Free radical damage in reflux esophagitis of rats induced by 24-hr duo
denojejunal ligation was studied. Oxygen free radicals were selectivel
y blocked. Groups were: sham operation, reflux, reflux + superoxide di
smutase (SOD), catalase, dimethylthiourea, allopurinol, and inactivate
d SOD or inactivated catalase alone or in the combination SOD + catala
se or SOD + catalase + dimethylthiourea + allopurinol. Macroscopic eso
phagitis was inhibited only by SOD, alone or in combination with other
agents. Esophageal mucosal lipid peroxidation was 10-fold increased i
n the reflux group compared to the sham group (P < 0.05). This respons
e was damped by SOD > catalase (P < 0.05) but not by the inactivated e
nzymes, dimethylthiourea or allopurinol. SOD + catalase showed no sign
ificant improvement on SOD alone. Total inhibition of lipid peroxidati
on was achieved by combining all scavengers. Total glutathione (GSH) i
n the esophageal mucosa was stimulated by reflux. This response was in
hibited by scavengers equivalent to their efficacy in preventing lipid
peroxidation. It is concluded that reflux esophagitis is associated w
ith free radical release with O-2(-) being the main source. Free radic
als appear to stimulate GSH production in this prolonged oxidative str
ess.