Duodenoesophageal reflux induces apoptosis in rat esophageal epithelium

The esophageal epithelial damage caused by duodenoesophageal reflux was examined by assessing histology, free radicals, and apoptosis in rats with an end-to-side esophagoduodenostomy (reflux group) or sham operation. Rats were sacrificed at 1, 6, or 12 weeks after surgery. Reflux-associated hyperplasia was noted in the reflux group at 6 and 12 weeks. The reflux group manifested glutathione (GSH) overproduction at one and six weeks. Apoptotic cells were detected by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling method. Significantly increased numbers of apoptotic cells were seen on the epithelial surface in the reflux group at 6 and 12 weeks. Duodenoesophageal reflux causes esophageal injury with hyperplasia. Early GSH overproduction indicated that reflux esophagitis may be partly mediated by free radicals. Increased apoptosis may counteract increased proliferation and may be a protective mechanism against increased genotoxic events.