Reflux esophagitis in humans is mediated by oxygen-derived free radicals.
BACKGROUND
Oxidative stress in reflux esophagitis was investigated before and after antireflux surgery.


METHODS
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 Barrett's esophagus), and in patients who had a Nissen fundoplication. Oxidative stress was assessed by chemiluminescence, lipid peroxidation (LP), and by measuring superoxide dismutase (SOD).


RESULTS
Chemiluminescence and LP increased with the degree of esophagitis and was highest in patients with Barrett's esophagus; SOD decreased with damage, except in cases of Barrett's 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.


CONCLUSIONS
Reflux esophagitis is mediated by free radicals depleting SOD. Barrett's esophagus is a severe form of oxidative damage; in some patients, high SOD levels may prevent severe esophagitis. Antireflux surgery prevents oxidative damage.
D001471:Barrett Esophagus / Q000378:metabolism; D004942:Esophagitis, Peptic / Q000378:metabolism*; D004947:Esophagus / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism*; D018662:Fundoplication; D005753:Gastric Mucosa / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation; D008163:Luminescent Measurements; D018384:Oxidative Stress; D013482:Superoxide Dismutase / Q000378:metabolism
D005609:Free Radicals; D013482:Superoxide Dismutase