclude that H₂O₂ has profound effects on sphincter of Oddi motility and that the actions of H₂O₂ are probably mediated through OH.