Abstract
To study the expression of heme-oxygenase-1 (HO-1), an enzyme induced by oxidative stress, in specimens obtained from an experimental model in rats that evaluated the role of gastric and duodenal reflux in esophageal carcinogenesis. Esophageal specimens embedded in paraffin obtained from different experimental groups of rats were used for immunohistochemistry analysis of HO-1 expression. The rats had been divided into the following groups and were killed after 22 weeks: (1) cardioplasty to induce acid reflux; (2) esophagoduodenal anastomosis to induce duodenal reflux; (3) no treatment; (4) cardioplasty + diethylnitrosamine (DEN); (5) esophagoduodenal anastomosis + DEN; and (6) DEN. The study sample comprised 3 specimens from each group with the most severe histopathological lesions found on each study branch. The expression of HO-1 was seen only in rat specimens submitted to esophagoduodenal anastomosis (Groups 2 and 5), and the analysis of mean fluorescence intensity revealed a significant increase of HO-1 expression (4.8 and 4.6 fold, respectively) when compared with the control group (Group 3) (p<0.05). The main target for HO-1 induction was the inflammatory cells inside the tumor or in subepithelial areas. Rats exposed to gastric reflux had no HO-1 expression. Reflux esophagitis induced by reflux of duodenal contents, which provoked considerable oxidative stress, may play an important role in esophageal carcinogenesis. Acid reflux did not induce oxidative stress in this experimental model.
Highlights
Esophageal cancer is the eighth most common cancer worldwide
A total of 100 Wistar rat esophageal specimens embedded in paraffin were available from a previous experimental study conducted in our institution to evaluate histopathological lesions caused by gastric and duodenoesophageal reflux, isolated or in association with diethylnitrosamine (DEN) in an experimental esophageal carcinogenesis model[29]
HO-1 immunoreactivity was evaluated in a sample containing three different esophageal specimens from each group; the specimens selected had the most severe histopathological changes found in each experimental branch
Summary
Esophageal cancer is the eighth most common cancer worldwide. It has received considerable attention in recent years because of the rapid increase of the adenocarcinoma histological subtype in Western countries[1,2]. Chronic reflux is a risk factor for esophageal metaplasia (Barrett’s esophagus) and adenocarcinoma[4,5]. Only 10% of individuals with reflux develop Barrett’s esophagus (BE), and the estimated lifetime risk for a middle-aged individual with BE to develop adenocarcinoma is 10-15%6,7. Factors other than acid reflux alone might contribute to the progression from normal epithelia to BE and cancer. Mixed reflux of gastric and duodenal juices is more common in patients with BE than in normal subjects[8,9]. The precise mechanisms by which duodenal reflux causes esophageal injury and cancer are unclear, but one of the driving forces may be oxidative stress[10,11]
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