Reflux esophagitis in humans is mediated by oxygen-derived free radicals

: Oxidative stress in reflux esophagitis was investigated before and after antireflux surgery. : Oxidative stress was studied in the distal and proximal esophagus of control patients (without esophagitis, but with other gastrointestinal disorders), of patients with various grades of esophagitis (including Barrettʹs esophagus), and in patients who had a Nissen fundoplication. Oxidative stress was assessed by chemiluminescence, lipid peroxidation (LP), and by measuring superoxide dismutase (SOD). : Chemiluminescence and LP increased with the degree of esophagitis and was highest in patients with Barrettʹs esophagus; SOD decreased with damage, except in cases of Barrettʹs esophagus associated with mild esophagitis. Chemiluminescence and LP in reflux patients were higher in the distal than in the proximal esophagus, and SOD was lower, whereas no such difference was found in controls. Findings after Nissen fundoplication were similar to those of controls. : Reflux esophagitis is mediated by free radicals depleting SOD. Barrettʹs esophagus is a severe form of oxidative damage; in some patients, high SOD levels may prevent severe esophagitis. Antireflux surgery prevents oxidative damage.